Aflatoxin - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

AFLATOXIN A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES J AMES N. ...

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AFLATOXIN A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES

J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS

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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2004 by ICON Group International, Inc. Copyright 2004 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1

Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Aflatoxin: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-497-00034-2 1. Aflatoxin-Popular works. I. Title.

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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.

Copyright Notice If a physician wishes to copy limited passages from this book for patient use, this right is automatically granted without written permission from ICON Group International, Inc. (ICON Group). However, all of ICON Group publications have copyrights. With exception to the above, copying our publications in whole or in part, for whatever reason, is a violation of copyright laws and can lead to penalties and fines. Should you want to copy tables, graphs, or other materials, please contact us to request permission (E-mail: [email protected]). ICON Group often grants permission for very limited reproduction of our publications for internal use, press releases, and academic research. Such reproduction requires confirmed permission from ICON Group International, Inc. The disclaimer above must accompany all reproductions, in whole or in part, of this book.

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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on aflatoxin. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.

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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.

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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes&Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health

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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON AFLATOXIN ............................................................................................... 3 Overview........................................................................................................................................ 3 Federally Funded Research on Aflatoxin ....................................................................................... 3 E-Journals: PubMed Central ....................................................................................................... 23 The National Library of Medicine: PubMed ................................................................................ 44 CHAPTER 2. NUTRITION AND AFLATOXIN ..................................................................................... 91 Overview...................................................................................................................................... 91 Finding Nutrition Studies on Aflatoxin ...................................................................................... 91 Federal Resources on Nutrition ................................................................................................... 99 Additional Web Resources ......................................................................................................... 100 CHAPTER 3. ALTERNATIVE MEDICINE AND AFLATOXIN ............................................................. 101 Overview.................................................................................................................................... 101 National Center for Complementary and Alternative Medicine................................................ 101 Additional Web Resources ......................................................................................................... 121 General References ..................................................................................................................... 123 CHAPTER 4. DISSERTATIONS ON AFLATOXIN ............................................................................... 125 Overview.................................................................................................................................... 125 Dissertations on Aflatoxin ......................................................................................................... 125 Keeping Current ........................................................................................................................ 126 CHAPTER 5. PATENTS ON AFLATOXIN .......................................................................................... 127 Overview.................................................................................................................................... 127 Patents on Aflatoxin .................................................................................................................. 127 Patent Applications on Aflatoxin .............................................................................................. 149 Keeping Current ........................................................................................................................ 151 CHAPTER 6. BOOKS ON AFLATOXIN ............................................................................................. 153 Overview.................................................................................................................................... 153 Book Summaries: Online Booksellers......................................................................................... 153 Chapters on Aflatoxin ................................................................................................................ 154 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 159 Overview.................................................................................................................................... 159 NIH Guidelines.......................................................................................................................... 159 NIH Databases........................................................................................................................... 161 Other Commercial Databases..................................................................................................... 163 APPENDIX B. PATIENT RESOURCES ............................................................................................... 165 Overview.................................................................................................................................... 165 Patient Guideline Sources.......................................................................................................... 165 Finding Associations.................................................................................................................. 167 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 169 Overview.................................................................................................................................... 169 Preparation................................................................................................................................. 169 Finding a Local Medical Library................................................................................................ 169 Medical Libraries in the U.S. and Canada ................................................................................. 169 ONLINE GLOSSARIES................................................................................................................ 175 Online Dictionary Directories ................................................................................................... 175 AFLATOXIN DICTIONARY ....................................................................................................... 177 INDEX .............................................................................................................................................. 229

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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with aflatoxin is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about aflatoxin, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to aflatoxin, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on aflatoxin. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to aflatoxin, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on aflatoxin. The Editors

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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.

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CHAPTER 1. STUDIES ON AFLATOXIN Overview In this chapter, we will show you how to locate peer-reviewed references and studies on aflatoxin.

Federally Funded Research on Aflatoxin The U.S. Government supports a variety of research studies relating to aflatoxin. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to aflatoxin. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore aflatoxin. The following is typical of the type of information found when searching the CRISP database for aflatoxin: •

Project Title: ADDUCT INDUCED FRAMESHIFT MUTAGENESIS Principal Investigator & Institution: Stone, Michael P.; Professor; Chemistry; Vanderbilt University 3319 West End Ave. Nashville, Tn 372036917 Timing: Fiscal Year 2002; Project Start 15-FEB-1992; Project End 31-DEC-2003 Summary: The goal is to understand relationships between conformational perturbations of DNA which has been adducted by endogenous and exogenous

2 Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).

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chemical mutagens, and the subsequent biological processing of adducted DNA, e.g., during error-prone replication. We seek to understand what features of adduct structure promote frameshifts vs. substitutions. Using a frameshift-prone sequence from the Salmonella typhimurium hisD3052 gene, we will examine whether the primary adduct of malondialdehyde, M1G, induces frameshift mutations as a consequence of the ability of duplex DNA to spontaneously ring-open this adduct to its derivative N2-(3-oxo-lpropenyl)-dG. We propose that N2-(3-oxo-l- propenyl)-dG induces/promotes strand slippage structures subsequent to incorporation of dCTP, possibly as a consequence of the positioning of the propenyl moiety in the minor groove of the duplex, fostering dissociation/reassociation of the polymerase due to potential disruption of protein DNA interactions involving the thumb region of the polymerase. We will examine the potential formation of DNA crosslinks by the N2-(3-oxo-l-propenyl)-dG derivative. We will examine why the planar intercalated trans-8,9-dihydro-8-(N7-guanyl)-9hydroxyaflatoxin B1 adduct is not a strong inducer of frameshifts, using the codon 249 sequence of the p53 tumor suppressor gene, which has been linked to human cancer via aflatoxin-induced G yields T mutations. This adduct stabilizes DNA, and perhaps discourages strand slippage intermediates, which we propose reduces the propensity for frameshifts. The adduct may not disrupt minor groove interactions between DNA polymerase and the duplex. We will compare this adduct with its imidazole ringopened derivative, the FAPY adduct, which induces greater stabilization of the DNA duplex. We will examine structural hypotheses to explain the G yields T and G yields A transitions induced by the trans-8,9-dihydro-8- (N7-guanyl)-9-hydroxyaflatoxin B1. A proposed mechanism for the "signature" 5'-neighbor mutation C yields T will be examined. Our working hypothesis posits that the adduct alters or inhibits extension following the correct incorporation of cytosine, possibly by misaligning the primer terminous for further extension. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: AFLATOXIN B1 BIOSYNTHESIS IN ASPERGILLUS PARASITICUS Principal Investigator & Institution: Linz, John E.; Food Science & Human Nutrition; Michigan State University 301 Administration Bldg East Lansing, Mi 48824 Timing: Fiscal Year 2003; Project Start 01-JAN-1991; Project End 31-MAR-2007 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: SYNTHESIS

AFLATOXIN

BIOSYNTHESIS

AND

TYPE

I

POLYKETIDE

Principal Investigator & Institution: Townsend, Craig A.; Professor; Chemistry; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2003; Project Start 01-FEB-1978; Project End 31-MAR-2008 Summary: (provided by applicant): Studies of the potent environmental carcinogen aflatoxin B1 will be continued. This mycotoxin enters the food supply through contamination of grains by the molds Aspergitlus fiavus, A. parasiticus and A. nomius, which produce this compound as a normal metabolite. Chronic ingestion leads to liver tumors that are a major cause of premature death in Asia, Africa and Central America. A direct link has been forged between the interaction of the metabolically activated form of the toxin and DNA, particularly at a "hot spot" in the p53 gene leading to mutation of the encoded protein. Alterations in p53 are associated with ca. 50% of human cancers. An understanding of its biosynthesis presents problems of fundamental interest in

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bioorganic chemistry and may afford means to control the occurrence of this environmental hazard. The investigation has two major goals. The first seeks understanding of fungal Type t polyketide synthases (PKSs)-how iterative function is accomplished, how "programming" is achieved to control polyketide chain length, cyclization geometry and oxidation state. A particularly interesting example of this class lies at the heart of aflatoxin biosynthesis in a complex of the PKS with two specialized yeast-like fatty acid synthase (FAS) subunits in a catalytic complex, NorS. The function of NorS will be examined both in "dissection" experiments using expressed domains of the PKS and FASs, and with the intact recombinant subunits themselves. A newly developed algorithm (UMA) to identify linker regions in multidomainal proteins will guide the experiments to examine function, physical association and structure of domains individually and in groups. The second goal focuses on the three principal oxidative skeletal rearrangement steps that characterize the progression of the biosynthetic pathway from the initially formed anthraquinone to the final substituted coumarin of aflatoxin B1. These are the rearrangement of averufin to l'hydroxyversicolorone, versicolorin A to demethylsterigmatocystin, and Omethylsterigmatocystin to aflatoxin. Gene disruption experiments have identified as many as 3 proteins mediating a single transformation, but in each case a particular cytochrome P450 has been identified. The mechanisms of these reactions are of interest in themselves, and in the broader context of acetogenin biosynthesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ALDO-KETO REDUCTASES AS PART OF CHEMICAL STRESS RESPONSE Principal Investigator & Institution: Barski, Oleg A.; Pediatrics; Baylor College of Medicine 1 Baylor Plaza Houston, Tx 77030 Timing: Fiscal Year 2002; Project Start 17-AUG-2000; Project End 31-JUL-2004 Summary: Aldo-keto reductases provide protection against environmental and nutritional toxins and carcinogens by detoxification of reactive aldehydes capable of modifying cellular macromolecules. Chemical stress induces the expression of a number of detoxification enzymes. Thus, aflatoxin reductase is induced by ethoxyquin and other antioxidants. Recently it was shown that ethoxyquin and antiobiotic tunicamycin also induce aldehyde reductase, another member of the aldo-keto reductase family. A crucial element of the human aldehyde reductase gene promoter binds transcription factor CHOP, which is induced in cells exposed to chemical stress. Preliminary results suggest that CHOP mediates the induction of aldehyde reductase expression and that both aflatoxin and aldehyde reductases are part of the cellular chemical stress response system, hence their expression is induced in response to toxic insult. The application proposes to: a) evaluate the ability of physiologically relevant compounds to induce aldehyde reductase expression and to find out whether induction of both reductases goes through the CHOP-dependent pathway. B) test the compounds of the two major groups: toxic substrates and chemoprotectors that are known to induce aflatoxin reductase and other drug metabolizing enzymes (e.g. glutathione-S-transferase). C) test the Selected stimuli for their ability to induce CHOP. D) determine whether CHOP plays a role in inducing aflatoxin and aldehyde reductase by testing the effect of CHOP overexpression and deficiency, and known CHOP-inducing agents on the of the reductases expression. e) clone and sequence aflatoxin reductase promoter and examine it for a CHOP-binding element and response elements described to direct antioxidant induction in other detoxification genes. Understanding the nature and mechanism of regulation of aldehyde and aflatoxin reductase expression will potentially assist in the

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prevention of harmful and carcinogenic effects of toxic aldehydes as well as provide a basis for identifying populations with increased susceptibility to certain environmental agents. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ANALYTICAL CHEMISTRY CORE Principal Investigator & Institution: Wishnok, John S.; Senior Research Scientist; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 07-APR-1993; Project End 31-MAY-2007 Summary: (provided by applicant): This Core operates as a service, a developmental laboratory, and a resource for the Program Project. Both the overall objectives and the specific aims of the Core laboratories follow primarily from those of the individual projects; e.g., development of methods for identification or quantitation of carcinogennucleic acid adducts, carcinogen-protein adducts, and carcinogen metabolites and/or their conjugates. This includes continued evaluation of capillary HPLC-LIF for quantitation of protein or DNA damage and continued development of capillary HPLC and nanoelectrospray/microelectrospray tandem MS techniques to characterize and quantitate modified proteins or DNA. Development or adaptation of methods to quantitate DNA or protein adducts or urinary levels of PhIP or 2-amino-3,8dimethylimidazo-[4,5-f]quinoxaline (MeIQx) or their metabolites during previous funding periods, for example, was in direct response to the needs of epidemiological studies that evolved into Project 1 in this proposal. Many of the methods listed below were adapted or developed by the Core in this context and some methods, such as quantitation of aromatic amine-hemoglobin adducts by NICI GC-MS have in some cases become the methods of choice for other laboratories that carry out related investigations. The specific aims of the various research projects involve quantitation in urine, physiological fluids or tissue, of DNA and protein adducts of several carcinogens including aflatoxin and aromatic amines and related compounds (e.g., alkylated anilines) and quantitation of urinary excretion of the food-related carcinogen, PhIP, and its metabolites or conjugates. Literature methods are often based on pure or in vitro samples, so methods are developed for the isolation or concentration of low levels of these compounds in complex biological mixtures using, for example, solid-phase extractions or affinity chromatography. Where necessary, for example with tandem MS methods for analyses of modified oligonucleotides, the developmental work is done in the Core laboratories. Specific objectives for additional analyses or techniques include: (1) development and applications of ultrasensitive MS methods for nucleobase and deoxyribonucleoside adducts; (2) development and applications of HPLC-LIF methods for quantitation of derivatized adducts; and (3) transfer of HPLC-LIF technology to the Johns Hopkins University (Project 1 and Core). Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: BIOLOGICAL MARKERS OF AFLATOXIN EXPOSURE Principal Investigator & Institution: Santella, Regina M.; Professor; Environmental Health Sciences; Columbia University Health Sciences Po Box 49 New York, Ny 10032 Timing: Fiscal Year 2002; Project Start 01-JAN-1990; Project End 30-JUN-2005 Summary: (provided by applicant): This project will continue to focus on the identification of environmental and genetic risk factors for development of hepatocellular carcinoma (HCC) in Taiwan. We have demonstrated that, in conjunction with hepatitis B or C virus (HBV and HCV) infection, aflatoxin B1 (AFB1), 4-

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aminobiphenyl, and polycyclic aromatic hydrocarbons (PAH), increase HCC risk. Synergistic interactions between virus and chemical were also observed. Deletion o glutathione S-transferase M1(GSTM1) further increased risk in exposed subjects. The current proposal will focus on a case-control study nested in a cohort established by our collaborator Dr. Chien Jen Chen in which 25,611 subjects were recruited and a total of approximately 350 HCC cases will be identified by the end of the next four years. We will analyze blood samples from cases and controls for urinary aflatoxin metabolites and AFB1- and PAH-albumin adducts as markers of exposure. We will also begin to investigate the role of oxidative stress in risk for HCC by analyzing for variants in genes that encode enzymes with pro-oxidant and anti-oxidant activities. damage from ROS and carcinogenic metabolites that are not detoxified may be prevented from contributing to carcinogenesis by DNA repair; thus, we will extend our investigation of genetic susceptibility to DNA repair genes in the base excision and nucleotide excision repair pathways. We hypothesize that cases will more frequently be carriers of "higher risk" alleles than controls and that there will also be an interaction between environmental exposures and genotype. Finally, we will carry out a small exploratory study to determine whether tumor DNA can be detected in plasma of HCC cases. Other studies have demonstrated that tumor DNA circulating in blood contains the same genetic alterations as are found in the tumor. We will begin to investigate this phenomena in our HCC cases specifically looking at p.53 mutations and methylation of p16. These pilot studies will allow us to determine whether tumor DNA can be found at a high enough frequency to be useful in diagnosis and studies of etiology, when in the cancer process they are detectable. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BIOSTATISTICS/EPIDEMIOLOGY CORE Principal Investigator & Institution: Munoz, Alvaro; Associate Professor; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 07-APR-1993; Project End 31-MAY-2007 Summary: (provided by applicant): During the previous 2 cycles of this Program Project on "Molecular Biomarkers for Environmental Carcinogens," the investigators have established close links with the Projects which have led to several publications. As part of the renewal of the Program Project, they will continue to collaborate with investigators of Projects in the Program Project for the design of studies using specimens collected as part of previous studies, for the analysis of data, and for the development of methods relevant to the issues of the research Projects. The design and analysis of the experiments and studies to be conducted under the auspices of the Program Project will benefit by the inclusion of expertise in biostatistics and epidemiology. The specific aims of the Biostatistics/Epidemiology Core are: (1) To establish methods that promote adherence to standard protocols with particular attention to data collection and management. The Biostatistics/Epidemiology Core will assist with the selection of appropriate samples for testing; monitor data entry; implement data editing procedures design a data base to expedite analysis and linkage of the different projects; and establish systems for data security and backup. (2) To collaborate with investigators in the Projects of the Program Project for the purpose of data analysis. Data from the projects will require the implementation of multivariate (e.g., exposure to aflatoxin, HBV status and p53 mutation on codon 249) regression methods for analyses of longitudinal data and for binary and continuous outcomes. Furthermore, they will use methods for the evaluation of treatments administered in clinical trials using changes of biomarkers as the primary outcome measure. (3) To develop new statistical methods

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appropriate for the data generated by the Projects which will allow for testing and estimating parameters relevant to the specific aims of the Program Project. First, they will investigate the use of sequential designs to minimize sample testing. Second, a salient feature of the data from the proposed Projects is that most biomarkers will be a mixture of discrete (% undetectable) and continuous (level among those detectable) components. Methods that treat the data as left censored, as opposed to assigning all undetectable observations a given value, are preferred and will be developed and implemented as part of this application. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CATALYTIC AND STEREOSELECTIVE C-C BOND FORMING REACTION Principal Investigator & Institution: Hoveyda, Amir H.; J. T. & P. Vanderslice Millennium Profes; Chemistry; Boston College 140 Commonwealth Ave Newton, Ma 02467 Timing: Fiscal Year 2002; Project Start 01-MAY-1992; Project End 30-APR-2005 Summary: (Applicant's Description) Efficient and selective preparation of organic molecules is critical to the synthesis of therapeutics. Thus development of catalytic and stereoselective addition of alkylmetals to olefins stands as an important objective. Catalytic olefin alkylation offers a practical and inexpensive route for synthesis of C-C bonds; these reactions require readily available substrates and alkylmetals. A catalytic enatioselective version would be most useful especially if it were to afford molecules that are readily amenable to further functionalization. Similar to carbomagnesation, the reactions proposed herein are Zr-catalyzed, but they proceed by an entirely different mechanism and will be significantly more general. In catalytic carbometalations reported to-date, the alkyl group of the alkyl metal is typically incorporated within the final product; here it is the alkyl moiety of an electrophilic reagent that is transferred to the product. Thus, the new Zr-catalyzed reactions are unusual: there is efficient reaction between the alkene substrate and the electrophile, but there is little or no reaction between the alkylmetal and the electrophile. The following specific objectives will be pursued: I. Development of regio- and stereoselective Zr-catalyzed alkylation and carbometalation of olefins with alkyl electrophiles. Mechanistic evidence from our previous studies will be used to develop unique methods for catalytic regio- and diastereoselective synthesis of C-C bonds. These transformations offer a new approach to C-C bond formation, where readily available olefinic substrates, alkylmetals and electrophiles can be used. II. Development of diastereoselective intramolecular Zrcatalyzed electrophilic alkylations and carbometalations. The intramolecular version of the Zr-catalyzed alkylation should allow for an unprecedented and efficient synthesis of various carbo- and heterocycles with high regio- and diastereoselectivity. III.Development of Zr-catalyzed enantioselective electrophilic alkylations and carbometalations. We will develop a catalytic and asymmetric alkylation and carbometalation of olefins with various electrophiles. These transformations offer unique and selective routes to the enantioselective synthesis of easily functionalizable molecules. The utility of the new methods will be demonstrated by synthesis of anticancer LY300502, antispastic baclofen, anti-fungal aflatoxin B2, antidepressant gemfexine and anti-leukemic helianane. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CHEMOPREVENTION OF GREEN TEA POLYPHENOL ON LIVER CANCER Principal Investigator & Institution: Wang, Jia-Sheng; None; Texas Tech University Box 42013 Lubbock, Tx 79409 Timing: Fiscal Year 2003; Project Start 16-JUN-2003; Project End 31-MAY-2008 Summary: (provided by applicant): The long-term goal of this revised application is to design effective prevention strategies for reducing the incidence of liver cancer in highrisk populations. Primary liver cancer, mainly hepatocellular carcinoma (HCC), is one of the most common cancers in Asia and Africa. The poor prognosis of this malignancy results in it being the third most common cause of cancer deaths in the world. Chronic infection with hepatitis B viruses (HBV) and dietary aflatoxin exposure are two major etiologic risk factors for HCC in high-risk areas. The great challenge in cancer prevention and control is how to manage those who have already been exposed to carcinogens, such as individuals who are HBsAg carriers and have long-term aflatoxin exposure. Chemoprevention has been proposed as the good tool to target these high-risk populations. Among various identified chemopreventive agents, green tea polyphenols (GTP) have been shown to be safe and high effective in inhibition of carcinogen-induced mutagenesis and tumorigenesis in bioassays and animal models for different target organ sites, including aflatoxin-induced liver tumors. The specific aims for this study are (1) to incorporate molecular biomarkers analysis for aflatoxin exposure, HBV infection, and oxidative DNA damage into an on-going randomized, double blinded, and placebocontrolled intervention trial of GTP in 1,800 residents who are double seropositive of HBsAg and aflatoxin-albumin adduct in Fusui County, Guangxi Zhuang Autonomous Region, People's Republic of China; efficacy of the chemopreventive trial will be determined by monitoring changes of levels of risk-factor specific molecular biomarkers and the actual incidence of HCC in the studied population. (2) to examine and assess the efficacy of GTP in reducing aflatoxin biomarkers by measuring aflatoxin-albumin adducts in serum and various aflatoxin biomarkers in urine collected from 300 participants in different time of the study. Difference in metabolic phenotypes/genotypes as they related to aflatoxin biomarker levels will be determined. (3) to evaluate the inhibitory effect of GTP on HBV-associated markers including HBVDNA replication and HBV-induced immunologic changes in serum samples. (4) to determine antioxidative role of GTP in inhibition of the level of 8-hydroxy-2'deoxyguanosine in urine samples collected from the study participants and (5) to determine and assess long-term bioavailability and biotransformation of GTP and the long-term toxicological effect of GTP on study participants. The results of this study would help to evaluate the chemoprotective effect of GTP against human HCC and to understand the molecular mechanisms of GTP in chemoprevention of human HCC caused by well-defined major risk factors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CHLOROPHYLLS AS TRANS-SPECIES BLOCKING AGENTS Principal Investigator & Institution: Bailey, George S.; Distinguished Professor & Center Directo; Oregon State University Corvallis, or 973391086 Timing: Fiscal Year 2003; Project Start 17-MAR-2003; Project End 28-FEB-2008 Summary: This Project aims to compare in depth the mechanisms and dose-response characteristics for two plant-based blocking agents, native chlorophyll (Chla) and its derivative Cu-chlorophyllin (CHL). Our working hypothesis is that these agents act in vivo primarily via strong non-covalent complexation with carcinogens having

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Aflatoxin

complementary planar aromatic structure, thereby reducing carcinogen uptake and systemic bioavailability. Though CHL studies have progressed to an initial clinical intervention trial against aflatoxin B1 (AFB1), its mechanisms against this and other carcinogens are not fully defined. We recently showed native Chla to also strongly reduce dibenzo(alpha,1)pyrene (DBP)-DNA adduction in trout, but beyond this promising result, almost nothing is known of Chla chemoprevention in vivo. Finally, since few if any blocking agents are 100% effective, additional strategies are needed to fully abrogate the effects of genotoxins such as AFB1 and DBP. To address these issues we use 5 models: AFB1 hepatic tumors in rats; AFB1 hepatic tumors in trout; the trout multi-organ DBP model; DBP rat mammary tumors; and human 14C-AFB2 exposures. AIMS 1A-C compare CHL and Chla efficacy in four tumor models, including a 10,000 trout dose-dose matrix design to test the molecular dose hypothesis that Chla-mediated reduction in DNA adduct biomarkers quantitatively predicts tumor outcome over all DBP doses. AIM 1D investigates CHL and Chla effects on AFB2 uptake in humans. AIM 2 compares CHL and Chla protective mechanisms, both systemic (complex stoichiometry and stability; degree and specificity of effects on carcinogen pharmacokinetics; predictivity of complex Kd on CHL efficacy) and cellular (P450 inhibition; electrophile destabilization). AIM 3 investigates combined chemoprevention as a strategy to supplement the incomplete blocking effects of chlorophylls. It examines initiator-specificity and basic mechanisms of tumor suppression in trout, and establishes quantitative interactions between CHL as a blocking agent and ellagie acid (EA) or tea catechins as suppressing agents in the trout stomach tumor model. It provides the first dose-dose matrix quantification of tumor suppression ever conducted, and provides a model to establish rigorously if CHL blocking and EA/tea suppression are synergistic in combined chemoprevention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CHROMOSOMAL CARCINOGENS

PROBES

FOR

MUTAGENESIS

BY

Principal Investigator & Institution: Essigmann, John M.; Professor of Chemistry & Toxicology; Division of Toxicology; Massachusetts Institute of Technology Room E19750 Cambridge, Ma 02139 Timing: Fiscal Year 2002; Project Start 01-JUL-1998; Project End 30-JUN-2003 Summary: The stated goal of the work is to investigate the mechanisms by which sample alkylating agents and the potent human live carcinogen aflatoxin induce mutations. Natural bases in the genome of viruses of plasmids will be replaced by DNA adduct known to be formed by alkylating agents and by aflatoxin. The genomes containing adducts at specific sites will be constructed by using a combination of chemical synthesis and recombinant DNA techniques. Following their construction, the modified genomes will be introduced into bacterial or mammalian cells, where the adducts will be exposed to and processed by the natural repair and replicative systems of the host. Progeny will be isolated and characterized for the type and frequency of mutation induced at or near the original site of the adduct. The genetic requirements for mutagenesis will be characterized, as will the ability of the adduct to affect survival. This study can help to rank the genetic threats posed by the various DNA adducts formed by DNA-damaging agents. With aflatoxin, the hypothesis being tested is that some feature of the mutational spectrum of aflatoxin will correlate with the type of mutations induced by one or more of the DNA adducts. With alkylating agents, previous work has defined the types of mutations induced by the most mutagenic adducts. The field has now progressed to a deeper level of biochemical detail, in which

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probing the extent to which the context (the neighboring sequence of nucleotides) of a lesion determines the likelihood that the lesion will be repaired or mutate. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: COLON ACETAMINOPHEN

AND

LIVER

ANTICARCINOGENICITY

BY

Principal Investigator & Institution: Williams, Gary M.; Professor; Pathology; New York Medical College Valhalla, Ny 10595 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-AUG-2005 Summary: (provided by applicant): The overall objective of the proposed research is to examine the hypothesis that phenolic compounds can act as anticarcinogens at low levels by blocking the cellular effects of carcinogens that operate as reactive electrophiles. In testing this hypothesis, we will conduct a series of in vivo studies in rats with the widely used analgesic acetaminophen (APAP), which has demonstrated anticarcinogenic properties in colon. As model carcinogens in the rat, 3,2'-dimethyl-4aminobiphenyl (DMAB) and 2-amino-3-methyl-3H-imidazo [4,5-f]quinoline (IQ) will be used to produce a moderate level of initiation in rat colon as well as liver. We will establish the ability of low levels of APAP to inhibit the early carcinogen-induced effects that underlie initiation of colon and liver carcinogenesis, such as enhanced cell proliferation, decreased apoptosis and induction of preneoplastic lesions, and will study the mechanism(s) of this inhibition, focusing on blocking of intracellular reactivity of the carcinogens (i.e., adduct formation). These experiments will be pursued in three specific aims as follows: 1. Define low doses of the carcinogens 3,2'-dimethyl-4-aminobiphenyl (DMAB) and 2-amino-3-methyl-3H-imidazo[4,5-f]quinoline (IQ) that produce a moderate level of initiation in rat colon and liver to be studied for inhibition by low levels of APAP; 2. Establish the dose responses for inhibition of carcinogen-induced initiation by low levels of APAP against selected doses of carcinogens in order to determine conditions for mechanistic studies and 3. Determine whether low levels of APAP inhibit initiation by reduction of formation of IQ DNA adducts in order to gain insight into potential mechanisms of anticarcinogenicity. These experiments will provide the basis for future studies of prophylaxis against human carcinogens, such as aflatoxin B1. In addition, these experiments will provide support for the epidemiological observations of reduced cancer risk associated with the use of APAP. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CPG METHYLATION AND MUTATION Principal Investigator & Institution: Pfeifer, Gerd P.; Professor; City of Hope National Medical Center Duarte, Ca 91010 Timing: Fiscal Year 2002; Project Start 01-JUL-2000; Project End 30-JUN-2004 Summary: Mutations in p53 from different human cancers show mutagenic patterns that are presumed to provide insight into mutagenic mechanism. mC->T mutations are prominent in colon cancer, breast cancer and leukemias and are generally thought to be due to spontaneous deamination of m5C. In lung cancer there is a preponderance of G>T mutations in the non-transcribed strand of p53, which is reminiscent of mutagenesis by bulky agents, notably polycyclic aromatic hydrocarbons (PAHs) such as benzo[a]pyrene (BP). In liver cancer, which is associated with aflatoxin B1 (AFB1) exposure, there is an extraordinary hotspot (a G->T mutation at codon 249) in p53. The PI and collaborators have been involved in several significant studies, including one showing that slow DNA repair of UV damage correlated with skin cancer hotspots in

12

Aflatoxin

p53, and hotspots for BP adduction (and slow DNA repair) correlated with lung cancer hotspots in p53. Such correlations are consistent with (but not proof of) a role for these etiological agents in carcinogenesis involving p53 mutations. In this proposal, the PI wishes to investigate these associations at a deeper level by studying the effect of adduction hotspots and differential repair directly on mutagenesis (using a variety of assays) by a number of agents. The focus will be on the mechanism of CpG mutational hotspots associated with the presence of m5C. The PI proposes three specific aims. (1) Sites for DNA adduct formation, repair and mutagenesis with BP and AFB1 will be determined in a single system (fibroblasts from the Big Blue mouse having a lacI mutational target). (2) UV-, BP- and AFB1-induced mutations in a yeast p53-containing vector system will be collected and compared to p53 mutations from human tumors. (3) The PI will investigate whether C->T hotspots at CpGs might be due to one of four endogenous mutagens, which might generate mutations preferentially at m5C residues. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DIETARY FACTORS IN THE ETIOLOGY OF CANCER IN SHANGHAI Principal Investigator & Institution: Ross, Ronald K.; Professor; Preventive Medicine; University of Southern California 2250 Alcazar Street, Csc-219 Los Angeles, Ca 90033 Timing: Fiscal Year 2002; Project Start 01-APR-1987; Project End 30-JUN-2002 Summary: (Adapted from the Applicant's Abstract): We are requesting continued support for an ongoing cohort study of 18,244 men, ages 45-64, living in a geographically defined area of metropolitan Shanghai, Peoples Republic of China. All cohort members have completed detailed diet and medical histories and have blood and urine samples. Questionnaires have been edited and computerized and blood and urine samples have been processed, aliquoted, and continuously stored at both -20_C and 70_C. The cohort was fully established in 1989. Follow-up of the cohort is proceeding through cancer registration by the population-based Shanghai Cancer Registry, by routine ascertainment of death certificates, and by annual recontact of all cohort members. As of March 1994, 606 have developed cancer and 989 have died. The leading cancers include lung, stomach, liver, and colorectal cancers, while stroke is the number one cause of death. Major accomplishments achieved through this cohort to date include: (1) the first direct evidence linking aflatoxin ingestion to human hepatocellular carcinoma (HCC); (2) strong evidence of synergy between aflatoxin biomarkers and chronic infection with hepatitis B virus in establishing risk of HCC; (3) failure to find an association between H. pylori serology and stomach cancer risk; (4) the absence of an inverse association between antioxidants and fatal stroke; and (5) the first comprehensive and systematic evaluations of smoking-related cancer incidence and mortality in China. We propose to continue to follow this cohort for an additional five years. We will continue to evaluate risk factors for major health outcomes in the cohort, building on previous observations and continuing to exploit the serum and urine banks available for biomarker studies. Although we did not collect buffy coats for genetic studies on cohort members, we have demonstrated that the stored serum samples contain sufficient cells for conducting selected PCR-based genetic studies. Among the scientific goals for the next five years are: (1) to continue to evaluate the aflatoxin/HCC association and to assess the impact of sequence variations in genes involved in aflatoxin metabolism (GSTM1 and EPHX) in modifying risk; (2) to continue to assess the role of H. pylori in gastric cancer etiology in Shanghai, and to assess the possible protective effect of tea polyphenols on risk; and (3) to better understand the complex interrelationships among carotenoids, smoking, and lung cancer and to assess the

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possible risk modifying impact of genes involved in metabolism of smoking-related carcinogens. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EPIDEMIOLOGY OF HEPATOCELLULAR HEPATITIS B VIRUS IN 3 POPULATIONS

CARCINOMA

&

Principal Investigator & Institution: London, W. Thomas.; Senior Member; Fox Chase Cancer Center Philadelphia, Pa 191112434 Timing: Fiscal Year 2002; Project Start 01-APR-2001; Project End 31-MAR-2003 Summary: (Applicant's Description) Prospective studies of 60,984 men in Haimen City, China and 19,469 men in Senegal, west Africa revealed a 14-fold greater death rate from hepatocellular carcinoma (HCC) among the Haimen (168 per 100,000) than the Senegalese cohort (12 per 100,000). Even though chronic infection with hepatitis B virus (HBV) is the major risk factor for HCC in both populations, the age-adjusted prevalence of chronic infection is about 20% in both cohorts. Exposure to aflatoxin, a postulated major risk factor for HCC, is also similar or greater in the Senegalese population. The prevalence of viremia (HBV DNA in serum) among HBV carriers throughout adult life, however, is much higher among the Chinese than the Senegalese population. Nevertheless, within the Chinese cohort, viremia at study entry is not a risk factor for HCC after four years of follow-up. The aims of this project focus on factors that may account for variation in HCC risk in the Chinese and Senegalese cohorts and a cohort of Asian-American HBV carriers living in the Philadelphia area. Continued tracking of these three cohorts will test the hypothesis that with longer duration of follow-up, H B V v iremia and liver damage at study entry are associated with person-specific risks of HCC and that aflatoxin-B1 (AFB1)-albumin adducts are a s s ociated with development of HCC among viremic individuals and/or genotypically determined poor detoxifiers of AFB1 (in collaboration with Project 2). In close cooperation with the studies of WHV in woodchucks (Project 3), an intensive longitudinal study of 1000 male and female HBV carriers in these three populations will be conducted to: a) examine whether perturbations of the stability of HBV serum markers are associated with acute illnesses, aflatoxin exposure, and/or outgrowth of viral mutants; b) assay hepatocyte turnover and immune responses in liver biopsies; c) correlate these measures with viral load; d) examine the relationship of sex differences in changes in HBV serum markers over time to the lower HCC risk of female HBV carriers. Because present studies show that an episode of acute hepatitis in adulthood approximately doubles HCC risk among both HBV carriers and non-carriers, the causes and outcomes of 200 cases of acute hepatitis in Haimen City will be characterized. This research will lead to a new level of understanding of the factors that lead to HCC and to new strategies for the prevention of this lethal disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GENETIC EPIDEMIOLOGY OF PRIMARY HEPATOCELLULAR CARCINOMA Principal Investigator & Institution: Buetow, Kenneth H.; Chief; Fox Chase Cancer Center Philadelphia, Pa 191112434 Timing: Fiscal Year 2002 Summary: The risk of common cancer is produced through gene-gene, and/or geneenvironment interactions. These interactions are poorly understood for most cancers in part due to the diversity and complexity of the exposures. Primary hepatocellular

14

Aflatoxin

carcinoma (HCC) represents a unique opportunity to investigate a complex cancer phenotype in humans. Epidemiologic studies have firmly established the role of chronic hepatitis B virus infection (HBV) and aflatoxin B1 (AFB1) exposure as environmental risk factors. These exposures are well described and are amenable to exposure assessment. it is therefore conceptually possible to examine their relationship to host genetic constitution in determining HCC susceptibility. Significant progress has been made during the current funding period toward understanding the genetic components of the HCC complex phenotype. Statistical analyses has demonstrated familial aggregation consistent with genetic susceptibility of HCC. Comprehensive genomewide allele loss studies have identified multiple regions which could contain novel tumor suppressor genes. An interaction between host genetic constitution, HBV/AFB1 exposures, and HCC was established in c case-control study and confirmed in a cohortderived study population. It is the goal of the of the current application to continue the integrated genetic epidemiologic analysis of HCC. Familial aggregation of HCC and its relationship to HBV and AFB1 exposure will be examined in a significantly expanded collection of families. Comparative genome hybridization (CGH) will be added to permit the localization of putative tumor suppressor genes and oncogenes. Regions observed to have high frequency changes in tumors will be studied by genetic mapping methods to assess their role in familial transmission. The role of genetic variability in candidate genes that modulate responses to HBV infection and AFB1 exposure will be assessed. This will be accomplished by expressing human xenobiotic metabolizing P450 cDNAs and their polymorphic variants in Saccharomyces cerevisiae and determining which ones in combination with AFB1 cause genetic alterations. Human gene mapping methods using a family-based case-control population will be used to test the role polymorphic variants of candidate AFB1 metabolizing loci in HCC. The influence of lipotrope insufficiency and genetic variability in lipotrope metabolism to HCC related end-points will be assessed. Finally, the interaction of major susceptibility genes, risk modifying loci, and environmental exposures and their role in determining risk and familial aggregation will be examined. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GLOBAL RESPONSES TO AFLATOXIN B1 & ALKYLATING AGENTS Principal Investigator & Institution: Samson, Leona D.; Professor; Biomedical Engineering; Massachusetts Institute of Technology Room E19-750 Cambridge, Ma 02139 Timing: Fiscal Year 2002; Project Start 30-SEP-2001; Project End 31-JUL-2006 Summary: (provided by applicant) In response to RFA:ES-01-002, this is an application to become a member of the NIEHS-sponsored Toxicogenomics Research Consortium. The have proposed a highly integrated plan to explore the transcriptional responses of a variety of organisms, including humans, to a broad range of toxic agents found in the environment. Transcriptional profiling is expected to reveal a truly global view of how cells, tissues and animals attempt to recover, not always successfully from environmental insults. The investigators hope to learn what features of environmentally induced transcriptional responses are predictive of success or failure, and in addition to learn what features correlate with specific outcomes of toxic exposures, for instance, cell death, apoptosis, mutagenesis and carcinogenesis. The model environmental agents to be studied are Aflatoxin B1 and its metabolites, plus a range of SNI and SN2 alkylating agents. Together these agents are representative of toxic agents found in the external environment, food supply, the endogenous cellular environment, and the cancer chemotherapy clinic. The model organisms and cell systems whose transcriptional

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responsiveness will be scrutinized include E. coli, S. cerevisiae, cultured rodent and human cell lines, engineered rat and mouse liver tissues, rats and mice. The investigators have integrated an in vitro tissue engineering Project into this application with the goal of developing an alternative to using animals to test for toxicity and carcinogenicity. It seems to the investigators that appropriate transcriptional responsiveness in this system represents a rigorous test of its similarity to in vivo tissues. Two platforms for mRNA profiling will be employed, namely, Affymetrix GeneChip DNA oligonucleotide microarrays, and cDNA arrays fabricated in the MIT BioMicro Center. The Microarraying and Bioinformatics Core will have its center of gravity in the MIT BioMicro Center, and this Core will serve as the focal point for three Research Projects and the Toxicology Research Core Project (TRCP). The TRCP activities will be closely aligned with the activities of the other 4 or 5 members of the Toxicogenomics Research Consortium. Together the overarching goals will be to establishing good working practices in transcriptional profiling as it relates to the area of toxicogenomics, and to contribute to the development of an extensive relational database as a repository for high quality data emerging from the field of toxicogenomics. The investigators anticipate that this research will uncover a myriad of hitherto unknown ways in which cells respond to environmental agents. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: HEPTOCYTE PROLIFERATION AND AFLATOXIN METABOLISM Principal Investigator & Institution: Sell, Stewart; Professor; Pathology and Lab Medicine; Albany Medical College of Union Univ Albany, Ny 12208 Timing: Fiscal Year 2002; Project Start 01-APR-2000; Project End 31-MAR-2003 Summary: The hypothesis that continued proliferation of hepatocytes is associated with an transgenic immature phenotype in regard to metabolism of aflatoxin (AFB1) and development of hepatocellular carcinoma (HCC) will be analyzed in p53 null and p53ser246 mutant transgenic, and HBV mice. World-wide HCC is arguably the tumor that causes the highest cancer mortality. HCCs occurring in high-risk areas of the world are associated with continued proliferation of liver cells in response to liver injury (HBV and HCV), and with aflatoxin (AFB1) exposure. AFB1/HBV associated HCCs have a high frequency of mutations in the tumor suppressor gene p53 at codon 249 (p53ser249). Recently we reported that hepatocytes of p53 null mice continue to proliferate into adulthood and do not become polyploid with aging. In addition, hepatocytes of p53ser246 transgenic mice (equivalent to p53ser249 of humans) maintain a high number of cells in G1. P53 null and p53ser246 mice also have increased susceptibility to AFB1 hepatocarcinogenesis when the carcinogen is administered during the first week of life, and HBV transgenic mice are susceptible to AFB1 carcinogenesis, even when the carcinogen is administered at one month of age when normal mice of the same strain are resistant. We wish to test the hypothesis that the changes in status of cells in the livers of these mice reflects a less-differentiated phenotype associated with increase production of carcinogenic metabolites and increased risk of HCC development in adult mice. In specific aim 1, the metabolism of AFB1 at different ages of normal and transgenic mice will be examined by AFB1 epoxide and adduct formation, glutathione-s-transferase activity and p450 isoenzyme distribution. In addition, oval cells or small hepatocytes will be isolated from cocaine-treated mice and from neonatal and adult transgenic livers to determine if there is distinctive metabolism of AFB1 in these cells. The effect of proliferation of "mature" hepatocytes will be determined using microsomes from partially hepatectomized livers, and metabolism of AFB1 by cultured liver cells at different stages of differentiation will be examined. In Specific Aim 2, AFB1 will be

16

Aflatoxin

administered after one month (when normal mice are not susceptible to carcinogenesis) to p53+/- hemizygous mice, to p53-/- null mice, to p53ser246 hemizygous and homozygous transgenic mice, and to F1 mice of p53ser246 mice cross-bred to p53 null mice and the development of HCC determined. the effect Of HBV associated injury and AFB I hepatocarcinogensis in these mice. In Specific Aim 3, the effect of HBV associated injury and AFB1 hepatocarcinogenesis in these mice will be examined. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MECHANISM OF CELL DEATH INDUCED BY AFLATOXIN B1 Principal Investigator & Institution: Kosa, Jessica L.; Division of Toxicology; Massachusetts Institute of Technology Room E19-750 Cambridge, Ma 02139 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-MAY-2003 Summary: (Adapted from the Applicant?s Abstract): The goal of this study is to determine how aflatoxin B1 (AFB1) kills hepatocytes. First, I shall probe the sequence of biochemical events that leads to liver cell death. Seond, since aflatoxin is believed to exert its biological effects by inflicting DNA damage, I shall determine which of the several types of DNA damage induced by aflatoxin induces the pattern of gene expression that precedes death. Third, I shall screen for novel genes whose mRNA levels change during AFB1-induced cell death, employing a DNA microarray approach. Apoptosis is the mechanism by which the liver eliminates pre-neoplastic cells, and is known to be induced by AFB1 in transformed liver cells. Initial experiments will test the hypothesis that apoptosis is responsible for the cytotoxicity of AFB1. Expression of genes know to participate in apoptosis is responsible for the cytotoxicity of AFB1. Expression of genes known to participate in apoptosis will be examined by quantitative RT-PCR in order to identify the specific pathways involved in the induction of apoptosis, thereby establishing which genes are vulnerable to oncogenic mutations. Primary rat hepatocytes will be employed in order to model in vivo AFB1 exposure realistically. In order to pinpoint the molecular pathway from DNA damage to cell death, DNA containing the AFB1-induced lesions AFB1-N7-Gua, AFB1-FAPY, and AP sites will be introduced into hepatocytes. The impact of each lesion on cell death, and apoptosis gene expression, will be measured to determine which specific DNA adduct(s) induce cell death. Finally, a microarray of rat genes will be constructed and used to search for novel genes that are induced or repressed during AFB1-induced cell death. Genes whose expression is altered by AFB1 exposure, and especially those that appear to be co-regulated with known apoptosis genes, are likely to participate in the cellular response to the toxin. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

•

Project Title: MITOCHONDRIAL DNA DAMAGE AND REPAIR Principal Investigator & Institution: Bogenhagen, Daniel F.; Professor; State University New York Stony Brook Stony Brook, Ny 11794 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2003 Summary: Mitochondrial DNA is a frequent target of chemical damage. Base loss, oxidative damage and reaction with carcinogenic compounds such as benzo(a)pyrene and aflatoxin are thought to occur at rates equal to or greater than the corresponding rates of damage to nuclear DNA. Mitochondria are able to repair some types of DNA damage, such as abasic sites and oxidative lesions (e.g., 8-oxo-dG), but probably not others. Very little is known concerning the enzymology of DNA repair in mitochondria. Replication through DNA adducts or attempts at repair may contribute to the incidence

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of point mutations and deletions observed in a growing list of human diseases. These diseases range from point mutations associated with rare neuromuscular diseases identified with the acronyms MELAS, MERRF, and NARP to large deletions observed in Kearns Sayre Syndrome. Recent studies have found a correlation between mtDNA damage and type 11 diabetes, Parkinson's disease and aging, although more research is required to establish a role for mtDNA damage in the etiology of these conditions. We propose to investigate the effects of specifically localized lesions in DNA templates prepared by our collaborators in this project on DNA replication by the purified mitochondrial DNA polymerase gamma. These studies will employ templates containing abasic sites, 8-oxo-dG, aminofluorene and benzo(a)pyrene adducts. We will also search for accessory factors that may facilitate translesional synthesis by DNA polymerase gamma. We propose experiments to characterize enzymes involved in mtDNA repair and to attempt to reconstitute repair of abasic sites or 8-oxo-dG lesions in mtDNA. Certain lesions, such as cyclobutane pyrimidine dimers in mtDNA are not thought to be repaired efficiently. We will attempt to increase the efficiency of repair by using molecular genetic techniques to direct repair enzymes such as photolyase or T4 endonuclease (denV) to mitochondria. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: MOLECULAR FUNGITOXICANTS

MODE

OF

ACTION

OF

SELECTED

Principal Investigator & Institution: Thompson, Dorothy P.; Southern Univ A&M Col Baton Rouge College Baton Rouge Baton Rouge, La 70813 Timing: Fiscal Year 2002 Summary: This abstract is not available. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NEUTROPHILS AND HEPATOTOXICITY Principal Investigator & Institution: Roth, Robert A.; Professor; Pharmacology and Toxicology; Michigan State University 301 Administration Bldg East Lansing, Mi 48824 Timing: Fiscal Year 2002; Project Start 15-JUN-1986; Project End 31-MAR-2004 Summary: (Adapted from the investigator's abstract). The overall goal of the proposed research is to understand how the inflammatory response to gram-negative bacterial endotoxin (lipopolysaccharide, LPS) acts as a determinant of susceptibility to intoxication by xenobiotic agents. In concert with this goal, the major focus of this proposal is to understand the role of the neutrophil in LPS-induced amplification of hepatotoxic responses to xenobiotic agents. Evidence has emerged indicating that exposure to small, nontoxic amounts of LPS is an important determinant of the magnitude of response to several hepatotoxicants. Experiments in the first specific aim will determine in rats whether LPS influences the response to chemicals (e.g., aflatoxin B1, monocrotaline) that initiate hepatotoxicity by different mechanisms and produce different lesions. Neutrophils activated in tissues are likely to play an important role in the mechanism by which LPS amplifies hepatotoxic responses, and Aim 2 will address this hypothesis in vivo and in a co-culture system of neutrophils and hepatocytes (HCs). Previous studies indicate that activated neutrophils damage hepatic parenchymal cells (HCs) through the release of toxic proteases such as cathepsin G and elastase. Studies in Aim 3 will determine if cathepsin G and elastase appear in plasma before the onset of liver injury, if administration of anti-proteases prevents LPS potentiation of liver injury, if administration of the proteases into the portal vein of rats reproduces the effects of

18

Aflatoxin

LPS in vivo, and if exposure of HCs in vitro to small concentrations of selected hepatotoxicants renders these cells more vulnerable to injury from cathepsin G and elastase. Tumor necrosis factor-alpha (TNF alpha) is released during LPS exposure and has pro-inflammatory effects on both neutrophils and hepatocytes. Aim 4 will explore the role of this important cytokine in the augmentation of chemical hepatotoxicity by LPS. In Aim 5, specific protein targets of neutrophil proteases on hepatocellular plasma membranes will be identified and their association with enhanced HC injury determined. Identification of such targets will provide important clues as to cellular mechanisms by which neutrophil proteases injure hepatocytes. These studies will reveal the role of neutrophils in LPS amplification of hepatotoxicity and mechanisms by which they act to increase susceptibility to hepatocellular damage from exposure to xenobiotic agents. The results will provide new knowledge about how LPS and the inflammatory events it generates may act as a determinant of the magnitude of response to toxicants. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PILOT--EFFECT PEROXISOMES OF TROUT

OF

TEMPERATURE

ACCLIMATION

ON

Principal Investigator & Institution: Carpenter, Hillary; Oregon State University Corvallis, or 973391086 Timing: Fiscal Year 2002 Summary: There is no text on file for this abstract. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: REGULATION OF XENOBIOTIC-METABOLIZING CYP3A Principal Investigator & Institution: Zangar, Richard C.; Senior Research Scientist; Battelle Pacific Northwest Laboratories Box 999, 902 Battelle Blvd Richland, Wa 99352 Timing: Fiscal Year 2002; Project Start 30-SEP-1999; Project End 31-AUG-2004 Summary: (Adapted from the Investigator's Abstract) Cytochrome P450 3A (CYP3A) levels are important determinants of aflatoxin and acetaminophen toxicity and the uptake and elimination of numerous therapeutic agents. CYP3A protein has been reported to be stabilized by some CYP3A substrates. The PI reported that several structurally and functionally distinct agents that are not known CYP3A substrates alter CYP3A protein stability in primary cultured rat hepatocytes. The changes in CYP3A stability are consistent with effects of these agents on phospholipase C or D (PLC or PLD, respectively). Studies in microsomes have indicated that the PLD metabolite, phosphatidic acid (PA), is important in determining CYP3A stability. We propose to test this hypothesis that CYP3A protein stability is dependent upon microsomal PA levels and to further elucidate the molecular mechanism by which phospholipases and other enzymes that regulate PA levels contribute to CYP3A protein stability. The specific aims are: 1) To further establish the role of PLD and PLC in the regulation of CYP3A protein stability. 2) To determine if agents that alter CYP3A stability in primary cultured hepatocytes also function in in vitro incubations. 3.) To determine if PA analogs with different fatty acid moieties have distinct effects on CYP3A protein stability in microsomal samples. 4) To determine whether agents that regulate rat CYP3A stability act in a like manner in human primary cultured hepatocytes and microsomes. These studies will provide information that can be used to predict drug interactions by providing an understanding of the underlying molecular mechanisms involved in the post-translational regulation of CYP3A, and will test a new hypothesis regarding the interactions of phospholipase activities and a key drug-metabolizing enzyme.

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Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: REMEDIATION PROCESS FOR AFLATOXIN CONTAMINATED FOODS Principal Investigator & Institution: Denvir, Adrian J.; Lynntech, Inc. College Station, Tx 77840 Timing: Fiscal Year 2002; Project Start 25-SEP-2002; Project End 25-JUN-2004 Summary: (provided by applicant): Mycotoxins are carcinogenic compounds that are produced by Aspergillus, Penicillium and Fusarium molds on agricultural produce and affect up to 25 per cent of the worlds food crops. Aflatoxins are naturally occurring mycotoxins produced by two types of mold: Aspergillus flavus and Aspergillus parasiticus. The Food and Drug Administration (FDA) has established action levels of 20 ppb for aflatoxin present in food and 0.5 ppb for aflatoxin M1 in milk. These limits are established by the Agency to provide an adequate margin of safety to protect human and animal health. As such there is an ongoing need for economic processes for detoxifying aflatoxin contaminated agricultural products intended for human and animal consumption. Remediation methods such as oxidation using ozone or ammoniation leave undesirable taste and odor residues on the product. The research in the Phase I will seek to determine the feasibility and economics of extracting aflatoxins in nuts and nut products using a cheap and environmentally benign solvent, which removes the toxin without producing or leaving toxic residues, retains nutritive value and does not alter significantly the technological properties of the nut. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: SPECIES DIFFERENCE IN THE BIOTRANSFORMATION OF AFLATOXIN Principal Investigator & Institution: Eaton, David L.; Professor and Associate Dean; Environmental and Occupational Health Studies; University of Washington Grant & Contract Services Seattle, Wa 98105 Timing: Fiscal Year 2002; Project Start 01-MAY-1991; Project End 31-JUL-2004 Summary: Numerous studies have demonstrated that biologically active, natural components of the diet may confer resistance to chemical carcinogens via induction and/or inhibition of biotransformation enzymes. In particular, specific chemical components of the diet, such as flavonoids, isocyanates, glucosinolates, indoles, dithiolthiones, and polyphenols have been identified as effective inducers and/or inhibitors of carcinogen activation/detoxification pathways in animal models. There is much supporting data from human epidemiological studies on the important relationship between diet and cancer in humans, although the diversity and complexity of the diet, and uncertainty of specific exposures, in such studies makes identification of specific active components nearly impossible. Although animal models are useful for "hypothesis testing", species differences in carcinogen activation and detoxification pathways, as well as differences in gene regulation and expression in response to inducers, make extrapolation of animal data to the human situation tentative, at best. Thus, there is a need to develop model systems that utilize human cells/tissues to determine the efficacy of specific dietary components and/or putative chemoprotectant drugs to favorably modify the biotransformation of human carcinogens. One such model human carcinogen is aflatoxin B1. Aflatoxins are mycotoxins produced by the common fungal molds, Aspergillus flavus and Aspergillus parasiticus. Worldwide, aflatoxins are considered a major public health problem because of their potent

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Aflatoxin

carcinogenic effects. Human epidemiological data has documented that humans are susceptible to AFB-induced hepatocarcinogenesis, especially in combination with hepatitis B virus infection. However, there are large species differences in the susceptibility to aflatoxin carcinogenesis. Rats are highly sensitive, whereas mice are very resistant. The mechanism for this difference is associated with the expression of a specific enzyme, glutathione S-transferase A3-3 (mGSTA3-3), which is present in the livers of mice, but not rats. Treatment of rats with the drug, oltipraz, or the food additive, ethoxyquin, protects rats from aflatoxin-induced liver cancer. The mechanism for this protection is due to the ability of these chemicals to "turn on" a gene for a glutathione S-transferase, rGSTA5-5, that is normally not expressed in rat liver, but which efficiently detoxifies aflatoxin. Human liver tissue has very low ability to detoxify aflatoxin -- in fact, worse than the poor ability of rats. There has been considerable interest in devising a dietary or chemointervention strategy for humans that increases resistance to AFB by induction of GSTs. The long range goals of this proposal are to: 1) establish in vitro models that utilize isolated human hepatocytes in culture and human cDNA expressing yeast, to assess the efficacy of specific dietary components as putative chemoprotectors against AFB and other chemical carcinogens, and 2) complete the characterization of species differences in glutathione S-transferases with activity toward AFB-epoxide. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: SYMPOSIUM ON ALDO-KETO REDUCTASES & TOXICANT METABOLISM Principal Investigator & Institution: Penning, Trevor M.; Professor; Pharmacology; University of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JUL-2003 Summary: (provided by applicant): This proposal is a request for financial support for a half-day symposium on "The Emerging Role of Aldo-keto reductases (AKRs) in the Metabolism of Toxic Substances" to be presented at the American Chemical Society National Meeting, Boston, MA August 18-22nd, 2002. AKRs are a superfamily of monomeric oxidoreductases that play central roles in the metabolism of aldose-sugars, prostaglandins, steroid hormones, and chemical carcinogens. Often they catalyze the conversion of carbonyl groups to alcohols so that the parent compound can be conjugated and eliminated. AKRs are highly conserved in both prokaryotes and eukaryotes. There are currently 150 proteins classified into 12 families and crystal structures exist for many of the proteins. In humans, these enzymes also catalyze the formation of hyperosmotic sugars, the detoxification of reactive a,B-unsaturated aldehydes that result from the decomposition of lipid hydroperoxides, and the metabolism of chemical carcinogens including aflatoxin dialdehyde, nicotine derived nitrosamino-ketones and polycyclic aromatic trans-dihydrodiols. Their emerging role in the metabolism of endogenous and exogenous toxins suggests that the family may be ultimately as important as the well-studied CYP superfamily in drug and xenobiotic metabolism. The speakers chosen for this symposium will cover each of the areas listed. In addition an overview of the AKR superfamily and its nomenclature (accepted by the Human Genome Project) will be given and approaches to studying functional genomics of AKRs in yeast will be presented. Each of the speakers has an international reputation in their area of expertise. The goal of the symposium will be to bring together experts in the AKR field so that they will be able to educate the scientific community concerning these enzymes with the hope of attracting new investigators to the field. Issues that are unexplored include the role of AKR isoforms in drug metabolism; their role in

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chemotherapeutic drug resistance; the regulation of human AKR genes; and AKR pharmacogenomics with emphasis on human polymorphisms that may affect individual response to toxicants and susceptibility to chemical carcinogenesis. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: USE OF BIOMARKERS IN HUMAN INTERVENTIONS Principal Investigator & Institution: Kensler, Thomas W.; Professor; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 07-APR-1993; Project End 31-MAY-2007 Summary: (provided by applicant): The goals of this Project are to incorporate the use of biomarkers into primary and secondary (chemoprevention) interventions in high risk populations exposed to aflatoxins. In all preventive interventions there must be objective metrics with which to quantify success. Subsequently, the cost-benefit balance of the intervention can be analyzed and appropriately targeted toward high risk subgroups or individuals within a population. One of the tenets of the molecular epidemiology paradigm is that a mechanistic understanding of the actions of carcinogens can lead to novel prevention technologies. Therefore, the aims of this Project are 3-fold. First, it is to improve existent liquid chromatography-electrospray ionization tandem mass spectroscopy (LC-ESI-MS/MS) methodology for quantitative analysis of major urinary aflatoxin metabolites (e.g., aflatoxin-N7-guanine, aflatoxin M1, aflatoxin P1, aflatoxin-mercapturic acid). Second, it is to determine the impact of primary prevention strategies in West Africa using targeted contamination reduction strategies in community settings. The investigators will develop interventions aimed at: (1) mothers and young children during the weaning period when mycotoxin-contaminated maize-based foods are first introduced into the child?s diet; and (2) local subsistence farmers attempting to reduce contamination of their dietary staple crops, groundnuts and maize. Aflatoxin and fumonisin biomarkers will be used as outcome measures, while in part (1) the investigators will also examine the effects of intervention on child growth and immune parameters. Third, it is to follow up initial results of the investigators' chlorophyllin intervention where they demonstrated a significantly reduced excretion of aflatoxin-N7-guanine at 3 months by examining the impact of the intervention on biomarker modulation at additional time points. They will also analyze urine samples collected during the course of a one-year long intervention with oltipraz in Qidong for magnitude and persistence of modulatory effects on DNA adduct and other aflatoxin biomarkers. It is the hypothesis that levels of biomarkers for the biologically effective dose of carcinogens will be predictive of the efficacy of primary and chemopreventive interventions. The specific aims of this Project have been designed to translate the biomarkers developed and validated in Projects 1 and 4 into metrics to determine the impact of the interventions in high risk populations. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

•

Project Title: VALIDATION AND APPLICATION OF RISK, BIOMARKERS IN HUMAN STUDIES Principal Investigator & Institution: Groopman, John D.; Associate Director of Cancer Prevention; Johns Hopkins University 3400 N Charles St Baltimore, Md 21218 Timing: Fiscal Year 2002; Project Start 07-APR-1993; Project End 31-MAY-2007 Summary: (provided by applicant): The goals of this Project are to develop and validate biomarkers of biologically effective dose and risk induced by environmental carcinogens. It is now axiomatic in human cancer that ambient exposures to multiple

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environmental carcinogens are significant factors in the development and progression of many cancer types. Thus, an understanding of the dose-response relationships between exposure and outcomes in critical targets such as DNA may characterize disease potential. While Dr. Tannenbaum's Project has a major focus on the development of novel, sensitive methods for the detection of DNA and protein adducts, this Project extends these strategies into risk-biomarker analysis. Since there are critical genetic targets in cells, such as tumor suppressor genes, for environmental carcinogens, then it is possible that these targets might prove to be useful biomarkers for risk analysis. Cooccurring environmental exposures and genetic susceptibility may modify the above dose-response effects and consequently these parameters will also be considered. The linkage between carcinogen-induced DNA damage and heritable change in genetic targets is a cornerstone of this Program Project's paradigm. Recently, the discovery that DNA from cells undergoing apoptosis and other turnover processes is found in the blood has resulted in the ability to noninvasively measure mutations in targets such as p53 offering the potential to quantify early biological effects in risk individuals. Therefore, a combined use of biologically effective dose biomarkers, susceptibility biomarkers and genetic biomarkers might reveal the subset of high risk people within a population who will benefit from targeted interventions, which is the outcome of studies proposed in Project 3. It is the hypothesis that levels of biomarkers of biologically effective dose in combination with gene mutations are predictive of disease outcome characterizing risk in individuals. Thus, specific aim 1 is to determine the power of p53 mutations and other genetic alterations in sera using the Short Oligonucleotide Mass Analysis (SOMA) methodology combined with aflatoxin-DNA adducts in urine to predict cancer outcome and disease risk in cohorts in rural China and West Africa. Specific aim 2 is designed to extend the investigators' observations on the high level of aflatoxin biomarkers in West African children in order to assess the impact on growth and immune status, including susceptibility to hepatitis B virus (HBV) infection. West African children, unlike adults, have elevated aflatoxin biomarker levels when infected with HBV. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EXPRESSION

ZEBRAFISH

CARCINOGENESIS

AND

CYTOCHROME

P450

Principal Investigator & Institution: Buhler, Donald R.; Professor; Environ & Molecular Toxicology; Oregon State University Corvallis, or 973391086 Timing: Fiscal Year 2002; Project Start 01-SEP-2001; Project End 31-AUG-2005 Summary: (provided by applicant): Cytochrome P450s (P450s or CYPs) are a superfamily of heme-containing enzyme that catalyze Phase I oxidative, reductive and peroxidative reactions of both endogenous (steroids, fatty acids, vitamins, prostaglandins, retinoids, etc.) and exogenous substrates (chemical pollutants, drugs and carcinogen). The zebrafish (Danio rerio) has become a widely used animal model for studying embryogenesis and developmental genetics and as an animal model to investigate mechanisms of chemical carcinogenesis. Compared to rainbow trout (Oncorhynchus mykiss), however, zebrafish are relatively resistant to certain carcinogens such as aflatoxin B1 (AFB1) and dibenzo[a,1]pyrene (DBP), thus reducing their utility as carcinogenesis models. Their is considerable interest, therefore, in finding zebrafish strains that are more sensitive to carcinogens. Because of their central roles in bioactivation and metabolism processes, it also has become important to establish the contribution of different CYP forms to carcinogenesis and tumor tissue selectivity in the zebrafish and to utilize bioactivating or detoxifying CYP expression as a tool to help

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select sensitive zebrafish strains. Therefore, the objectives of this project are to: 1) clone, sequence, heterologously express, enzymatically and kinetically characterize and map major zebrafish CYPs potentially involved in carcinogen activation and detoxification; 2) use zebrafish CYP isozyme specific oligonucleotide probes to determine their tissue and cell-specific expression patterns in zebrafish mutant lines used to assess the sensitivity of the fish to selected carcinogens; 3) select mutant zebrafish line on the basis of inactivating mutations of tumor suppressor genes and/or high carcinogen bioactivating CYP isoform expression; and 4) determine the sensitivity of wild-type and mutant zebrafish lines to AFB1 and DBP. This proposed work should add significantly to the foundation of CYP and carcinogenesis research in zebrafish. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “aflatoxin” (or synonyms) into the search box. This search gives you access to fulltext articles. The following is a sample of items found for aflatoxin in the PubMed Central database: •

A beta-glucuronidase reporter gene construct for monitoring aflatoxin biosynthesis in Aspergillus flavus. by Flaherty JE, Weaver MA, Payne GA, Woloshuk CP.; 1995 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167519

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A viral genome containing an unstable aflatoxin B1-N7-guanine DNA adduct situated at a unique site. by Bailey EA, Iyer RS, Harris TM, Essigmann JM.; 1996 Jul 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=146009

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Accumulation of Only Aflatoxin B2 by a Strain of Aspergillus flavus. by Schroeder HW, Carlton WW.; 1973 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=380751

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Action of phosphine on production of aflatoxins by various Aspergillus strains isolated from foodstuffs. by Leitao J, de Saint-Blanquat G, Bailly JR.; 1987 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=204108

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Activation of ras oncogene in aflatoxin-induced rat liver carcinogenesis. by Sinha S, Webber C, Marshall CJ, Knowles MA, Proctor A, Barrass NC, Neal GE.; 1988 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=280280

3 4

Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.

With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.

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Activation of the c-Ki-ras Oncogene in Aflatoxin B1-Induced Hepatocellular Carcinoma and Adenoma in the Rat: Detection by Denaturing Gradient Gel Electrophoresis. by Soman NR, Wogan GN.; 1993 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=46017

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Aflatoxin and cyclopiazonic acid production by a sclerotium-producing Aspergillus tamarii strain. by Goto T, Wicklow DT, Ito Y.; 1996 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168224

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Aflatoxin and sterigmatocystin contamination of pistachio nuts in orchards. by Sommer NF, Buchanan JR, Fortlage RJ.; 1976 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=170006

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Aflatoxin B1 dihydrodiol antibody: production and specificity. by Pestka JJ, Chu FS.; 1984 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=239704

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Aflatoxin B1 Induction of Lysogenic Bacteria. by Lillehoj EB, Ciegler A.; 1970 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=377046

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Aflatoxin B1 Indues the Transversion of G [right arrow] T in Codon 249 of the p53 Tumor Suppressor Gene in Human Hepatocytes. by Aguilar F, Hussain SP, Cerutti P.; 1993 Sep 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=47402

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Aflatoxin B1 Uptake by Flavobacterium aurantiacum and Resulting Toxic Effects. by Lillehoj EB, Ciegler A, Hall HH.; 1967 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=315019

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Aflatoxin biosynthesis: detection of transient, acetate-dependent intermediates in Aspergillus by kinetic pulse-labeling. by Zamir LO, Ginsburg R.; 1979 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=218091

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Aflatoxin contamination in soybeans: role of proteinase inhibitors, zinc availability, and seed coat integrity. by Stossel P.; 1986 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203394

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Aflatoxin contamination of maize in flooded areas of Bhagalpur, India. by Sinha KK.; 1987 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203877

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Aflatoxin Contamination of Preharvest Corn as Influenced by Timing and Method of Inoculation. by Widstrom NW, Wilson DM, McMillian WW.; 1981 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=243998

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•

Aflatoxin contamination of some common drug plants. by Roy AK, Sinha KK, Chourasia HK.; 1988 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=202555

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Aflatoxin in corn: ammonia inactivation and bioassay with rainbow trout. by Brekke OL, Sinnhuber RO, Peplinski AJ, Wales JH, Putnam GB, Lee DJ, Ciegler A.; 1977 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=242584

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Aflatoxin inhibition of viral interferon induction. by Hahon N, Booth JA, Stewart JD.; 1979 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=352845

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Aflatoxin localization by the enzyme-linked immunocytochemical technique. by Lawellin DW, Grant DW, Joyce BK.; 1977 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=242593

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Aflatoxin metabolism in humans: detection of metabolites and nucleic acid adducts in urine by affinity chromatography. by Groopman JD, Donahue PR, Zhu JQ, Chen JS, Wogan GN.; 1985 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=390743

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Aflatoxin Production in Meats. I. Stored Meats. by Bullerman LB, Hartman PA, Ayres JC.; 1969 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=378076

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Aflatoxin Production in Meats. II. Aged Dry Salamis and Aged Country Cured Hams. by Bullerman LB, Hartman PA, Ayres JC.; 1969 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=378077

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Aflatoxin Production in Peanut Varieties by aspergillus flavus Link and Aspergillus parasiticus Speare. by Nagarajan V, Bhat RV.; 1973 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=380798

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Aflatoxin Production of Species and Strains of the Aspergillus flavus Group Isolated from Field Crops. by Schroeder HW, Boller RA.; 1973 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=380934

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Aflatoxin production via cross-feeding of pathway intermediates during cofermentation of aflatoxin pathway-blocked Aspergillus parasiticus mutants. by Cleveland TE, Bhatnagar D, Brown RL.; 1991 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183895

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Aflatoxin variability in pistachios. by Mahoney NE, Rodriguez SB.; 1996 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167886

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Aflatoxin-Producing Strains of Aspergillus flavus Detected by Fluorescence of Agar Medium Under Ultraviolet Light. by Hara S, Fennell DI, Hesseltine CW.; 1974 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=380219

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Altered DNA Mutation Spectrum in Aflatoxin B1-Treated Transgenic Mice That Express the Hepatitis B Virus X Protein. by Madden CR, Finegold MJ, Slagle BL.; 2002 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=136763

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An Ethoxyquin-Inducible Aldehyde Reductase from Rat Liver that Metabolizes Aflatoxin B1 Defines a Subfamily of Aldo-Keto Reductases. by Ellis EM, Judah DJ, Neal GE, Hayes JD.; 1993 Nov 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=47772

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An intercalation inhibitor altering the target selectivity of DNA damaging agents: Synthesis of site-specific aflatoxin B1 adducts in a p53 mutational hotspot. by Kobertz WR, Wang D, Wogan GN, Essigmann JM.; 1997 Sep 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23223

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Analysis of mechanisms regulating expression of the ver-1 gene, involved in aflatoxin biosynthesis. by Liang SH, Wu TS, Lee R, Chu FS, Linz JE.; 1997 Mar; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168396

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Antimicrobial Activity of Aflatoxins. by Arai T, Ito T, Koyama Y.; 1967 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=314968

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Appearance of enzyme activities catalyzing conversion of sterigmatocystin to aflatoxin B1 in late-growth-phase Aspergillus parasiticus cultures. by Cleveland TE, Lax AR, Lee LS, Bhatnagar D.; 1987 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203939

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Aspergillus flavus Infection and Aflatoxin Production in Corn: Influence of Trace Elements. by Lillehoj EB, Garcia WJ, Lambrow M.; 1974 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=186821

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Aspergillus flavus infection and aflatoxin production in fig fruits. by Buchanan JR, Sommer NF, Fortlage RJ.; 1975 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=187160

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Aspergillus parasiticus growth and aflatoxin production on black and white pepper and the inhibitory action of their chemical constituents. by Madhyastha MS, Bhat RV.; 1984 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=241521

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Averufanin is an aflatoxin B1 precursor between averantin and averufin in the biosynthetic pathway. by McCormick SP, Bhatnagar D, Lee LS.; 1987 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203593

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avnA, a gene encoding a cytochrome P-450 monooxygenase, is involved in the conversion of averantin to averufin in aflatoxin biosynthesis in Aspergillus parasiticus. by Yu J, Chang PK, Cary JW, Bhatnagar D, Cleveland TE.; 1997 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168428

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Base substitution mutations induced by metabolically activated aflatoxin B1. by Foster PL, Eisenstadt E, Miller JH.; 1983 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=393894

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Biochemical Alternations in Bacillus megaterium as Produced by Aflatoxin B1. by Beuchat LR, Lechowich RV.; 1971 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=377129

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Biological Activity of Aflatoxin B2a. by Lillehoj EB, Ciegler A.; 1969 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=377733

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Biosynthetic relationship among aflatoxins B1, B2, G1, and G2. by Yabe K, Ando Y, Hamasaki T.; 1988 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=202810

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Biosynthetic relationship among aflatoxins B1, B2, M1, and M2. by Dutton MF, Ehrlich K, Bennett JW.; 1985 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=241735

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Biotransformation of aflatoxin B1 and its conjugated metabolites by rat gastrointestinal microfloras. by Wei C, Macy JM, Hsieh DP.; 1981 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=243730

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Bright greenish-yellow fluorescence and aflatoxin in agricultural commodities. by Bothast RJ, Hesseltine CW.; 1975 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=187179

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Caffeine inhibition of aflatoxin production: mode of action. by Buchanan RL, Hoover DG, Jones SB.; 1983 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=239540

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Caffeine inhibition of aflatoxin synthesis: probable site of action. by Buchanan RL, Lewis DF.; 1984 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=240199

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Characterization of aflJ, a Gene Required for Conversion of Pathway Intermediates to Aflatoxin. by Meyers DM, Obrian G, Du WL, Bhatnagar D, Payne GA.; 1998 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=106528

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Characterization of c-Ki-ras and N-ras oncogenes in aflatoxin B1-induced rat liver tumors. by McMahon G, Davis EF, Huber LJ, Kim Y, Wogan GN.; 1990 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=53419

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Characterization of the Critical Amino Acids of an Aspergillus parasiticus Cytochrome P-450 Monooxygenase Encoded by ordA That Is Involved in the Biosynthesis of Aflatoxins B1, G1, B2, and G2. by Yu J, Chang PK, Ehrlich KC, Cary JW, Montalbano B, Dyer JM, Bhatnagar D, Cleveland TE.; 1998 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=90931

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Characterization of the function of the ver-1A and ver-1B genes, involved in aflatoxin biosynthesis in Aspergillus parasiticus. by Liang SH, Skory CD, Linz JE.; 1996 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168283

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Characterization of the polyketide synthase gene (pksL1) required for aflatoxin biosynthesis in Aspergillus parasiticus. by Feng GH, Leonard TJ.; 1995 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=177466

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Chlorophyllin intervention reduces aflatoxin --DNA adducts in individuals at high risk for liver cancer. by Egner PA, Wang JB, Zhu YR, Zhang BC, Wu Y, Zhang QN, Qian GS, Kuang SY, Gange SJ, Jacobson LP, Helzlsouer KJ, Bailey GS, Groopman JD, Kensler TW.; 2001 Dec 4; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=64728

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Chromosomal Location Plays a Role in Regulation of Aflatoxin Gene Expression in Aspergillus parasiticus. by Chiou CH, Miller M, Wilson DL, Trail F, Linz JE.; 2002 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=126543

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Cloning and characterization of a cDNA from Aspergillus parasiticus encoding an Omethyltransferase involved in aflatoxin biosynthesis. by Yu J, Cary JW, Bhatnagar D, Cleveland TE, Keller NP, Chu FS.; 1993 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182499

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Cloning and Characterization of the O-Methyltransferase I Gene (dmtA) from Aspergillus parasiticus Associated with the Conversions of Demethylsterigmatocystin to Sterigmatocystin and Dihydrodemethylsterigmatocystin to Dihydrosterigmatocystin in Aflatoxin Biosynthesis. by Motomura M, Chihaya N, Shinozawa T, Hamasaki T, Yabe K.; 1999 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=91671

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Cloning of the afl-2 gene involved in aflatoxin biosynthesis from Aspergillus flavus. by Payne GA, Nystrom GJ, Bhatnagar D, Cleveland TE, Woloshuk CP.; 1993 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=202071

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Cloning of the Aspergillus parasiticus apa-2 gene associated with the regulation of aflatoxin biosynthesis. by Chang PK, Cary JW, Bhatnagar D, Cleveland TE, Bennett JW, Linz JE, Woloshuk CP, Payne GA.; 1993 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182448

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Coconut as a Medium for the Experimental Production of Aflatoxin. by Arseculeratne SN, De Silva LM, Wijesundera S, Bandunatha CH.; 1969 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=377895

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Comparative mapping of aflatoxin pathway gene clusters in Aspergillus parasiticus and Aspergillus flavus. by Yu J, Chang PK, Cary JW, Wright M, Bhatnagar D, Cleveland TE, Payne GA, Linz JE.; 1995 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167508

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Comparative Studies on the Detoxification of Aflatoxins by Sodium Hypochlorite and Commercial Bleaches. by Yang CY.; 1972 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=380691

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Comparison of antibody production against aflatoxin B1 in goats and rabbits. by Gaur PK, El-Nakib O, Chu FS.; 1980 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291637

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Conditions for induction of bacteriophage from lysogenic Bacillus megaterium with aflatoxin B1. by Whittaker BL, Chipley JR.; 1979 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=243254

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Conversion of a new metabolite to aflatoxin B2 by Aspergillus parasiticus. by Cleveland TE, Bhatnagar D, Foell CJ, McCormick SP.; 1987 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=204202

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Correlation of Aflatoxin Contamination With Zinc Content of Chicken Feed. by Jones FT, Hagler WM Jr, Hamilton PB.; 1984 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=239705

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Correlation of Zn2+ content with aflatoxin content of corn. by Failla LJ, Lynn D, Niehaus WG Jr.; 1986 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203395

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Country Cured Ham as a Possible Source of Aflatoxin. by Strzelecki E, Lillard HS, Ayres JC.; 1969 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=378119

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Cryptic speciation and recombination in the aflatoxin-producing fungus Aspergillus flavus. by Geiser DM, Pitt JI, Taylor JW.; 1998 Jan 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18233

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Culture Conditions Control Expression of the Genes for Aflatoxin and Sterigmatocystin Biosynthesis in Aspergillus parasiticus and A. nidulans. by Feng GH, Leonard TJ.; 1998 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=106313

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Detection of Aflatoxin B1 in Silkworm Larvae Attacked by an Aspergillus flavus Isolate from a Sericultural Farm. by Ohtomo T, Murakoshi S, Sugiyama J, Kurata H.; 1975 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=376585

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Detection of aflatoxin D1 in ammoniated corn by mass spectrometry-mass spectrometry. by Grove MD, Plattner RD, Peterson RE.; 1984 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=241638

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Development of Aflatoxin B1-Lysine Adduct Monoclonal Antibody for Human Exposure Studies. by Wang JS, Abubaker S, He X, Sun G, Strickland PT, Groopman JD.; 2001 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92929

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Dietary aflatoxin exposure and impaired growth in young children from Benin and Togo: cross sectional study. by Gong YY, Cardwell K, Hounsa A, Egal S, Turner PC, Hall AJ, Wild CP.; 2002 Jul 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=116667

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Differentiation of aflatoxins from territrems. by Ling KH, Yang CK, Huang HC.; 1979 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=243220

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Direct visual detection of aflatoxin synthesis by minicolonies of Aspergillus species. by Lemke PA, Davis ND, Creech GW.; 1989 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=202954

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Dothistroma pini, a Forest Pathogen, Contains Homologs of Aflatoxin Biosynthetic Pathway Genes. by Bradshaw RE, Bhatnagar D, Ganley RJ, Gillman CJ, Monahan BJ, Seconi JM.; 2002 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123981

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Effect of Aflatoxin B1 on Cell Cultures. by Gabliks J, Schaeffer W, Friedman L, Wogan G.; 1965 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=315716

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Effect of aflatoxin B1 on chromatin-bound ribonucleic acid polymerase and nucleic acid and protein synthesis in germinating maize seeds. by Tripathi RK, Misra RS.; 1981 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=244025

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Effect of aflatoxin on phagocytosis of Aspergillus fumigatus spores by rabbit alveolar macrophages. by Richard JL, Thurston JR.; 1975 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=187111

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Effect of aflatoxins on rat peritoneal macrophages. by Cusumano V, Costa GB, Seminara S.; 1990 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=184993

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Effect of C6 to C9 alkenals on aflatoxin production in corn, cottonseed, and peanuts. by Zeringue HJ Jr.; 1991 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183592

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Effect of dietary aflatoxin on fertility, hatchability, and progeny performance of broiler breeder hens. by Howarth B Jr, Wyatt RD.; 1976 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291175

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Effect of initial pH on aflatoxin production. by Buchanan RL Jr, Ayres JC.; 1975 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=376591

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Effect of ochratoxin and aflatoxin on serum proteins, complement activity, and antibody production to Brucella abortus in guinea pigs. by Richard JL, Thurston JR, Deyoe BL, Booth GD.; 1975 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=186904

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Effect of phenolic antioxidants on the mutagenicity of aflatoxin B1. by Shelef LA, Chin B.; 1980 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291718

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Effect of pyridazinone herbicides on growth and aflatoxin release by Aspergillus flavus and Aspergillus parasiticus. by Bean GA, Southall A.; 1983 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=239431

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Effect of specific amino acids on growth and aflatoxin production by Aspergillus parasiticus and Aspergillus flavus in defined media. by Payne GA, Hagler WM Jr.; 1983 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=239471

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Effect of temperature cycling on the production of aflatoxin by Asperfillus parasiticus. by Stutz HK, Krumperman PH.; 1976 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=170065

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Effect of temperature on aflatoxin production in Mucuna pruriens seeds. by Roy AK, Chourasia HK.; 1989 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=184149

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Effect of zinc on adenine nucleotide pools in relation to aflatoxin biosynthesis in Aspergillus parasiticus. by Gupta SK, Maggon KK, Venkitasubramanian TA.; 1976 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=170456

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Effects of Aflatoxin on Germination and Growth of Lettuce. by Crisan EV.; 1973 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=380808

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Effects of Aflatoxin on Seeding Growth and Ultrastructure in Plants. by Crisan EV.; 1973 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=379944

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Effects of Light, Temperature, and pH Value on Aflatoxin Production In Vitro. by Joffe AZ, Lisker N.; 1969 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=378018

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Effects of Moisture Content and Temperature on Aflatoxin Production in Corn. by Trenk HL, Hartman PA.; 1970 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=376788

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Effects of soil moisture and temperature on preharvest invasion of peanuts by the Aspergillus flavus group and subsequent aflatoxin development. by Hill RA, Blankenship PD, Cole RJ, Sanders TH.; 1983 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=242335

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Effects of trace metals on the production of aflatoxins by Aspergillus parasiticus. by Marsh PB, Simpson ME, Trucksess MW.; 1975 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=187113

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Enzymatic Conversion of Averufin to Hydroxyversicolorone and Elucidation of a Novel Metabolic Grid Involved in Aflatoxin Biosynthesis. by Yabe K, Chihaya N, Hamamatsu S, Sakuno E, Hamasaki T, Nakajima H, Bennett JW.; 2003 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=152417

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Enzymatic conversion of norsolorinic acid to averufin in aflatoxin biosynthesis. by Yabe K, Nakamura Y, Nakajima H, Ando Y, Hamasaki T.; 1991 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182952

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Enzymatic conversion of sterigmatocystin into aflatoxin B1 by cell-free extracts of Aspergillus parasiticus. by Singh R, Hsieh DP.; 1976 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291187

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Enzymatic Formation of G-Group Aflatoxins and Biosynthetic Relationship between G- and B-Group Aflatoxins. by Yabe K, Nakamura M, Hamasaki T.; 1999 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=99713

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Enzymatic formation of the bisfuran structure in aflatoxin biosynthesis. by Wan NC, Hsieh DP.; 1980 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291292

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Enzymatic Function of the Nor-1 Protein in Aflatoxin Biosynthesis in Aspergillus parasiticus. by Zhou R, Linz JE.; 1999 Dec; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=91775

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Enzyme-linked immunosorbent analysis for aflatoxin B1. by Lawellin DW, Grant DW, Joyce BK.; 1977 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=242594

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Enzymes and aflatoxin biosynthesis. by Dutton MF.; 1988 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=373139

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Evidence for cytochrome P-450NF, the nifedipine oxidase, being the principal enzyme involved in the bioactivation of aflatoxins in human liver. by Shimada T, Guengerich FP.; 1989 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=286490

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Evidence for involvement of multiple forms of cytochrome P-450 in aflatoxin B1 metabolism in human liver. by Forrester LM, Neal GE, Judah DJ, Glancey MJ, Wolf CR.; 1990 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=54944

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Field accumulation of aflatoxin in cottonseed as influenced by irrigation termination dates and pink bollworm infestation. by Russell TE, Watson TF, Ryan GF.; 1976 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291181

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Five of 12 forms of vaccinia virus-expressed human hepatic cytochrome P450 metabolically activate aflatoxin B1. by Aoyama T, Yamano S, Guzelian PS, Gelboin HV, Gonzalez FJ.; 1990 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=54203

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Further Characterization of Tissue Distribution and Metabolism of [14C]Aflatoxin B1 in Chickens. by Chipley JR, Mabee MS, Applegate KL, Dreyfuss MS.; 1974 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=186876

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Genetic transformation system for the aflatoxin-producing fungus Aspergillus flavus. by Woloshuk CP, Seip ER, Payne GA, Adkins CR.; 1989 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=184058

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High Aflatoxin Production on a Chemically Defined Medium. by Reddy TV, Viswanathan L, Venkitasubramanian TA.; 1971 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=376320

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High-affinity monoclonal antibodies for aflatoxins and their application to solidphase immunoassays. by Groopman JD, Trudel LJ, Donahue PR, Marshak-Rothstein A, Wogan GN.; 1984 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=392225

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Homologs of Aflatoxin Biosynthesis Genes and Sequence of aflR in Aspergillus oryzae and Aspergillus sojae. by Watson AJ, Fuller LJ, Jeenes DJ, Archer DB.; 1999 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=91020

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Identification and Aflatoxin Production of Molds Isolated from Country Cured Hams. by Sutic M, Ayres JC, Koehler PE.; 1972 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=380403

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Identification of aflatoxin biosynthesis genes by genetic complementation in an Aspergillus flavus mutant lacking the aflatoxin gene cluster. by Prieto R, Yousibova GL, Woloshuk CP.; 1996 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168161

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Identification of an activated c-Ki-ras oncogene in rat liver tumors induced by aflatoxin B1. by McMahon G, Hanson L, Lee JJ, Wogan GN.; 1986 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=387149

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Identification of averantin as an aflatoxin B1 precursor: placement in the biosynthetic pathway. by Bennett JW, Lee LS, Shoss SM, Boudreaux GH.; 1980 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291429

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Identification of O-methylsterigmatocystin as an aflatoxin B1 and G1 precursor in Aspergillus parasiticus. by Bhatnagar D, McCormick SP, Lee LS, Hill RA.; 1987 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203804

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Improved method of screening for aflatoxin with a coconut agar medium. by Davis ND, Iyer SK, Diener UL.; 1987 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203916

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Improved Yield of Aflatoxin by Incremental Increases of Temperature. by West S, Wyatt RD, Hamilton PB.; 1973 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=380959

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In vitro reactions of aflatoxin B1-adducted DNA. by Groopman JD, Croy RG, Wogan GN.; 1981 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=348762

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Inactivation of aflatoxin B1 by using the synergistic effect of hydrogen peroxide and gamma radiation. by Patel UD, Govindarajan P, Dave PJ.; 1989 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=184132

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Incidence of aflatoxin in California almonds. by Schade JE, McGreevy K, King AD Jr, Mackey B, Fuller G.; 1975 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=186909

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Incorporation of (2-14C)acetate into lipids of mink (Mustela vison) liver and intestine during in vitro and in vivo treatment with aflatoxin B1. by Chou CC, Marth EH.; 1975 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=376573

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Increased expression of Aspergillus parasiticus aflR, encoding a sequence-specific DNA-binding protein, relieves nitrate inhibition of aflatoxin biosynthesis. by Chang PK, Ehrlich KC, Yu J, Bhatnagar D, Cleveland TE.; 1995 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167509

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Increased production of aflatoxins by Aspergillus parasiticus Speare in the presence of rubratoxin B. by Moss MO, Badii F.; 1982 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=241938

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Induction of base substitution mutations by aflatoxin B1 is mucAB dependent in Escherichia coli. by Foster PL, Groopman JD, Eisenstadt E.; 1988 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=211309

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Influence of Fungicides and Irrigation Practice on Aflatoxin in Peanuts Before Digging. by Pettit RE, Taber RA, Schroeder HW, Harrison AL.; 1971 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=376377

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Influence of inoculum size of Aspergillus parasiticus spores on aflatoxin production. by Sharma A, Behere AG, Padwal-Desai SR, Nadkarni GB.; 1980 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291709

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Influence of modified atmosphere storage on aflatoxin production in high moisture corn. by Wilson DM, Jay E.; 1975 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=186948

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Influence of temperature cycling on the production of aflatoxins B1 and G1 by Aspergillus parasiticus. by Lin YC, Ayres JC, Koehler PE.; 1980 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291576

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Influence of tricarboxylic acid cycle intermediates and related metabolites on the biosynthesis of aflatoxin by resting cells of Aspergillus flavus. by Shantha T, Murthy VS.; 1981 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=244103

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Influence of white light on production of aflatoxins and anthraquinones in Aspergillus parasiticus. by Bennett JW, Dunn JJ, Goldsman CI.; 1981 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=243721

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Influence of yield on in vitro accumulation of aflatoxins in pecan (Carya illinoensis (Wang.) K. Koch) nutmeats. by McMeans JL.; 1983 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=242351

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Inhibition of aflatoxin biosynthesis by tolnaftate. by Khan SN, Maggon KK, Venkitasubramanian TA.; 1978 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291213

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Inhibition of aflatoxin formation by 2-mercaptoethanol. by Gupta SK, Maggon KK, Venkitasubramanian TA.; 1976 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=170064

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Inhibition of Aflatoxin Production and Tentative Identification of an Aflatoxin Intermediate "Versiconal Acetate" from Treatment with Dichlorvos. by Schroeder HW, Cole RJ, Grigsby RD, Hein H Jr.; 1974 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=380041

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Inhibition of aflatoxin production by selected insecticides. by Draughon FA, Ayres JC.; 1981 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=243843

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Inhibition of Aflatoxin Production by Surfactants. by Rodriguez SB, Mahoney NE.; 1994 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201276

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Inhibition of Aspergillus growth and aflatoxin release by derivatives of benzoic acid. by Chipley JR, Uraih N.; 1980 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291580

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Inhibition of deoxyribonucleic acid synthesis in Flavobacterium aurantiacum by aflatoxin B1. by Lillehoj EB, Ciegler A.; 1967 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=251955

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Integrated process for ammonia inactivation of aflatoxin-contaminated corn and ethanol fermentation. by Bothast RJ, Nofsinger GW, Lagoda AA, Black LT.; 1982 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=241949

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Interaction between Streptococcus lactis and Aspergillus flavus on production of aflatoxin. by Coallier-Ascah J, Idziak ES.; 1985 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=238363

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Interconversion of aflatoxin B1 and aflatoxicol by several fungi. by Nakazato M, Morozumi S, Saito K, Fujinuma K, Nishima T, Kasai N.; 1990 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=184431

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Involvement of Two Cytosolic Enzymes and a Novel Intermediate, 5[prime prime or minute]-Oxoaverantin, in the Pathway from 5[prime prime or minute]Hydroxyaverantin to Averufin in Aflatoxin Biosynthesis. by Sakuno E, Yabe K, Nakajima H.; 2003 Nov; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=262255

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Isolation and characterization of a gene from Aspergillus parasiticus associated with the conversion of versicolorin A to sterigmatocystin in aflatoxin biosynthesis. by Skory CD, Chang PK, Cary J, Linz JE.; 1992 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=183140

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Isolation and characterization of Aspergillus parasiticus mutants with impaired aflatoxin production by a novel tip culture method. by Yabe K, Nakamura H, Ando Y, Terakado N, Nakajima H, Hamasaki T.; 1988 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=202809

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Mechanism of action of aflatoxin B1 in Bacillus megaterium. by Tiwari RP, Dham CK, Bhalla TC, Saini SS, Vadehra DV.; 1985 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=238467

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Metabolic effects of low aflatoxin B1 levels on broiler chicks. by Maurice DV, Bodine AB, Rehrer NJ.; 1983 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=242400

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Metabolism of aflatoxin B1 by rat hepatic microsomes induced by polyhalogenated biphenyl congeners. by Halvorson MR, Phillips TD, Safe SH, Robertson LW.; 1985 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=238464

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Metabolism of aflatoxin, ochratoxin, zearalenone, and three trichothecenes by intact rumen fluid, rumen protozoa, and rumen bacteria. by Kiessling KH, Pettersson H, Sandholm K, Olsen M.; 1984 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=240059

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Mold flora and aflatoxin contamination of stored and cooked samples of pearl millet in the Paharia tribal belt of Santhal paragana, Bihar, India. by Mishra NK, Daradhiyar SK.; 1991 Apr; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182872

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Molecular characterization of aflR, a regulatory locus for aflatoxin biosynthesis. by Woloshuk CP, Foutz KR, Brewer JF, Bhatnagar D, Cleveland TE, Payne GA.; 1994 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201664

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Molecular characterization of an Aspergillus parasiticus dehydrogenase gene, norA, located on the aflatoxin biosynthesis gene cluster. by Cary JW, Wright M, Bhatnagar D, Lee R, Chu FS.; 1996 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167807

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Molecular cloning of genes related to aflatoxin biosynthesis by differential screening. by Feng GH, Chu FS, Leonard TJ.; 1992 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=195269

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Monitoring the Production of Aflatoxin B1 in Wheat by Measuring the Concentration of nor-1 mRNA. by Mayer Z, Farber P, Geisen R.; 2003 Feb; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=143586

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Monoclonal antibody to aflatoxin B1-modified DNA detected by enzyme immunoassay. by Haugen A, Groopman JD, Hsu IC, Goodrich GR, Wogan GN, Harris CC.; 1981 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=319740

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Morphological Alterations in Bacillus megaterium as Produced by Aflatoxin B1. by Beuchat LR, Lechowich RV.; 1971 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=377130

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Mutant of Aspergillus flavus producing more aflatoxin B2 than B1. by Papa KE.; 1977 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=170625

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Mutational Properties of the Primary Aflatoxin B1-DNA Adduct. by Bailey EA, Iyer RS, Stone MP, Harris TM, Essigmann JM.; 1996 Feb 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39975

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New Additive for Culture Media for Rapid Identification of Aflatoxin-Producing Aspergillus Strains. by Fente CA, Ordaz JJ, Vazquez BI, Franco CM, Cepeda A.; 2001 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=93241

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Occurrence of Aflatoxins and Aflatoxin-Producing Strains of Aspergillus spp. in Soybeans. by Bean GA, Schillinger JA, Klarman WL.; 1972 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=376537

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Occurrence of aflatoxins in oilseeds providing cocoa-butter substitutes. by Kershaw SJ.; 1982 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=244209

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ord1, an oxidoreductase gene responsible for conversion of O-methylsterigmatocystin to aflatoxin in Aspergillus flavus. by Prieto R, Woloshuk CP.; 1997 May; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=168459

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Persistence of Aflatoxin During the Fermentation of Soy Sauce. by Maing IY, Ayres JC, Koehler PE.; 1973 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=380958

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Physical and transcriptional map of an aflatoxin gene cluster in Aspergillus parasiticus and functional disruption of a gene involved early in the aflatoxin pathway. by Trail F, Mahanti N, Rarick M, Mehigh R, Liang SH, Zhou R, Linz JE.; 1995 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167540

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Possible implications of reciprocity between ethylene and aflatoxin biogenesis in Aspergillus flavus and Aspergillus parasiticus. by Sharma A, Padwal-Desai SR, Nadkarni GB.; 1985 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=238348

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Precursor recognition by kinetic pulse-labeling in a toxigenic aflatoxin B1-producing strain of Aspergillus. by Zamir LO, Hufford KD.; 1981 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=243979

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Preharvest aflatoxin contamination: effect of moisture and substrate variation in developing cottonseed and corn kernels. by Lillehoj EB, Wall JH, Bowers EJ.; 1987 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203710

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Preparation of Labeled Aflatoxins with High Specific Activities. by Hsieh DP, Mateles RI.; 1971 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=377379

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Presence of aflatoxin M1 in commercial ultra-high-temperature-treated milk. by Blanco JL, Dominguez L, Gomez-Lucia E, Garayzabal JF, Garcia JA, Suarez G.; 1988 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=202709

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Production and characterization of aflatoxin B2a antiserum. by Gaur PK, Lau HP, Pestka JJ, Chu FS.; 1981 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=243719

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Production and characterization of antibody against aflatoxin Q1. by Fan TS, Zhang GS, Chu FS.; 1984 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=239714

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Production and characterization of monoclonal antibodies against aflatoxin M1. by Woychik NA, Hinsdill RD, Chu FS.; 1984 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=241692

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Production of aflatoxin by an Aspergillus flavus isolate cultured under a limited oxygen supply. by Clevstrom G, Ljunggren H, Tegelstrom S, Tideman K.; 1983 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=239402

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Production of Aflatoxin M in a Liquid Medium. by Pai MR, Bai NJ, Venkitasubramanian TA.; 1975 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=187091

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Production of aflatoxin on soybeans. by Gupta SK, Venkitasubramanian TA.; 1975 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=187088

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Production of aflatoxins B1 and G1 by Aspergillus flavus and Aspergillus parasiticus isolated from market pecans. by Koehler PE, Hanlin RT, Beraha L.; 1975 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=187233

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Production of Aflatoxins by Aspergillus flavus Cultured on Flue-Cured Tobacco. by Pattee HE.; 1969 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=378129

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Production of antibody against aflatoxin B1. by Chu FS, Ueno I.; 1977 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=170837

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Purification and Characterization of O-Methyltransferase I Involved in Conversion of Demethylsterigmatocystin to Sterigmatocystin and of Dihydrodemethylsterigmatocystin to Dihydrosterigmatocystin during Aflatoxin Biosynthesis. by Yabe K, Matsushima KI, Koyama T, Hamasaki T.; 1998 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=124688

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Purification and Characterization of Two Versiconal Hemiacetal Acetate Reductases Involved in Aflatoxin Biosynthesis. by Matsushima KI, Ando Y, Hamasaki T, Yabe K.; 1994 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201684

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Purification of a 40-kilodalton methyltransferase active in the aflatoxin biosynthetic pathway. by Keller NP, Dischinger HC Jr, Bhatnagar D, Cleveland TE, Ullah AH.; 1993 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=202130

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Quantitation of aflatoxin B1 adduction within the ribosomal RNA gene sequences of rat liver DNA. by Irvin TR, Wogan GN.; 1984 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=344895

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Quantitation of aflatoxin B1 and aflatoxin B1 antibody by an enzyme-linked immunosorbent microassay. by Pestka JJ, Gaur PK, Chu FS.; 1980 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=291716

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Reaction of aflatoxin B1 exo-8,9-epoxide with DNA: Kinetic analysis of covalent binding and DNA-induced hydrolysis. by Johnson WW, Guengerich FP.; 1997 Jun 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=21012

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Reactivity of aflatoxin B2a antibody with aflatoxin B1-modified DNA and related metabolites. by Pestka JJ, Li YK, Chu FS.; 1982 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=242163

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Regional Differences in Production of Aflatoxin B1 and Cyclopiazonic Acid by Soil Isolates of Aspergillus flavus along a Transect within the United States. by Horn BW, Dorner JW.; 1999 Apr; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=91204

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Regulated expression of the nor-1 and ver-1 genes associated with aflatoxin biosynthesis. by Skory CD, Chang PK, Linz JE.; 1993 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182131

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Regulation of aflatoxin biosynthesis: assessment of the role of cellular energy status as a regulator of the induction of aflatoxin production. by Buchanan RL, Jones SB, Gerasimowicz WV, Zaika LL, Stahl HG, Ocker LA.; 1987 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203845

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Regulation of aflatoxin biosynthesis: effect of glucose on activities of various glycolytic enzymes. by Buchanan RL, Lewis DF.; 1984 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=241508

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Regulation of aflR and Its Product, AflR, Associated with Aflatoxin Biosynthesis. by Liu BH, Chu FS.; 1998 Oct; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=106529

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Restricted repair of aflatoxin B1 induced damage in alpha DNA of monkey cells. by Leadon SA, Zolan ME, Hanawalt PC.; 1983 Aug 25; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=326306

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Role of blastospores in protecting Aspergillus parasiticus NRRL 3240 from high levels of aflatoxins. by Bhatnagar RK, Ahmad S, Mukerji KG, Venkitasubramanian TA.; 1982 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=242061

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Role of versicolorin A and its derivatives in aflatoxin biosynthesis. by Dutton MF, Anderson MS.; 1982 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=241872

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Sensitivity of aflatoxin b1 to ionizing radiation. by Van Dyck PJ, Tobback P, Feyes M, van de Voorde H.; 1982 Jun; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=244234

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Sequence context effects in DNA replication blocks induced by aflatoxin B1. by Refolo LM, Conley MP, Sambamurti K, Jacobsen JS, Humayun MZ.; 1985 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=397721

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Sequence specificity in aflatoxin B1--DNA interactions. by Muench KF, Misra RP, Humayun MZ.; 1983 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=393298

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Sequence variability in homologs of the aflatoxin pathway gene aflR distinguishes species in Aspergillus section Flavi. by Chang PK, Bhatnagar D, Cleveland TE, Bennett JW.; 1995 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167259

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Silica gel medium to detect molds that produce aflatoxin. by Torrey GS, Marth EH.; 1976 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=170073

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Simple fluorescence method for rapid estimation of aflatoxin levels in a solid culture medium. by Cotty PJ.; 1988 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=202434

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Simple method for screening aflatoxin-producing molds by UV photography. by Yabe K, Ando Y, Ito M, Terakado N.; 1987 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203642

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Simultaneous occurrence of deoxynivalenol, zearalenone, and aflatoxin in 1982 scabby wheat from the midwestern United States. by Hagler WM Jr, Tyczkowska K, Hamilton PB.; 1984 Jan; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=239627

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Site-specific targeting of aflatoxin adduction directed by triple helix formation in the major groove of oligodeoxyribonucleotides. by Jones WR, Stone MP.; 1998 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=147363

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Sodium bicarbonate reduces viability and alters aflatoxin distribution of Aspergillus parasiticus in Czapek's agar. by Montville TJ, Goldstein PK.; 1987 Oct; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=204104

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Some Cultural Conditions That Control Biosynthesis of Lipid and Aflatoxin by Aspergillus parasiticus. by Shih CN, Marth EH.; 1974 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=380064

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Stability of aflatoxin B-1 and ochratoxin A in brewing. by Chu FS, Chang CC, Ashoor SH, Prentice N.; 1975 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=186972

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Stable expression of rat cytochrome P-450IIB1 cDNA in Chinese hamster cells (V79) and metabolic activation of aflatoxin B1. by Doehmer J, Dogra S, Friedberg T, Monier S, Adesnik M, Glatt H, Oesch F.; 1988 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=281846

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Step of Dichlorvos Inhibition in the Pathway of Aflatoxin Biosynthesis. by Yao RC, Hsieh DP.; 1974 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=186587

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Stereochemistry during aflatoxin biosynthesis: conversion of norsolorinic acid to averufin. by Yabe K, Matsuyama Y, Ando Y, Nakajima H, Hamasaki T.; 1993 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182310

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Stereochemistry during aflatoxin biosynthesis: cyclase reaction in the conversion of versiconal to versicolorin B and racemization of versiconal hemiacetal acetate. by Yabe K, Hamasaki T.; 1993 Aug; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=182311

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Stimulation by Hyphopichia burtonii and Bacillus amyloliquefaciens of aflatoxin production by Aspergillus flavus in irradiated maize and rice grains. by Cuero RG, Smith JE, Lacey J.; 1987 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203822

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Stimulation of aflatoxin B1 and T-2 toxin production by sorbic acid. by Gareis M, Bauer J, von Montgelas A, Gedek B.; 1984 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=239684

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Structural and functional analysis of the nor-1 gene involved in the biosynthesis of aflatoxins by Aspergillus parasiticus. by Trail F, Chang PK, Cary J, Linz JE.; 1994 Nov; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201939

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Structure and function of fas-1A, a gene encoding a putative fatty acid synthetase directly involved in aflatoxin biosynthesis in Aspergillus parasiticus. by Mahanti N, Bhatnagar D, Cary JW, Joubran J, Linz JE.; 1996 Jan; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=167785

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Surface Binding of Aflatoxin B1 by Lactic Acid Bacteria. by Haskard CA, El-Nezami HS, Kankaanpaa PE, Salminen S, Ahokas JT.; 2001 Jul; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=92985

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Susceptibility to Hepatocellular Carcinoma is Associated with Genetic Variation in the Enzymatic Detoxification of Aflatoxin B1. by McGlynn KA, Rosvold EA, Lustbader ED, Hu Y, Clapper ML, Zhou T, Wild CP, Xia X, Baffoe-Bonnie A, Ofori-Adjei D, Chen G, London WT, Shen F, Buetow KH.; 1995 Mar 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=42488

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The aflatoxin B1 formamidopyrimidine adduct plays a major role in causing the types of mutations observed in human hepatocellular carcinoma. by Smela ME, Hamm ML, Henderson PT, Harris CM, Harris TM, Essigmann JM.; 2002 May 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=124458

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The alcohol dehydrogenase gene adh1 is induced in Aspergillus flavus grown on medium conducive to aflatoxin biosynthesis. by Woloshuk CP, Payne GA.; 1994 Feb; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201364

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The Carboxy-Terminal Portion of the Aflatoxin Pathway Regulatory Protein AFLR of Aspergillus parasiticus Activates GAL1::lacZ Gene Expression in Saccharomyces cerevisiae. by Chang PK, Yu J, Bhatnagar D, Cleveland TE.; 1999 Jun; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=91370

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Tissue Distribution and Metabolism of Aflatoxin B1-14C in Broiler Chickens. by Mabee MS, Chipley JR.; 1973 May; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=380908

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Toxicity of aflatoxin B1 to penaeid shrimp. by Wiseman MO, Price RL, Lightner DV, Williams RR.; 1982 Dec; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=242216

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Two distinct O-methyltransferases in aflatoxin biosynthesis. by Yabe K, Ando Y, Hashimoto J, Hamasaki T.; 1989 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=203052

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Use of aflatoxin-producing ability medium to distinguish aflatoxin-producing strains of Aspergillus flavus. by Wicklow DT, Shotwell OL, Adams GL.; 1981 Mar; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=243762

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Variability among atoxigenic Aspergillus flavus strains in ability to prevent aflatoxin contamination and production of aflatoxin biosynthetic pathway enzymes. by Cotty PJ, Bhatnagar D.; 1994 Jul; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=201639

The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with aflatoxin, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “aflatoxin” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for aflatoxin (hyperlinks lead to article summaries):

6 PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.

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A follow-up study of urinary markers of aflatoxin exposure and liver cancer risk in Shanghai, People's Republic of China. Author(s): Qian GS, Ross RK, Yu MC, Yuan JM, Gao YT, Henderson BE, Wogan GN, Groopman JD. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 1994 January-February; 3(1): 3-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8118382

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A review on biological control and metabolism of aflatoxin. Author(s): Mishra HN, Das C. Source: Critical Reviews in Food Science and Nutrition. 2003; 43(3): 245-64. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12822672

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A survey of ethnic foods for microbial quality and aflatoxin content. Author(s): Candlish AAG, Pearson SM, Aidoo KE, Smith JE, Kelly B, Irvine H. Source: Food Additives and Contaminants. 2001 February; 18(2): 129-36. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11288910

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Activation of the insulin-like growth factor II transcription by aflatoxin B1 induced p53 mutant 249 is caused by activation of transcription complexes; implications for a gain-of-function during the formation of hepatocellular carcinoma. Author(s): Lee YI, Lee S, Das GC, Park US, Park SM, Lee YI. Source: Oncogene. 2000 August 3; 19(33): 3717-26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10949925

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Activation of toxic chemicals by cytochrome P450 enzymes: regio- and stereoselective oxidation of aflatoxin B1. Author(s): Guengerich FP, Ueng YF, Kim BR, Langouet S, Coles B, Iyer RS, Thier R, Harris TM, Shimada T, Yamazaki H, Ketterer B, Guillouzo A. Source: Advances in Experimental Medicine and Biology. 1996; 387: 7-15. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8794188

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Aflatoxin and kwashiorkor. Author(s): Mahoud B. Source: Acta Paediatrica (Oslo, Norway : 1992). 2001 January; 90(1): 103. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11227326

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Aflatoxin and liver cancer. Author(s): Jackson PE, Groopman JD. Source: Bailliere's Best Practice & Research. Clinical Gastroenterology. 1999 December; 13(4): 545-55. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10654919

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Aflatoxin and outcome from acute lower respiratory infection in children in The Philippines. Author(s): Denning DW, Quiepo SC, Altman DG, Makarananda K, Neal GE, Camallere EL, Morgan MR, Tupasi TE. Source: Annals of Tropical Paediatrics. 1995 September; 15(3): 209-16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8534039

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Aflatoxin as a human carcinogen. Author(s): Wogan GN. Source: Hepatology (Baltimore, Md.). 1999 August; 30(2): 573-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10421671

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Aflatoxin B1 8,9-epoxide hydrolysis in the presence of rat and human epoxide hydrolase. Author(s): Johnson WW, Yamazaki H, Shimada T, Ueng YF, Guengerich FP. Source: Chemical Research in Toxicology. 1997 June; 10(6): 672-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9208174

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Aflatoxin B1 aldehyde reductase (AFAR) genes cluster at 1p35-1p36.1 in a region frequently altered in human tumour cells. Author(s): Praml C, Savelyeva L, Schwab M. Source: Oncogene. 2003 July 24; 22(30): 4765-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12879023

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Aflatoxin B1-adduct formation in rat and human small bowel enterocytes. Author(s): Kolars JC, Benedict P, Schmiedlin-Ren P, Watkins PB. Source: Gastroenterology. 1994 February; 106(2): 433-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8299909

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Aflatoxin B1-induced DNA adduct formation and p53 mutations in CYP450expressing human liver cell lines. Author(s): Mace K, Aguilar F, Wang JS, Vautravers P, Gomez-Lechon M, Gonzalez FJ, Groopman J, Harris CC, Pfeifer AM. Source: Carcinogenesis. 1997 July; 18(7): 1291-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9230270

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Aflatoxin B1-induced immortalization of cultured skin fibroblasts from a patient with Li-Fraumeni syndrome. Author(s): Tsutsui T, Fujino T, Kodama S, Tainsky MA, Boyd J, Barrett JC. Source: Carcinogenesis. 1995 January; 16(1): 25-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7834802

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Aflatoxin contamination of Nigerian foods and feedingstuffs. Author(s): Atawodi SE, Atiku AA, Lamorde AG. Source: Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association. 1994 January; 32(1): 61-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8132166

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Aflatoxin exposure and cytogenetic alterations in individuals from the Gambia, West Africa. Author(s): Miele M, Donato F, Hall AJ, Whittle H, Chapot B, Bonatti S, De Ferrari M, Artuso M, Gallerani E, Abbondandolo A, Montesano R, Wild CP. Source: Mutation Research. 1996 February 1; 349(2): 209-17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8600352

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Aflatoxin exposure and DNA damage in the comet assay in individuals from the Gambia, West Africa. Author(s): Anderson D, Yu TW, Hambly RJ, Mendy M, Wild CP. Source: Teratogenesis, Carcinogenesis, and Mutagenesis. 1999; 19(2): 147-55. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10332811

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Aflatoxin exposure in Singapore: blood aflatoxin levels in normal subjects, hepatitis B virus carriers and primary hepatocellular carcinoma patients. Author(s): Chao TC, Lo DS, Bloodworth BC, Gunasegaram R, Koh TH, Ng HS. Source: Med Sci Law. 1994 October; 34(4): 289-98. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7830511

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Aflatoxin M1 contamination in commercial samples of milk and dairy products in Kuwait. Author(s): Srivastava VP, Bu-Abbas A, Alaa-Basuny, Al-Johar W, Al-Mufti S, Siddiqui MK. Source: Food Additives and Contaminants. 2001 November; 18(11): 993-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11665741

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Aflatoxin M1 in breast-milk of UAE women. Author(s): Abdulrazzaq YM, Osman N, Yousif ZM, Al-Falahi S. Source: Annals of Tropical Paediatrics. 2003 September; 23(3): 173-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14567832

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Aflatoxin M1 in human breast milk samples from Victoria, Australia and Thailand. Author(s): el-Nezami HS, Nicoletti G, Neal GE, Donohue DC, Ahokas JT. Source: Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association. 1995 March; 33(3): 173-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7896226

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Aflatoxin M1 in pasteurized and ultrapasteurized milk with different fat content in Mexico. Author(s): Carvajal M, Bolanos A, Rojo F, Mendez I. Source: J Food Prot. 2003 October; 66(10): 1885-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14572228

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Aflatoxin M1 occurrence in samples of Grana Padano cheese. Author(s): Peitri A, Bertuzzi T, Bertuzzi P, Piva G. Source: Food Additives and Contaminants. 1997 May-June; 14(4): 341-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9205562

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Aflatoxin related occupational exposure to maize processing workers. Author(s): Desai MR, Ghosh SK. Source: Cell Mol Biol (Noisy-Le-Grand). 2003 June; 49(4): 529-35. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12899445

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Aflatoxin, kwashiorkor, and morbidity. Author(s): Adhikari M, Gita-Ramjee, Berjak P. Source: Natural Toxins. 1994; 2(1): 1-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8032688

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Aflatoxin-albumin adducts: a basis for comparative carcinogenesis between animals and humans. Author(s): Wild CP, Hasegawa R, Barraud L, Chutimataewin S, Chapot B, Ito N, Montesano R. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 1996 March; 5(3): 179-89. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8833618

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An aflatoxin-associated mutational hotspot at codon 249 in the p53 tumor suppressor gene occurs in hepatocellular carcinomas from Mexico. Author(s): Soini Y, Chia SC, Bennett WP, Groopman JD, Wang JS, DeBenedetti VM, Cawley H, Welsh JA, Hansen C, Bergasa NV, Jones EA, DiBisceglie AM, Trivers GE, Sandoval CA, Calderon IE, Munoz Espinosa LE, Harris CC. Source: Carcinogenesis. 1996 May; 17(5): 1007-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8640905

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Association of aflatoxin B(1)-albumin adduct levels with hepatitis B surface antigen status among adolescents in Taiwan. Author(s): Chen SY, Chen CJ, Chou SR, Hsieh LL, Wang LY, Tsai WY, Ahsan H, Santella RM. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2001 November; 10(11): 1223-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11700273

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Associations of plasma aflatoxin B1-albumin adduct level with plasma selenium level and genetic polymorphisms of glutathione S-transferase M1 and T1. Author(s): Chen SY, Chen CJ, Tsai WY, Ahsan H, Liu TY, Lin JT, Santella RM. Source: Nutrition and Cancer. 2000; 38(2): 179-85. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11525595

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ATP-dependent transport of aflatoxin B1 and its glutathione conjugates by the product of the multidrug resistance protein (MRP) gene. Author(s): Loe DW, Stewart RK, Massey TE, Deeley RG, Cole SP. Source: Molecular Pharmacology. 1997 June; 51(6): 1034-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9187270

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Bacterial, fungal and aflatoxin contamination of cereals and cereal products in Bangkok. Author(s): Imwidthaya S, Anukarahanonta T, Komolpis P. Source: J Med Assoc Thai. 1987 July; 70(7): 390-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3668419

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Binding of aflatoxin B1 alters the adhesion properties of Lactobacillus rhamnosus strain GG in a Caco-2 model. Author(s): Kankaanpaa P, Tuomola E, El-Nezami H, Ahokas J, Salminen SJ. Source: J Food Prot. 2000 March; 63(3): 412-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10716575

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Binding of aflatoxin by plasma albumin in vitro. Author(s): Rao VN, Valmikinathan K, Verghese N. Source: Biochimica Et Biophysica Acta. 1968 September 3; 165(2): 288-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5683528

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Bioactivation and inactivation of aflatoxin B1 by human, mouse and rat liver preparations: effect on SCE in human mononuclear leucocytes. Author(s): Wilson AS, Williams DP, Davis CD, Tingle MD, Park BK. Source: Mutation Research. 1997 February 3; 373(2): 257-64. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9042408

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Bioactivation of aflatoxin B1 by human liver microsomes: role of cytochrome P450 IIIA enzymes. Author(s): Ramsdell HS, Parkinson A, Eddy AC, Eaton DL. Source: Toxicology and Applied Pharmacology. 1991 May; 108(3): 436-47. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1902334

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Biochemical and molecular aspects of mammalian susceptibility to aflatoxin B1 carcinogenicity. Author(s): Neal GE. Source: Human & Experimental Toxicology. 1995 July; 14(7): 619-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7576827

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Biochemical and molecular aspects of mammalian susceptibility to aflatoxin B1 carcinogenicity. Author(s): Massey TE, Stewart RK, Daniels JM, Liu L. Source: Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.). 1995 March; 208(3): 213-27. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7878060

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Biochemical basis for the extreme sensitivity of turkeys to aflatoxin B(1). Author(s): Klein PJ, Buckner R, Kelly J, Coulombe RA Jr. Source: Toxicology and Applied Pharmacology. 2000 May 15; 165(1): 45-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10814552

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Biological characteristics of the aflatoxin-induced hepatic tumor. Author(s): Woodhead AD. Source: Basic Life Sci. 1982; 21: 127-48. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6756374

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Biotransformation of aflatoxin B1 in human lung. Author(s): Donnelly PJ, Stewart RK, Ali SL, Conlan AA, Reid KR, Petsikas D, Massey TE. Source: Carcinogenesis. 1996 November; 17(11): 2487-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8968067

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Blood aflatoxin levels in patients with hepatocellular carcinoma in Singapore. Author(s): Tan CK, Lo DS, Law NM, Ng HS, Chao TC. Source: Singapore Med J. 1995 December; 36(6): 612-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8781632

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Cancer risks posed by aflatoxin M1. Author(s): Hsieh DP, Cullen JM, Hsieh LS, Shao Y, Ruebner BH. Source: Princess Takamatsu Symp. 1985; 16: 57-65. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3939566

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Case-control study of cigarette smoking and primary hepatoma in an aflatoxinendemic region of China: a protective effect. Author(s): Lin L, Yang F, Ye Z, Xu E, Yang C, Zhang C, Wu D, Nebert DW. Source: Pharmacogenetics. 1991 November; 1(2): 79-85. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1668964

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cDNA cloning, expression and activity of a second human aflatoxin B1-metabolizing member of the aldo-keto reductase superfamily, AKR7A3. Author(s): Knight LP, Primiano T, Groopman JD, Kensler TW, Sutter TR. Source: Carcinogenesis. 1999 July; 20(7): 1215-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10383892

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Cellular interactions and metabolism of aflatoxin: an update. Author(s): McLean M, Dutton MF. Source: Pharmacology & Therapeutics. 1995 February; 65(2): 163-92. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7540767

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Characterization of a murine p53ser246 mutant equivalent to the human p53ser249 associated with hepatocellular carcinoma and aflatoxin exposure. Author(s): Ghebranious N, Knoll BJ, Wu H, Lozano G, Sell S. Source: Molecular Carcinogenesis. 1995 June; 13(2): 104-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7605578

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Chemical and physical properties of the major serum albumin adduct of aflatoxin B1 and their implications for the quantification in biological samples. Author(s): Sabbioni G. Source: Chemico-Biological Interactions. 1990; 75(1): 1-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2114222

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Chromatographic and spectroscopic properties of hemiacetals of aflatoxin and sterigmatocystin metabolites. Author(s): Orti DL, Grainger J, Ashley DL, Hill RH Jr. Source: Journal of Chromatography. 1989 January 13; 462: 269-79. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2738124

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Chromosome damage by dothistromin in human peripheral blood lymphocyte cultures: a comparison with aflatoxin B1. Author(s): Ferguson LR, Parslow MI, McLarin JA. Source: Mutation Research. 1986 April-May; 170(1-2): 47-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3083246

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Chronic hepatitis B carriers with null genotypes of glutathione S-transferase M1 and T1 polymorphisms who are exposed to aflatoxin are at increased risk of hepatocellular carcinoma. Author(s): Chen CJ, Yu MW, Liaw YF, Wang LW, Chiamprasert S, Matin F, Hirvonen A, Bell DA, Santella RM. Source: American Journal of Human Genetics. 1996 July; 59(1): 128-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8659516

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Circumstances associated with the contamination of food by aflatoxin in a high primary liver cancer area. Author(s): Van Rensburg SJ, Kirsipuu A, Coutinho LP, Van Der Watt JJ. Source: South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde. 1975 May 24; 49(22): 877-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1145389

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Cirrhosis in children after consumption of aflatoxin-contaminated peanut meal. Author(s): Amla I, Parpia HA, Jayaraj AP. Source: The Journal of Pathology. 1971 February; 103(2): Pxix. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5567948

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Cirrhosis in children from peanut meal contaminated by aflatoxin. Author(s): Amla I, Kamala CS, Gopalakrishna GS, Jayaraj AP, Sreenivasamurthy V, Parpia HA. Source: The American Journal of Clinical Nutrition. 1971 June; 24(6): 609-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5581000

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Cloning and expression of succinic semialdehyde reductase from human brain. Identity with aflatoxin B1 aldehyde reductase. Author(s): Schaller M, Schaffhauser M, Sans N, Wermuth B. Source: European Journal of Biochemistry / Febs. 1999 November; 265(3): 1056-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10518801

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Cloning of cDNAs from fetal rat liver encoding glutathione S-transferase Yc polypeptides. The Yc2 subunit is expressed in adult rat liver resistant to the hepatocarcinogen aflatoxin B1. Author(s): Hayes JD, Nguyen T, Judah DJ, Petersson DG, Neal GE. Source: The Journal of Biological Chemistry. 1994 August 12; 269(32): 20707-17. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8051171

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Codon 249 of the human TP53 tumor suppressor gene is no hot spot for aflatoxin B1 in a heterologous background. Author(s): Sengstag C, Morbe JL, Weibel B. Source: Mutation Research. 1999 November 29; 430(1): 131-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10592324

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Comparative cytotoxicity of aflatoxin B1 and saxitoxin in cell cultures. Author(s): Gabliks J, Barter S. Source: Mol Toxicol. 1987 April-September; 1(2-3): 209-16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3130568

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Comparative ultrastructural effects of aflatoxin B1 on mouse, rat, and human hepatocytes in primary culture. Author(s): Cole KE, Hsu IC, Trump BF. Source: Cancer Research. 1986 March; 46(3): 1290-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3080241

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Comparison of rates of enzymatic oxidation of aflatoxin B1, aflatoxin G1, and sterigmatocystin and activities of the epoxides in forming guanyl-N7 adducts and inducing different genetic responses. Author(s): Baertschi SW, Raney KD, Shimada T, Harris TM, Guengerich FP. Source: Chemical Research in Toxicology. 1989 March-April; 2(2): 114-2. Erratum In: Chem Res Toxicol 1989 July-August; 2(4): 272. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2519710

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Comparison of S9 mix and hepatocytes as external metabolizing systems in mammalian cell cultures: cytogenetic effects of 7,12-dimethylbenzanthracene and aflatoxin B1. Author(s): Madle E, Tiedemann G, Madle S, Ott A, Kaufmann G. Source: Environ Mutagen. 1986; 8(3): 423-37. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3086074

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Co-mutagenicity of coumarin (1,2-benzopyrone) with aflatoxin B1 and human liver S9 in mammalian cells. Author(s): Goeger DE, Hsie AW, Anderson KE. Source: Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association. 1999 June; 37(6): 581-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10478826

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Contribution of the glutathione S-transferases to the mechanisms of resistance to aflatoxin B1. Author(s): Hayes JD, Judah DJ, McLellan LI, Neal GE. Source: Pharmacology & Therapeutics. 1991; 50(3): 443-72. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1754606

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Correlation of dietary aflatoxin B1 levels with excretion of aflatoxin M1 in human urine. Author(s): Zhu JQ, Zhang LS, Hu X, Xiao Y, Chen JS, Xu YC, Fremy J, Chu FS. Source: Cancer Research. 1987 April 1; 47(7): 1848-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3102051

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Correspondence re: G-S. Qian, et al., A follow-up study of urinary markers of aflatoxin exposure and liver cancer risk in Shanghai, People's Republic of China. Cancer Epidemiol., Biomarkers & Prev., 3:3-10, 1994, and C.C. Harris, Solving the viral-chemical puzzle of human liver carcinogenesis. Cancer Epidemiol., Biomarkers & Prev., 3:1-2, 1994. Author(s): Campbell TC. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 1994 September; 3(6): 519-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8000305

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Correspondence re: T. Colin Campbell et al., Nonassociation of aflatoxin with primary liver cancer in a cross-sectional ecological survey in the People's Republic of China. Cancer Res., 50:6882-6893, 1990. Author(s): Wild CP, Montesano R. Source: Cancer Research. 1991 July 15; 51(14): 3825-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2065337

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Cost-effectiveness of lowering the aflatoxin tolerance level. Author(s): Dichter CR, Weinstein MC. Source: Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association. 1984 June; 22(6): 439-45. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6429018

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CTNNB1 mutations and beta-catenin protein accumulation in human hepatocellular carcinomas associated with high exposure to aflatoxin B1. Author(s): Devereux TR, Stern MC, Flake GP, Yu MC, Zhang ZQ, London SJ, Taylor JA. Source: Molecular Carcinogenesis. 2001 June; 31(2): 68-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11429783

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Cytochrome P3-450 cDNA encodes aflatoxin B1-4-hydroxylase. Author(s): Faletto MB, Koser PL, Battula N, Townsend GK, Maccubbin AE, Gelboin HV, Gurtoo HL. Source: The Journal of Biological Chemistry. 1988 September 5; 263(25): 12187-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3137222

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Cytotoxic effects of aflatoxin B1 and its association with cellular components in chicken embryo primary cultured cells. Author(s): Iwaki M, Kitagawa T, Akamatsu Y, Aibara K. Source: Biochimica Et Biophysica Acta. 1990 August 17; 1035(2): 146-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1697481

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Cytotoxicity and mutagenicity of aflatoxin dichloride in normal and repair deficient diploid human fibroblasts. Author(s): Mahoney EM, Ball JC, Swenson DH, Richmond D, Maher VM, McCormick JJ. Source: Chemico-Biological Interactions. 1984 June; 50(1): 59-76. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6428759

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Cytotoxicity of aflatoxin B1 and its chemically synthesised epoxide derivative on the A549 human epithelioid lung cell line. Author(s): Palanee T, Dutton MF, Chuturgoon AA. Source: Mycopathologia. 2001; 151(3): 155-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11678590

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Defective repair of tryptophan pyrolysate (Trp P-1 and Trp P-2) and aflatoxin B1 damage in xeroderma pigmentosum cells. Author(s): Okui T, Fujiwara Y. Source: Journal of Radiation Research. 1983 December; 24(4): 356-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6427452

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Defenses against aflatoxin carcinogenesis in humans. Author(s): Masri MS. Source: Advances in Experimental Medicine and Biology. 1984; 177: 115-46. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6496216

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Detection and detoxification of aflatoxins: prevention of aflatoxicosis and aflatoxin residues with hydrated sodium calcium aluminosilicate. Author(s): Phillips TD, Clement BA, Kubena LF, Harvey RB. Source: Vet Hum Toxicol. 1990; 32 Suppl: 15-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1965459

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Detection of aflatoxin B1 in serum samples of male Japanese subjects by radioimmunoassay and high-performance liquid chromatography. Author(s): Tsuboi S, Nakagawa T, Tomita M, Seo T, Ono H, Kawamura K, Iwamura N. Source: Cancer Research. 1984 March; 44(3): 1231-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6420055

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Detection of exposure to aflatoxin in an African population. Author(s): Autrup H, Wakhisi J. Source: Iarc Sci Publ. 1988; (89): 63-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3143673

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Determinants of aflatoxin exposure in young children from Benin and Togo, West Africa: the critical role of weaning. Author(s): Gong YY, Egal S, Hounsa A, Turner PC, Hall AJ, Cardwell KF, Wild CP. Source: International Journal of Epidemiology. 2003 August; 32(4): 556-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12913029

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Determinants of specificity for aflatoxin B1-8,9-epoxide in alpha-class glutathione Stransferases. Author(s): McDonagh PD, Judah DJ, Hayes JD, Lian LY, Neal GE, Wolf CR, Roberts GC. Source: The Biochemical Journal. 1999 April 1; 339 ( Pt 1): 95-101. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10085232

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Determination of aflatoxin B1 biotransformation and binding to hepatic macromolecules in human precision liver slices. Author(s): Heinonen JT, Fisher R, Brendel K, Eaton DL. Source: Toxicology and Applied Pharmacology. 1996 January; 136(1): 1-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8560461

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Determination of aflatoxin B1 in baby food (infant formula) by immunoaffinity column cleanup liquid chromatography with postcolumn bromination: collaborative study. Author(s): Stroka J, Anklam E, Joerissen U, Gilbert J. Source: J Aoac Int. 2001 July-August; 84(4): 1116-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11501912

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Determination of aflatoxin M1 levels in cheese and milk consumed in Bursa, Turkey. Author(s): Oruc HH, Sonal S. Source: Vet Hum Toxicol. 2001 October; 43(5): 292-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11577937

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Determination of aflatoxin Q1 in urine by automated immunoaffinity column cleanup and liquid chromatography. Author(s): Kussak A, Andersson B, Andersson K. Source: Journal of Chromatography. B, Biomedical Applications. 1994 June 17; 656(2): 329-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7987484

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Determination of exposure to aflatoxins among Danish workers in animal-feed production through the analysis of aflatoxin B1 adducts to serum albumin. Author(s): Autrup JL, Schmidt J, Seremet T, Autrup H. Source: Scand J Work Environ Health. 1991 December; 17(6): 436-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1788537

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Detoxification of aflatoxin-polluted peanut cakes with monomethylamine/Ca(OH)2: pilot industrial application, nutrition experiments, toxicity evaluation. Author(s): Giddey C, Bunter G, Larroux R, Jemmali M, Rossi J. Source: Journal of Environmental Pathology, Toxicology and Oncology : Official Organ of the International Society for Environmental Toxicology and Cancer. 1992 JanuaryFebruary; 11(1): 60-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1740770

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Development of aflatoxin B(1)-lysine adduct monoclonal antibody for human exposure studies. Author(s): Wang JS, Abubaker S, He X, Sun G, Strickland PT, Groopman JD. Source: Applied and Environmental Microbiology. 2001 June; 67(6): 2712-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11375185

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Dietary clay in the chemoprevention of aflatoxin-induced disease. Author(s): Phillips TD. Source: Toxicological Sciences : an Official Journal of the Society of Toxicology. 1999 December; 52(2 Suppl): 118-26. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10630600

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Dietary exposure to aflatoxin in Benin City, Nigeria: a possible public health concern. Author(s): Ibeh IN, Uraih N, Ogonor JI. Source: International Journal of Food Microbiology. 1991 November; 14(2): 171-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1777386

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Dietary exposure to aflatoxin in human male infertility in Benin City, Nigeria. Author(s): Ibeh IN, Uraih N, Ogonar JI. Source: Int J Fertil Menopausal Stud. 1994 July-August; 39(4): 208-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7951403

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Dietary intake of aflatoxins and the level of albumin-bound aflatoxin in peripheral blood in The Gambia, West Africa. Author(s): Wild CP, Hudson GJ, Sabbioni G, Chapot B, Hall AJ, Wogan GN, Whittle H, Montesano R, Groopman JD. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 1992 March-April; 1(3): 229-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1339083

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Differential response of primary cultures of human and rat hepatocytes to aflatoxin B1-induced cytotoxicity and protection by the hepatoprotective agent (+)-cyanidanol3. Author(s): Begue JM, Baffet G, Campion JP, Guillouzo A. Source: Biology of the Cell / under the Auspices of the European Cell Biology Organization. 1988; 63(3): 327-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3147113

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Distribution and stability of aflatoxin M1 during processing, ripening and storage of Telemes cheese. Author(s): Govaris A, Roussi V, Koidis PA, Botsoglou NA. Source: Food Additives and Contaminants. 2001 May; 18(5): 437-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11358185

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DNA binding and adduct formation of aflatoxin B1 in cultured human and animal tracheobronchial and bladder tissues. Author(s): Stoner GD, Daniel FB, Schenck KM, Schut HA, Sandwisch DW, Gohara AF. Source: Carcinogenesis. 1982; 3(11): 1345-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6817939

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Do aflatoxin and polycyclic hydrocarbon carcinogens delete genes in the regions of chromosomes acted on by steroid hormones? Author(s): Money-Kyrle AF. Source: Medical Hypotheses. 1977 July-August; 3(4): 146-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=895590

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Do aflatoxin-DNA adduct measurements in humans provide accurate data for cancer risk assessment? Author(s): Groopman JD. Source: Iarc Sci Publ. 1988; (89): 55-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3143672

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Does aflatoxin B1 play a role in the etiology of hepatocellular carcinoma in the United States? Author(s): Hoque A, Patt YZ, Yoffe B, Groopman JD, Greenblatt MS, Zhang YJ, Santella RM. Source: Nutrition and Cancer. 1999; 35(1): 27-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10624703

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Dose dependency of aflatoxin B1 binding on human high molecular weight DNA in the activation of proto-oncogene. Author(s): Yang SS, Taub JV, Modali R, Vieira W, Yasei P, Yang GC. Source: Environmental Health Perspectives. 1985 October; 62: 231-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3002775

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Effect of aflatoxin B1 on human platelet protein kinase C. Author(s): Van den Heever LH, Dirr HW. Source: Int J Biochem. 1991; 23(9): 839-43. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1773888

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Effect of an extract of the root of Scutellaria baicalensis and its flavonoids on aflatoxin B1 oxidizing cytochrome P450 enzymes. Author(s): Kim BR, Kim DH, Park R, Kwon KB, Ryu DG, Kim YC, Kim NY, Jeong S, Kang BK, Kim KS. Source: Planta Medica. 2001 July; 67(5): 396-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11488450

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Effects of aflatoxin B1 on murine lymphocytic functions. Author(s): Reddy RV, Sharma RP. Source: Toxicology. 1989 January; 54(1): 31-44. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2492685

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Effects of aflatoxin on the immune system of the chick. Author(s): Virdi JS, Tiwari RP, Saxena M, Khanna V, Singh G, Saini SS, Vadehra DV. Source: Journal of Applied Toxicology : Jat. 1989 August; 9(4): 271-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2778263

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Effects of dietary oltipraz and ethoxyquin on aflatoxin B1 biotransformation in nonhuman primates. Author(s): Bammler TK, Slone DH, Eaton DL. Source: Toxicological Sciences : an Official Journal of the Society of Toxicology. 2000 March; 54(1): 30-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10746929

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Effects of hydrogen ion and fatty acid concentrations on the binding of aflatoxin B1 to human albumin. Author(s): Dirr HW. Source: Biochem Int. 1987 April; 14(4): 727-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3134025

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Elevated aflatoxin exposure and increased risk of hepatocellular carcinoma. Author(s): Chen CJ, Wang LY, Lu SN, Wu MH, You SL, Zhang YJ, Wang LW, Santella RM. Source: Hepatology (Baltimore, Md.). 1996 July; 24(1): 38-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8707279

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Elevated HPRT mutation frequencies in aflatoxin-exposed residents of daxin, Qidong county, People's Republic of China. Author(s): Wang SS, O'Neill JP, Qian GS, Zhu YR, Wang JB, Armenian H, Zarba A, Wang JS, Kensler TW, Cariello NF, Groopman JD, Swenberg JA. Source: Carcinogenesis. 1999 November; 20(11): 2181-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10545423

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Environmental and genetic determinants of aflatoxin-albumin adducts in the Gambia. Author(s): Wild CP, Yin F, Turner PC, Chemin I, Chapot B, Mendy M, Whittle H, Kirk GD, Hall AJ. Source: International Journal of Cancer. Journal International Du Cancer. 2000 April 1; 86(1): 1-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10728587

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Epidemiology of human aflatoxin exposures and their relationship to liver cancer. Author(s): Groopman JD, Scholl P, Wang JS. Source: Prog Clin Biol Res. 1996; 395: 211-22. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8895991

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Estimation of the daily exposure of Koreans to aflatoxin B1 through food consumption. Author(s): Park JW, Kim EK, Kim YB. Source: Food Additives and Contaminants. 2004 January; 21(1): 70-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14744682

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Evaluation of a commercial immunoassay system for sulfamethazine and aflatoxin detection in biological fluids and feeds. Author(s): Stahr HM, Pfeiffer RL, Mace B. Source: Vet Hum Toxicol. 1991 October; 33(5): 509-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1746151

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Evaluation of methods for quantitation of aflatoxin-albumin adducts and their application to human exposure assessment. Author(s): Wild CP, Jiang YZ, Sabbioni G, Chapot B, Montesano R. Source: Cancer Research. 1990 January 15; 50(2): 245-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2104776

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Evidence for human antibodies that recognize an aflatoxin epitope in groups with high and low exposure to aflatoxins. Author(s): Autrup H, Seremet T, Wakhisi J. Source: Archives of Environmental Health. 1990 January-February; 45(1): 31-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1690532

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Evidence for involvement of multiple forms of cytochrome P-450 in aflatoxin B1 metabolism in human liver. Author(s): Forrester LM, Neal GE, Judah DJ, Glancey MJ, Wolf CR. Source: Proceedings of the National Academy of Sciences of the United States of America. 1990 November; 87(21): 8306-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2122459

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Evidence for membrane-mediated chromosomal damage by aflatoxin B1 in human lymphocytes. Author(s): Amstad P, Levy A, Emerit I, Cerutti P. Source: Carcinogenesis. 1984 June; 5(6): 719-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6426812

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Evidence that mutational activation of the ras genes may not be involved in aflatoxin B(1)-induced human hepatocarcinogenesis, based on sequence analysis of the ras and p53 genes. Author(s): Chao HK, Tsai TF, Lin CS, Su TS. Source: Molecular Carcinogenesis. 1999 October; 26(2): 69-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10506750

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Excision repair of aflatoxin B1-DNA adducts in human fibroblasts. Author(s): Leadon SA, Tyrrell RM, Cerutti PA. Source: Cancer Research. 1981 December; 41(12 Pt 1): 5125-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6796265

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Exposure of infants to aflatoxin M1 from mothers' breast milk in Abu Dhabi, UAE. Author(s): Saad AM, Abdelgadir AM, Moss MO. Source: Food Additives and Contaminants. 1995 March-April; 12(2): 255-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7781822

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Expression of stably transfected murine glutathione S-transferase A3-3 protects against nucleic acid alkylation and cytotoxicity by aflatoxin B1 in hamster V79 cells expressing rat cytochrome P450-2B1. Author(s): Fields WR, Morrow CS, Doehmer J, Townsend AJ. Source: Carcinogenesis. 1999 June; 20(6): 1121-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10357798

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Failure of dietary dimethylsulfoxide to protect against aflatoxin in young broiler chickens. Author(s): Yen CC, Hamilton PB. Source: Poultry Science. 1982 February; 61(2): 255-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7088790

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Field studies of aflatoxin exposure, metabolism and induction of genetic alterations in relation to HBV infection and hepatocellular carcinoma in The Gambia and Thailand. Author(s): Wild CP, Shrestha SM, Anwar WA, Montesano R. Source: Toxicology Letters. 1992 December; 64-65 Spec No: 455-61. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1471197

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Five of 12 forms of vaccinia virus-expressed human hepatic cytochrome P450 metabolically activate aflatoxin B1. Author(s): Aoyama T, Yamano S, Guzelian PS, Gelboin HV, Gonzalez FJ. Source: Proceedings of the National Academy of Sciences of the United States of America. 1990 June; 87(12): 4790-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2162057

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Food additives and plant components control growth and aflatoxin production by toxigenic aspergilli: a review. Author(s): Rusul G, Marth EH. Source: Mycopathologia. 1988 January; 101(1): 13-23. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3281019

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Food surveillance in the Basque Country (Spain). II. Estimation of the dietary intake of organochlorine pesticides, heavy metals, arsenic, aflatoxin M1, iron and zinc through the Total Diet Study, 1990/91. Author(s): Urieta I, Jalon M, Eguilero I. Source: Food Additives and Contaminants. 1996 January; 13(1): 29-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8647305

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Formation and removal of aflatoxin B1-induced DNA lesions in epithelioid human lung cells. Author(s): Wang TC, Cerutti PA. Source: Cancer Research. 1979 December; 39(12): 5165-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=498143

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Genetic polymorphisms of glutathione S-transferases M1 and T1 associated with susceptibility to aflatoxin-related hepatocarcinogenesis among chronic hepatitis B carriers: a nested case-control study in Taiwan. Author(s): Sun CA, Wang LY, Chen CJ, Lu SN, You SL, Wang LW, Wang Q, Wu DM, Santella RM. Source: Carcinogenesis. 2001 August; 22(8): 1289-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11470760

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Genotoxicity of aflatoxin B1: evidence for a recombination-mediated mechanism in Saccharomyces cerevisiae. Author(s): Sengstag C, Weibel B, Fasullo M. Source: Cancer Research. 1996 December 1; 56(23): 5457-65. Erratum In: Cancer Res 1997 February 15; 57(4): 793. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8968101

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Glutathione conjugation of aflatoxin B1 exo- and endo-epoxides by rat and human glutathione S-transferases. Author(s): Raney KD, Meyer DJ, Ketterer B, Harris TM, Guengerich FP. Source: Chemical Research in Toxicology. 1992 July-August; 5(4): 470-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1391613

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Glutathione S-transferase-catalyzed conjugation of bioactivated aflatoxin B(1) in human lung: differential cellular distribution and lack of significance of the GSTM1 genetic polymorphism. Author(s): Stewart RK, Smith GB, Donnelly PJ, Reid KR, Petsikas D, Conlan AA, Massey TE. Source: Carcinogenesis. 1999 October; 20(10): 1971-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10506113

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Health risk and regulatory aspects of aflatoxin. Author(s): Robens JF. Source: Vet Hum Toxicol. 1980 August; 22(4): 264-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7404988

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Hepatitis B infection and aflatoxin biomarker levels in Gambian children. Author(s): Turner PC, Mendy M, Whittle H, Fortuin M, Hall AJ, Wild CP. Source: Tropical Medicine & International Health : Tm & Ih. 2000 December; 5(12): 83741. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11169271

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Hepatitis B, aflatoxin B(1), and p53 codon 249 mutation in hepatocellular carcinomas from Guangxi, People's Republic of China, and a meta-analysis of existing studies. Author(s): Stern MC, Umbach DM, Yu MC, London SJ, Zhang ZQ, Taylor JA. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2001 June; 10(6): 617-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11401911

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Hepatocarcinogenic material in urine specimens from humans consuming aflatoxin. Author(s): Campbell TC, Sinnhuber RO, Lee DJ, Wales JH, Salamat L. Source: Journal of the National Cancer Institute. 1974 May; 52(5): 1647-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4364740

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Hepatocellular carcinoma and aflatoxin exposure in Zhuqing Village, Fusui County, People's Republic of China. Author(s): Wang JS, Huang T, Su J, Liang F, Wei Z, Liang Y, Luo H, Kuang SY, Qian GS, Sun G, He X, Kensler TW, Groopman JD. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2001 February; 10(2): 143-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11219772

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Hepatocellular carcinoma and dietary aflatoxin in Mozambique and Transkei. Author(s): Van Rensburg SJ, Cook-Mozaffari P, Van Schalkwyk DJ, Van der Watt JJ, Vincent TJ, Purchase IF. Source: British Journal of Cancer. 1985 May; 51(5): 713-26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2986667

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Hepatocellular carcinoma p53 G > T transversions at codon 249: the fingerprint of aflatoxin exposure? Author(s): Lasky T, Magder L. Source: Environmental Health Perspectives. 1997 April; 105(4): 392-7. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9189703

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Heterologous expression of CYP2K1 and identification of the expressed protein (BVCYP2K1) as lauric acid (omega-1)-hydroxylase and aflatoxin B1 exo-epoxidase. Author(s): Yang YH, Miranda CL, Henderson MC, Wang-Buhler JL, Buhler DR. Source: Drug Metabolism and Disposition: the Biological Fate of Chemicals. 2000 November; 28(11): 1279-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11038153

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High frequency of promoter hypermethylation of RASSF1A and p16 and its relationship to aflatoxin B1-DNA adduct levels in human hepatocellular carcinoma. Author(s): Zhang YJ, Ahsan H, Chen Y, Lunn RM, Wang LY, Chen SY, Lee PH, Chen CJ, Santella RM. Source: Molecular Carcinogenesis. 2002 October; 35(2): 85-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12325038

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High serum concentrations of aflatoxin in Nepal as measured by enzyme-linked immunosorbent serum assay. Author(s): Denning DW, Sykes JA, Wilkinson AP, Morgan MR. Source: Human & Experimental Toxicology. 1990 May; 9(3): 143-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2165416

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HLA related genetic control of natural killer activity and aflatoxin B1 suppression of lymphocytic blastogenesis. Author(s): Wang CY, Yu XS, Hong JX, Lin TZ, Yang YQ. Source: Chinese Medical Journal. 1987 January; 100(1): 29-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3109821

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Human aflatoxin B1 metabolism: an investigation of the importance of aflatoxin Q1 as a metabolite of hepatic post-mitochondrial fraction. Author(s): Yourtee DM, Bean TA, Kirk-Yourtee CL. Source: Toxicology Letters. 1987 October; 38(3): 213-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3116726

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Human glutathione S-transferase-expressing Salmonella typhimurium tester strains to study the activation/detoxification of mutagenic compounds: studies with halogenated compounds, aromatic amines and aflatoxin B1. Author(s): Simula TP, Glancey MJ, Wolf CR. Source: Carcinogenesis. 1993 July; 14(7): 1371-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8330352

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Human hepatitis B virus and hepatocellular carcinoma. II. Experimental induction of hepatocellular carcinoma in tree shrews exposed to hepatitis B virus and aflatoxin B1. Author(s): Yan RQ, Su JJ, Huang DR, Gan YC, Yang C, Huang GH. Source: Journal of Cancer Research and Clinical Oncology. 1996; 122(5): 289-95. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8609152

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Human variability in hepatic glutathione S-transferase-mediated conjugation of aflatoxin B1-epoxide and other substrates. Author(s): Slone DH, Gallagher EP, Ramsdell HS, Rettie AE, Stapleton PL, Berlad LG, Eaton DL. Source: Pharmacogenetics. 1995 August; 5(4): 224-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8528269

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Identification of an aflatoxin G1-serum albumin adduct and its relevance to the measurement of human exposure to aflatoxins. Author(s): Sabbioni G, Wild CP. Source: Carcinogenesis. 1991 January; 12(1): 97-103. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1899057

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Identification of homozygous deletions at chromosome 16q23 in aflatoxin B1 exposed hepatocellular carcinoma. Author(s): Yakicier MC, Legoix P, Vaury C, Gressin L, Tubacher E, Capron F, Bayer J, Degott C, Balabaud C, Zucman-Rossi J. Source: Oncogene. 2001 August 23; 20(37): 5232-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11526514

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Immunobiological activities of mould products: functional impairment of human monocytes exposed to aflatoxin B1. Author(s): Cusumano V, Rossano F, Merendino RA, Arena A, Costa GB, Mancuso G, Baroni A, Losi E. Source: Research in Microbiology. 1996 June; 147(5): 385-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8763624

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Immunological and HPLC detection of aflatoxin adducts in human tissues after an acute poisoning incident in S.E. Asia. Author(s): Harrison JC, Garner RC. Source: Carcinogenesis. 1991 April; 12(4): 741-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1901526

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Immunoperoxidase detection of 8-hydroxydeoxyguanosine in aflatoxin B1-treated rat liver and human oral mucosal cells. Author(s): Yarborough A, Zhang YJ, Hsu TM, Santella RM. Source: Cancer Research. 1996 February 15; 56(4): 683-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8630995

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In vitro inhibition of dihydropyridine oxidation and aflatoxin B1 activation in human liver microsomes by naringenin and other flavonoids. Author(s): Guengerich FP, Kim DH. Source: Carcinogenesis. 1990 December; 11(12): 2275-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2265479

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In vitro mutational spectrum of aflatoxin B1 in the human hypoxanthine guanine phosphoribosyltransferase gene. Author(s): Cariello NF, Cui L, Skopek TR. Source: Cancer Research. 1994 August 15; 54(16): 4436-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8044792

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Inability of aflatoxin B1 to stimulate arachidonic acid metabolism in human polymorphonuclear and mononuclear leukocytes. Author(s): Geissler FT, Henderson WR. Source: Carcinogenesis. 1988 July; 9(7): 1135-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2838195

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Incidence of aflatoxin contamination in non-perishable food commodities. Author(s): Munir MA, Saleem M, Malik ZR, Ahmed M, Ali A. Source: J Pak Med Assoc. 1989 June; 39(6): 154-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2504956

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Increased risk of hepatocellular carcinoma in male hepatitis B surface antigen carriers with chronic hepatitis who have detectable urinary aflatoxin metabolite M1. Author(s): Sun Z, Lu P, Gail MH, Pee D, Zhang Q, Ming L, Wang J, Wu Y, Liu G, Wu Y, Zhu Y. Source: Hepatology (Baltimore, Md.). 1999 August; 30(2): 379-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10421643

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Influence of four Nigerian food additives on the mutagenicity of aflatoxin B1. Author(s): Osowole OA, Ogidi HJ, Uwaifo AO. Source: Afr J Med Med Sci. 1992 December; 21(2): 83-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1308087

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Inhibition of aflatoxin B1 genotoxicity in human liver-derived HepG2 cells by kolaviron biflavonoids and molecular mechanisms of action. Author(s): Nwankwo JO, Tahnteng JG, Emerole GO. Source: European Journal of Cancer Prevention : the Official Journal of the European Cancer Prevention Organisation (Ecp). 2000 October; 9(5): 351-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11075889

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Inhibition of aflatoxin B1 mutagenicity by cyclopiazonic acid in the presence of human liver preparations. Author(s): Sabater Vilar M, Kuilman-Wahls ME, Fink-Gremmels J. Source: Toxicology Letters. 2003 August 28; 143(3): 291-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12849689

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Inhibition of CYP1A2 and CYP3A4 by oltipraz results in reduction of aflatoxin B1 metabolism in human hepatocytes in primary culture. Author(s): Langouet S, Coles B, Morel F, Becquemont L, Beaune P, Guengerich FP, Ketterer B, Guillouzo A. Source: Cancer Research. 1995 December 1; 55(23): 5574-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7585637

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In-house direct cELISA for determining aflatoxin B1 in Thai corn and peanuts. Author(s): Lipigorngoson S, Limtrakul P, Suttajit M, Yoshizawa T. Source: Food Additives and Contaminants. 2003 September; 20(9): 838-45. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=13129779

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Intracellular localization of aflatoxin B1 in rat and human livers. Author(s): Stora C. Source: Journal of Environmental Pathology, Toxicology and Oncology : Official Organ of the International Society for Environmental Toxicology and Cancer. 1990 May-June; 10(3): 129-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2174970

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In-utero exposure to aflatoxin in west Africa. Author(s): Wild CP, Rasheed FN, Jawla MF, Hall AJ, Jansen LA, Montesano R. Source: Lancet. 1991 June 29; 337(8757): 1602. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1675725

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Investigation of various extractants for the analysis of aflatoxin B1 in different food and feed matrices. Author(s): Stroka J, Petz M, Joerissen U, Anklam E. Source: Food Additives and Contaminants. 1999 August; 16(8): 331-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10645347

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Involvement of cytochrome P450, glutathione S-transferase, and epoxide hydrolase in the metabolism of aflatoxin B1 and relevance to risk of human liver cancer. Author(s): Guengerich FP, Johnson WW, Ueng YF, Yamazaki H, Shimada T. Source: Environmental Health Perspectives. 1996 May; 104 Suppl 3: 557-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8781383

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Involvement of NO, H2O2 and TNF-alpha in the reduced antitumor activity of murine peritoneal macrophages by aflatoxin B1. Author(s): Moon EY, Rhee DK, Pyo S. Source: Cancer Letters. 1999 March 1; 136(2): 167-76. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10355746

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Killing and mutation of human lymphoblast cells by aflatoxin B1: evidence for an inducible repair response. Author(s): Kaden DA, Call KM, Leong PM, Komives EA, Thilly WG. Source: Cancer Research. 1987 April 15; 47(8): 1993-2001. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3103909

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Kinds of mutations induced by aflatoxin B1 in a shuttle vector replicating in human cells transiently expressing cytochrome P4501A2 cDNA. Author(s): Trottier Y, Waithe WI, Anderson A. Source: Molecular Carcinogenesis. 1992; 6(2): 140-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1326989

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Kinetics of hydrolysis and reaction of aflatoxin B1 exo-8,9-epoxide and relevance to toxicity and detoxication. Author(s): Guengerich FP, Johnson WW. Source: Drug Metabolism Reviews. 1999 February; 31(1): 141-58. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10065369

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Letter: Aflatoxin--human colon carcinogenesis? Author(s): Deger GE. Source: Annals of Internal Medicine. 1976 August; 85(2): 204-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=942142

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Liquid chromatographic method for aflatoxin M1 in milk. Author(s): van Egmond HP, Dragacci S. Source: Methods in Molecular Biology (Clifton, N.J.). 2001; 157: 59-69. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11050994

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Liver carcinogen aflatoxin B1 as an inducer of mitotic recombination in a human cell line. Author(s): Stettler PM, Sengstag C. Source: Molecular Carcinogenesis. 2001 July; 31(3): 125-38. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11479921

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Liver injury induced by aflatoxin. Author(s): Butler WH. Source: Prog Liver Dis. 1970; 3: 408-18. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4908708

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Liver microsomal metabolism of aflatoxin B 1 to a reactive derivative toxic to Salmonella typhimurium TA 1530. Author(s): Garner RC, Miller EC, Miller JA. Source: Cancer Research. 1972 October; 32(10): 2058-66. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4404160

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Major differences exist in the function and tissue-specific expression of human aflatoxin B1 aldehyde reductase and the principal human aldo-keto reductase AKR1 family members. Author(s): O'connor T, Ireland LS, Harrison DJ, Hayes JD. Source: The Biochemical Journal. 1999 October 15; 343 Pt 2: 487-504. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10510318

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Manual sorting to eliminate aflatoxin from peanuts. Author(s): Galvez FC, Francisco ML, Villarino BJ, Lustre AO, Resurreccion AV. Source: J Food Prot. 2003 October; 66(10): 1879-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14572227

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Measurement of aflatoxin in Nigerian sera by enzyme-linked immunosorbent assay. Author(s): Denning DW, Onwubalili JK, Wilkinson AP, Morgan MR. Source: Transactions of the Royal Society of Tropical Medicine and Hygiene. 1988; 82(1): 169-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3140442

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Mechanisms of aflatoxin B1 lung tumorigenesis. Author(s): Massey TE, Smith GB, Tam AS. Source: Experimental Lung Research. 2000 December; 26(8): 673-83. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11195464

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Mechanisms of aflatoxin carcinogenesis. Author(s): Eaton DL, Gallagher EP. Source: Annual Review of Pharmacology and Toxicology. 1994; 34: 135-72. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8042848

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Metabolic behaviour of aflatoxin producing strain and non-toxigenic strain of Aspergillus flavus to different sources of nitrogen and glucose concentration. Author(s): Thapar GS. Source: Mycopathologia. 1988 April; 102(1): 9-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3138542

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Metabolism of aflatoxin B1 by human hepatocytes in primary culture. Author(s): Langouet S, Coles B, Morel F, Maheo K, Ketterer B, Guillouzo A. Source: Advances in Experimental Medicine and Biology. 1996; 387: 439-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8794238

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Metabolism of aflatoxin B1 by normal human bronchial epithelial cells. Author(s): Van Vleet TR, Klein PJ, Coulombe RA Jr. Source: Journal of Toxicology and Environmental Health. Part A. 2001 August 10; 63(7): 525-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11497333

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Micronuclei, chromosomal aberrations and aflatoxin-albumin adducts in experimental animals after exposure to aflatoxin B1. Author(s): Anwar WA, Khalil MM, Wild CP. Source: Mutation Research. 1994 July; 322(1): 61-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7517505

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Molecular biology of aflatoxin biosynthesis. Author(s): Trail F, Mahanti N, Linz J. Source: Microbiology (Reading, England). 1995 April; 141 ( Pt 4): 755-65. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7773383

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Molecular dosimetry of aflatoxin DNA adducts in humans and experimental rat models. Author(s): Groopman JD, Roebuck BD, Kensler TW. Source: Prog Clin Biol Res. 1992; 374: 139-55. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1320272

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Molecular dosimetry of aflatoxin-N7-guanine in human urine obtained in The Gambia, West Africa. Author(s): Groopman JD, Hall AJ, Whittle H, Hudson GJ, Wogan GN, Montesano R, Wild CP. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 1992 March-April; 1(3): 221-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1339082

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Molecular dosimetry of hepatic aflatoxin B1-DNA adducts: linear correlation with hepatic cancer risk. Author(s): Bechtel DH. Source: Regulatory Toxicology and Pharmacology : Rtp. 1989 August; 10(1): 74-81. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2505337

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Molecular dosimetry of urinary aflatoxin-DNA adducts in people living in Guangxi Autonomous Region, People's Republic of China. Author(s): Groopman JD, Zhu JQ, Donahue PR, Pikul A, Zhang LS, Chen JS, Wogan GN. Source: Cancer Research. 1992 January 1; 52(1): 45-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1727385

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Molecular epidemiology of aflatoxin exposures: validation of aflatoxin-N7-guanine levels in urine as a biomarker in experimental rat models and humans. Author(s): Groopman JD, Wild CP, Hasler J, Junshi C, Wogan GN, Kensler TW. Source: Environmental Health Perspectives. 1993 March; 99: 107-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8319607

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Mutagenic activation of aflatoxin B1 by P-450 HFLa in human fetal livers. Author(s): Kitada M, Taneda M, Ohi H, Komori M, Itahashi K, Nagao M, Kamataki T. Source: Mutation Research. 1989 September; 227(1): 53-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2549412

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Mutagenic effect of aflatoxin G1 in comparison with B1. Author(s): el-Zawahri MM, Morad MM, Khishin AF. Source: Journal of Environmental Pathology, Toxicology and Oncology : Official Organ of the International Society for Environmental Toxicology and Cancer. 1990 JanuaryApril; 10(1-2): 45-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2121957

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Mutational properties of the primary aflatoxin B1-DNA adduct. Author(s): Bailey EA, Iyer RS, Stone MP, Harris TM, Essigmann JM. Source: Proceedings of the National Academy of Sciences of the United States of America. 1996 February 20; 93(4): 1535-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8643667

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Mutations of p53 gene in hepatocellular carcinoma: roles of hepatitis B virus and aflatoxin contamination in the diet. Author(s): Hsia CC, Kleiner DE Jr, Axiotis CA, Di Bisceglie A, Nomura AM, Stemmermann GN, Tabor E. Source: Journal of the National Cancer Institute. 1992 November 4; 84(21): 1638-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1279184

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Mycological survey for potential aflatoxin and ochratoxin producers and their toxicological properties in harvested Brazilian black pepper. Author(s): Gatti MJ, Fraga ME, Magnoli C, Dalcero AM, da Rocha Rosa CA. Source: Food Additives and Contaminants. 2003 December; 20(12): 1120-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14726275

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Natural co-occurrence of aflatoxin and cyclopiazonic acid in peanuts grown in Argentina. Author(s): Fernandez Pinto V, Patriarca A, Locani O, Vaamonde G. Source: Food Additives and Contaminants. 2001 November; 18(11): 1017-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11665730

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Nitrogen fertilizer influence on aflatoxin contamination of corn in Louisiana. Author(s): Tubajika KM, Mascagni HJ Jr, Damann KE, Russin JS. Source: Journal of Agricultural and Food Chemistry. 1999 December; 47(12): 5257-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10606605

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Nonassociation of aflatoxin with primary liver cancer in a cross-sectional ecological survey in the People's Republic of China. Author(s): Campbell TC, Chen JS, Liu CB, Li JY, Parpia B. Source: Cancer Research. 1990 November 1; 50(21): 6882-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2208157

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Occupational exposure to airborne fungi among rice mill workers with special reference to aflatoxin producing A. flavus strains. Author(s): Desai MR, Ghosh S. Source: Annals of Agricultural and Environmental Medicine : Aaem. 2003; 10(2): 159-62. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14677906

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Occurrence of aflatoxin in commodities imported into Qatar, 1997-2000. Author(s): Abdulkadar AH, Al-Ali A, Al-Jedah JH. Source: Food Additives and Contaminants. 2002 July; 19(7): 666-70. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12113661

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Occurrence of aflatoxin M(1) in raw and market milk commercialized in Greece. Author(s): Roussi V, Govaris A, Varagouli A, Botsoglou NA. Source: Food Additives and Contaminants. 2002 September; 19(9): 863-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12396397

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Occurrence of Aspergillus section flavi and aflatoxin B1 in corn genotypes and corn meal in Argentina. Author(s): Etcheverry M, Nesci A, Barros G, Torres A, Chulze S. Source: Mycopathologia. 1999; 147(1): 37-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10872514

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Oltipraz chemoprevention trial in Qidong, People's Republic of China: modulation of serum aflatoxin albumin adduct biomarkers. Author(s): Kensler TW, He X, Otieno M, Egner PA, Jacobson LP, Chen B, Wang JS, Zhu YR, Zhang BC, Wang JB, Wu Y, Zhang QN, Qian GS, Kuang SY, Fang X, Li YF, Yu LY, Prochaska HJ, Davidson NE, Gordon GB, Gorman MB, Zarba A, Enger C, Munoz A, Helzlsouer KJ, et al. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 1998 February; 7(2): 127-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9488587

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Oltipraz-mediated changes in aflatoxin B(1) biotransformation in rat liver: implications for human chemointervention. Author(s): Buetler TM, Bammler TK, Hayes JD, Eaton DL. Source: Cancer Research. 1996 May 15; 56(10): 2306-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8625305

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On influence of aflatoxin B1 on the physical properties of the avian myeloblastosis virus BAI strain A (AMV) and on the biosynthesis of viral nucleic acids. Author(s): Kremen J, Lexova J+LEXOVA J, Sula J. Source: Neoplasma. 1974; 21(3): 275-83. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4371293

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Outbreak of acute hepatitis caused by aflatoxin poisoning in Kenya. Author(s): Ngindu A, Johnson BK, Kenya PR, Ngira JA, Ocheng DM, Nandwa H, Omondi TN, Jansen AJ, Ngare W, Kaviti JN, Gatei D, Siongok TA. Source: Lancet. 1982 June 12; 1(8285): 1346-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6123648

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Overexpression of cytochrome P-450 isoforms involved in aflatoxin B1 bioactivation in human liver with cirrhosis and hepatitis. Author(s): Kirby GM, Batist G, Alpert L, Lamoureux E, Cameron RG, Alaoui-Jamali MA. Source: Toxicologic Pathology. 1996 July-August; 24(4): 458-67. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8864187

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Oxidation of aflatoxin B1 by bacterial recombinant human cytochrome P450 enzymes. Author(s): Ueng YF, Shimada T, Yamazaki H, Guengerich FP. Source: Chemical Research in Toxicology. 1995 March; 8(2): 218-25. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7766804

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Oxidation of aflatoxins and sterigmatocystin by human liver microsomes: significance of aflatoxin Q1 as a detoxication product of aflatoxin B1. Author(s): Raney KD, Shimada T, Kim DH, Groopman JD, Harris TM, Guengerich FP. Source: Chemical Research in Toxicology. 1992 March-April; 5(2): 202-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1643250

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Oxidative metabolism of aflatoxin B1 by lipoxygenase purified from human term placenta and intrauterine conceptal tissues. Author(s): Datta K, Kulkarni AP. Source: Teratology. 1994 October; 50(4): 311-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7716738

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p53 codon 249ser mutations in hepatocellular carcinoma patients with low aflatoxin exposure. Author(s): Patel P, Stephenson J, Scheuer PJ, Francis GE. Source: Lancet. 1992 April 4; 339(8797): 881. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1347900

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P53 gene of chang-liver cells (Atcc-Ccl13) exposed to aflatoxin B1 (Afb): the effect of lysine on mutation at codon 249 of exon 7. Author(s): Uwaifo O. Source: Afr J Med Med Sci. 1999 March-June; 28(1-2): 71-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12953991

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p53 mutation in hepatocellular carcinoma after aflatoxin exposure. Author(s): Ozturk M. Source: Lancet. 1991 November 30; 338(8779): 1356-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1682737

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p53 mutations and aflatoxin B1 exposure in hepatocellular carcinoma patients from Thailand. Author(s): Hollstein MC, Wild CP, Bleicher F, Chutimataewin S, Harris CC, Srivatanakul P, Montesano R. Source: International Journal of Cancer. Journal International Du Cancer. 1993 January 2; 53(1): 51-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8380058

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p53 proteins and aflatoxin b1: the good, the bad, and the ugly. Author(s): Liang TJ. Source: Hepatology (Baltimore, Md.). 1995 October; 22(4 Pt 1): 1330-2. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7557889

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Plasma antioxidant vitamins, chronic hepatitis B virus infection and urinary aflatoxin B1-DNA adducts in healthy males. Author(s): Yu MW, Chiang YC, Lien JP, Chen CJ. Source: Carcinogenesis. 1997 June; 18(6): 1189-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9214602

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Policy forum: public health. Reducing liver cancer--global control of aflatoxin. Author(s): Henry SH, Bosch FX, Troxell TC, Bolger PM. Source: Science. 1999 December 24; 286(5449): 2453-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10636808

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Possible effects of aflatoxin consumption by man. Author(s): Copper P. Source: Food Cosmet Toxicol. 1976 April; 14(2): 151-2. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=178583

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Precipitins to an aflatoxin-producing strain of Aspergillus flavus in patients with malignancy. Author(s): Wray BB, Harmon CA, Rushing EJ, Cole RJ. Source: Journal of Cancer Research and Clinical Oncology. 1982; 103(2): 181-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6807994

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Preliminary study on serum enzyme changes in Long Evans rats given parenteral ochratoxin A, aflatoxin B1 and their combination. Author(s): Brownie CF, Brownie C. Source: Vet Hum Toxicol. 1988 June; 30(3): 211-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3133871

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Presence of aflatoxin B1 in human liver in the United States. Author(s): Phillips DL, Yourtee DM, Searles S. Source: Toxicology and Applied Pharmacology. 1976 May; 36(2): 403-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1273856

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Presence of aflatoxin B1 in human liver referred to as Reye's syndrome in Venezuela. Author(s): Burguera JA. Source: Acta Cient Venez. 1986; 37(3): 325-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3113145

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Prevalence of exposure to aflatoxin and hepatitis B and C viruses in Guinea, West Africa. Author(s): Diallo MS, Sylla A, Sidibe K, Sylla BS, Trepo CR, Wild CP. Source: Natural Toxins. 1995; 3(1): 6-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7749585

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Primary liver cancer and aflatoxin intake in Transkei. Author(s): van Rensburg SJ, van Schalkwyk GC, van Schalkwyk DJ. Source: Journal of Environmental Pathology, Toxicology and Oncology : Official Organ of the International Society for Environmental Toxicology and Cancer. 1990 JanuaryApril; 10(1-2): 11-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2231312

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Primary liver cancer is of multifactorial origin: importance of hepatitis B virus infection and dietary aflatoxin. Author(s): Saracco G. Source: Journal of Gastroenterology and Hepatology. 1995 September-October; 10(5): 604-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8963039

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Production of aflatoxicol from aflatoxin B1 by postmitochondrial liver fractions. Author(s): Salhab AS, Edwards GS. Source: Journal of Toxicology and Environmental Health. 1977 January; 2(3): 583-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=846007

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Proficiency testing for the evaluation of the ability of European Union-National Reference laboratories to determine aflatoxin M1 in milk at levels corresponding to the new European Union legislation. Author(s): Dragacci S, Grosso F, Pfauwathel-Marchond N, Fremy JM, Venant A, Lombard B. Source: Food Additives and Contaminants. 2001 May; 18(5): 405-15. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11358182

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Protective activity of different hepatic cytosolic glutathione S-transferases against DNA-binding metabolites of aflatoxin B1. Author(s): Quinn BA, Crane TL, Kocal TE, Best SJ, Cameron RG, Rushmore TH, Farber E, Hayes MA. Source: Toxicology and Applied Pharmacology. 1990 September 15; 105(3): 351-63. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2173169

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Protective effects of coffee diterpenes against aflatoxin B1-induced genotoxicity: mechanisms in rat and human cells. Author(s): Cavin C, Mace K, Offord EA, Schilter B. Source: Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association. 2001 June; 39(6): 549-56. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11346484

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Pulmonary interstitial fibrosis with evidence of aflatoxin B1 in lung tissue. Author(s): Dvorackova I, Pichova V. Source: Journal of Toxicology and Environmental Health. 1986; 18(1): 153-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3084802

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Quantification and validation of enzyme immunoassay for urinary aflatoxin B1-N7guanine adduct for biological monitoring of aflatoxins. Author(s): Nayak S, Sashidhar RB, Bhat RV. Source: The Analyst. 2001 February; 126(2): 179-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11235100

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Quantitation and mapping of aflatoxin B1-induced DNA damage in genomic DNA using aflatoxin B1-8,9-epoxide and microsomal activation systems. Author(s): Denissenko MF, Cahill J, Koudriakova TB, Gerber N, Pfeifer GP. Source: Mutation Research. 1999 April 6; 425(2): 205-11. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10216213

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Quantitation of aflatoxin B1-N7-guanine adduct in urine by enzyme-linked immunosorbent assay coupled with immunoaffinity chromatography. Author(s): Vidyasagar T, Vyjayanthi V, Sujatha N, Rao BS, Bhat RV. Source: J Aoac Int. 1997 September-October; 80(5): 1013-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9325579

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Quantitative analysis of aflatoxin-albumin adducts. Author(s): Sheabar FZ, Groopman JD, Qian GS, Wogan GN. Source: Carcinogenesis. 1993 June; 14(6): 1203-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8508508

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Rapid immunochemical screening method for aflatoxin B1 in human and animal urine. Author(s): Stubblefield RD, Greer JI, Shotwell OL, Aikens AM. Source: J Assoc Off Anal Chem. 1991 May-June; 74(3): 530-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1908454

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Recent aflatoxin exposure and mutation at codon 249 of the human p53 gene: lack of association. Author(s): Hsieh DP, Atkinson DN. Source: Food Additives and Contaminants. 1995 May-June; 12(3): 421-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7664937

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Reduction of aflatoxin B(1) adduct biomarkers by oltipraz in the tree shrew (Tupaia belangeri chinensis). Author(s): Li Y, Su J, Qin L, Egner PA, Wang J, Groopman JD, Kensler TW, Roebuck BD. Source: Cancer Letters. 2000 June 1; 154(1): 79-83. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10799742

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Reduction of aflatoxin B1 dialdehyde by rat and human aldo-keto reductases. Author(s): Guengerich FP, Cai H, McMahon M, Hayes JD, Sutter TR, Groopman JD, Deng Z, Harris TM. Source: Chemical Research in Toxicology. 2001 June; 14(6): 727-37. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11409944

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Regulation of glutathione S-transferases and aldehyde reductase by chemoprotectors: studies of mechanisms responsible for inducible resistance to aflatoxin B1. Author(s): Hayes JD, McLeod R, Ellis EM, Pulford DJ, Ireland LS, McLellan LI, Judah DJ, Manson MM, Neal GE. Source: Iarc Sci Publ. 1996; (139): 175-87. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8923030

80

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Regulatory surveillance for aflatoxin and other mycotoxins in feeds, meat, and milk. Author(s): Wessel JR, Stoloff L. Source: J Am Vet Med Assoc. 1973 December 1; 163(11): 1284-7. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4800880

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Relation between geographical distribution of liver cancer and climate-aflatoxin B1 in China. Author(s): Wang YB, Lan LZ, Ye BF, Xu YC, Liu YY, Li WG. Source: Sci Sin [b]. 1983 November; 26(11): 1166-75. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6422550

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Relationship between fungal growth and aflatoxin production in varities of maize and groundnut. Author(s): Priyadarshini E, Tulpule PG. Source: Journal of Agricultural and Food Chemistry. 1978 January-February; 26(1): 24952. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=621329

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Repair of DNA in human cells after treatment with activated aflatoxin B1. Author(s): Sarasin AR, Smith CA, Hanawalt PC. Source: Cancer Research. 1977 June; 37(6): 1786-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=192462

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Response of culture human skin fibroblasts to aflatoxin B1. Author(s): McCoy BJ, Llewellyn GC. Source: Bulletin of Environmental Contamination and Toxicology. 1980 July; 25(1): 7-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7459485

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Response: relative versus absolute risk modeling of aflatoxin. Author(s): Bowers JC. Source: Risk Analysis : an Official Publication of the Society for Risk Analysis. 1993 February; 13(1): 9-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8451464

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Response: risk assessment for aflatoxin. Author(s): Bruce RD. Source: Risk Analysis : an Official Publication of the Society for Risk Analysis. 1994 December; 14(6): 897. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7846323

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Risk assessment for aflatoxin B1: a modeling approach. Author(s): Wu-Williams AH, Zeise L, Thomas D. Source: Risk Analysis : an Official Publication of the Society for Risk Analysis. 1992 December; 12(4): 559-67. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1336206

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Risk assessment for aflatoxin: an evaluation based on the multistage model. Author(s): Bowers J, Brown B, Springer J, Tollefson L, Lorentzen R, Henry S. Source: Risk Analysis : an Official Publication of the Society for Risk Analysis. 1993 December; 13(6): 637-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8310162

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Risk assessment for aflatoxin: I. Metabolism of aflatoxin B1 by different species. Author(s): Gorelick NJ. Source: Risk Analysis : an Official Publication of the Society for Risk Analysis. 1990 December; 10(4): 539-59. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2287782

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Risk assessment for aflatoxin: II. Implications of human epidemiology data. Author(s): Bruce RD. Source: Risk Analysis : an Official Publication of the Society for Risk Analysis. 1990 December; 10(4): 561-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2287783

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Risk assessment for aflatoxin: III. Modeling the relative risk of hepatocellular carcinoma. Author(s): Hoseyni MS. Source: Risk Analysis : an Official Publication of the Society for Risk Analysis. 1992 March; 12(1): 123-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1315449

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Risk estimates of liver cancer due to aflatoxin exposure from peanuts and peanut products. Author(s): Dichter CR. Source: Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association. 1984 June; 22(6): 431-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6539733

82

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Role of genetic polymorphism of glutathione-S-transferase T1 and microsomal epoxide hydrolase in aflatoxin-associated hepatocellular carcinoma. Author(s): Tiemersma EW, Omer RE, Bunschoten A, van't Veer P, Kok FJ, Idris MO, Kadaru AM, Fedail SS, Kampman E. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2001 July; 10(7): 785-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11440964

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Role of human microsomal and human complementary DNA-expressed cytochromes P4501A2 and P4503A4 in the bioactivation of aflatoxin B1. Author(s): Gallagher EP, Wienkers LC, Stapleton PL, Kunze KL, Eaton DL. Source: Cancer Research. 1994 January 1; 54(1): 101-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8261428

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Screening method for the detection of aflatoxin and metabolites in human urine: aflatoxins B1, G1, M1, B2a, G2a, aflatoxicols I and II. Author(s): Lovelace CE, Njapau H, Salter LF, Bayley AC. Source: Journal of Chromatography. 1982 January 8; 227(1): 256-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6799532

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Selection and characterisation of recombinant single-chain antibodies to the hapten Aflatoxin-B1 from naive recombinant antibody libraries. Author(s): Moghaddam A, Lobersli I, Gebhardt K, Braunagel M, Marvik OJ. Source: Journal of Immunological Methods. 2001 August 1; 254(1-2): 169-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11406162

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Sequence specificity of aflatoxin B1-induced mutations in a plasmid replicated in xeroderma pigmentosum and DNA repair proficient human cells. Author(s): Levy DD, Groopman JD, Lim SE, Seidman MM, Kraemer KH. Source: Cancer Research. 1992 October 15; 52(20): 5668-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1394191

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Serum albumin adducts in the molecular epidemiology of aflatoxin carcinogenesis: correlation with aflatoxin B1 intake and urinary excretion of aflatoxin M1. Author(s): Gan LS, Skipper PL, Peng XC, Groopman JD, Chen JS, Wogan GN, Tannenbaum SR. Source: Carcinogenesis. 1988 July; 9(7): 1323-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3133131

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83

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Shuttle-vector mutagenesis by aflatoxin B1 in human cells: effects of sequence context on the supF mutational spectrum. Author(s): Courtemanche C, Anderson A. Source: Mutation Research. 1994 April 15; 306(2): 143-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7512213

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Site-specific synthesis of aflatoxin B(1) adducts within an oligodeoxyribonucleotide containing the human p53 codon 249 sequence. Author(s): Jones WR, Johnston DS, Stone MP. Source: Chemical Research in Toxicology. 1999 August; 12(8): 707-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10458704

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Species comparison of in vitro metabolism of aflatoxin B1. Author(s): Roebuck BD, Wogan GN. Source: Cancer Research. 1977 June; 37(6): 1649-56. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=404034

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Species susceptibility to aflatoxin B1 carcinogenesis: comparative kinetics of microsomal biotransformation. Author(s): Ramsdell HS, Eaton DL. Source: Cancer Research. 1990 February 1; 50(3): 615-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2105159

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Specificity of aflatoxin B1 binding on human proto-oncogene nucleotide sequence. Author(s): Modali R, Yang SS. Source: Prog Clin Biol Res. 1986; 207: 147-58. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3083425

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Stable expression of human cytochrome P450IA2 cDNA in a human lymphoblastoid cell line: role of the enzyme in the metabolic activation of aflatoxin B1. Author(s): Crespi CL, Steimel DT, Aoyama T, Gelboin HV, Gonzalez FJ. Source: Molecular Carcinogenesis. 1990; 3(1): 5-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2108694

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Study on the binding of aflatoxin B1 to cellular components. I. Binding of aflatoxin B1 to albumin in vitro. Author(s): Lu FJ, Ling KH. Source: Taiwan Yi Xue Hui Za Zhi. 1973 August; 72(8): 434-9. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4520340

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Substances with affinity to a monoclonal aflatoxin B1 antibody in Danish urine samples. Author(s): Dragsted LO, Bull I, Autrup H. Source: Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association. 1988 March; 26(3): 233-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2452776

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Suppression of the interleukin-2 gene expression by aflatoxin B1 is mediated through the down-regulation of the NF-AT and AP-1 transcription factors. Author(s): Han SH, Jeon YJ, Yea SS, Yang KH. Source: Toxicology Letters. 1999 July 30; 108(1): 1-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10472804

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Survey of the occurrence of aflatoxin M1 in dairy products marketed in Italy: second year of observation. Author(s): Galvano F, Galofaro V, Ritieni A, Bognanno M, De Angelis A, Galvano G. Source: Food Additives and Contaminants. 2001 July; 18(7): 644-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11469321

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Susceptibility to aflatoxin B1-related primary hepatocellular carcinoma in mice and humans. Author(s): McGlynn KA, Hunter K, LeVoyer T, Roush J, Wise P, Michielli RA, Shen FM, Evans AA, London WT, Buetow KH. Source: Cancer Research. 2003 August 1; 63(15): 4594-601. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12907637

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Susceptibility to hepatocellular carcinoma is associated with genetic variation in the enzymatic detoxification of aflatoxin B1. Author(s): McGlynn KA, Rosvold EA, Lustbader ED, Hu Y, Clapper ML, Zhou T, Wild CP, Xia XL, Baffoe-Bonnie A, Ofori-Adjei D, et al. Source: Proceedings of the National Academy of Sciences of the United States of America. 1995 March 14; 92(6): 2384-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7892276

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Synergism between hepatitis B virus and aflatoxin in hepatocellular carcinoma. Author(s): Ayoola EA. Source: Iarc Sci Publ. 1984; (63): 167-79. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6100268

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Synergistic hepatocarcinogenic effect of hepadnaviral infection and dietary aflatoxin B1 in woodchucks. Author(s): Bannasch P, Khoshkhou NI, Hacker HJ, Radaeva S, Mrozek M, Zillmann U, Kopp-Schneider A, Haberkorn U, Elgas M, Tolle T, et al. Source: Cancer Research. 1995 August 1; 55(15): 3318-30. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7614467

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Synergistic interaction between aflatoxin B1 and hepatitis B virus in hepatocarcinogenesis. Author(s): Kew MC. Source: Liver International : Official Journal of the International Association for the Study of the Liver. 2003 December; 23(6): 405-9. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14986813

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Systemic aspergillosis caused by an aflatoxin-producing strain of Aspergillus flavus. Author(s): Mori T, Matsumura M, Yamada K, Irie S, Oshimi K, Suda K, Oguri T, Ichinoe M. Source: Medical Mycology : Official Publication of the International Society for Human and Animal Mycology. 1998 April; 36(2): 107-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9776821

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Temporal patterns of aflatoxin-albumin adducts in hepatitis B surface antigenpositive and antigen-negative residents of Daxin, Qidong County, People's Republic of China. Author(s): Wang JS, Qian GS, Zarba A, He X, Zhu YR, Zhang BC, Jacobson L, Gange SJ, Munoz A, Kensler TW, et al. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 1996 April; 5(4): 253-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8722216

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The 1995 Pharmacological Society of Canada Merck Frosst Award. Cellular and molecular targets in pulmonary chemical carcinogenesis: studies with aflatoxin B1. Author(s): Massey TE. Source: Canadian Journal of Physiology and Pharmacology. 1996 June; 74(6): 621-8. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8909771

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The aflatoxin B(1) formamidopyrimidine adduct plays a major role in causing the types of mutations observed in human hepatocellular carcinoma. Author(s): Smela ME, Hamm ML, Henderson PT, Harris CM, Harris TM, Essigmann JM. Source: Proceedings of the National Academy of Sciences of the United States of America. 2002 May 14; 99(10): 6655-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12011430

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The aflatoxin-lysine adduct quantified by high-performance liquid chromatography from human serum albumin samples. Author(s): Sabbioni G, Ambs S, Wogan GN, Groopman JD. Source: Carcinogenesis. 1990 November; 11(11): 2063-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2121383

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The anticalmodulin effect of aflatoxin B1 on purified erythrocyte Ca(2+)-ATPase. Author(s): Adebayo AO, Okunade GW, Olorunsogo OO. Source: Bioscience Reports. 1995 August; 15(4): 209-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8562872

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The binding of aflatoxin B1 with serum albumin. Author(s): Bassir O, Bababunmi EA. Source: Biochemical Pharmacology. 1973 January 1; 22(1): 132-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4763240

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The chemistry and biology of aflatoxin B(1): from mutational spectrometry to carcinogenesis. Author(s): Smela ME, Currier SS, Bailey EA, Essigmann JM. Source: Carcinogenesis. 2001 April; 22(4): 535-45. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11285186

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The cytogenetic effects of aflatoxin and gamma-rays on human leukocytes in vitro. Author(s): Promchainant C, Baimai V, Nondasuta A. Source: Mutation Research. 1972 December; 16(4): 373-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=5084979

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The development of a human cell line stably expressing human CYP3A4: role in the metabolic activation of aflatoxin B1 and comparison to CYP1A2 and CYP2A3. Author(s): Crespi CL, Penman BW, Steimel DT, Gelboin HV, Gonzalez FJ. Source: Carcinogenesis. 1991 February; 12(2): 355-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1899812

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The endo-8,9-epoxide of aflatoxin B1: a new metabolite. Author(s): Raney KD, Coles B, Guengerich FP, Harris TM. Source: Chemical Research in Toxicology. 1992 May-June; 5(3): 333-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1504254

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The Escherichia coli DNA repair protein UvrA can re-associate with the UvrB: aflatoxin B1-DNA complex in vitro. Author(s): Allan JM, Routledge MN, Garner RC. Source: Mutation Research. 1996 April 2; 362(3): 261-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8637504

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The metabolism of aflatoxin B1 by human liver. Author(s): Moss EJ, Neal GE. Source: Biochemical Pharmacology. 1985 September 1; 34(17): 3193-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3929787

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The mutagenicity of aflatoxin Q1 to Salmonella typhimurium TA 100 with or without rat or human liver microsomal preparations. Author(s): Yourtee DM, Kirk-Yourtee CL. Source: Res Commun Chem Pathol Pharmacol. 1986 October; 54(1): 101-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3099349

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The role of aflatoxin metabolism in its toxic lesion. Author(s): Campbell TC, Hayes JR. Source: Toxicology and Applied Pharmacology. 1976 February; 35(2): 199-222. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4903

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The role of dietary aflatoxin in the genesis of hepatocellular cancer in developing countries. Author(s): Enwonwu CO. Source: Lancet. 1984 October 27; 2(8409): 956-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6149345

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The role of infection by Opisthorchis viverrini, hepatitis B virus, and aflatoxin exposure in the etiology of liver cancer in Thailand. A correlation study. Author(s): Srivatanakul P, Parkin DM, Jiang YZ, Khlat M, Kao-Ian UT, Sontipong S, Wild C. Source: Cancer. 1991 December 1; 68(11): 2411-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1657355

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The use of monoclonal antibody affinity columns for assessing DNA damage and repair following exposure to aflatoxin B1. Author(s): Groopman JD, Kensler TW. Source: Pharmacology & Therapeutics. 1987; 34(2): 321-34. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3120202

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Toward less misleading comparisons of uncertain risks: the example of aflatoxin and alar. Author(s): Finkel AM. Source: Environmental Health Perspectives. 1995 April; 103(4): 376-85. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7607139

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Toxicity testing in vitro. I. The effects of delta 9-tetrahydrocannabinol and aflatoxin B1 on the growth of cultured human fibroblasts. Author(s): Cooper JT, Goldstein S. Source: Canadian Journal of Physiology and Pharmacology. 1976 August; 54(4): 541-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=974881

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Transplacental transfer of aflatoxin in humans. Author(s): Denning DW, Allen R, Wilkinson AP, Morgan MR. Source: Carcinogenesis. 1990 June; 11(6): 1033-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2112058

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U.S. Food and Drug Administration approach to risk assessment of aflatoxin in human foods. Author(s): Henry SH, Scheuplein RJ, Bowers J, Tollefson L. Source: Quality Assurance (San Diego, Calif.). 1993 March-June; 2(1-2): 71-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8156225

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Uncertainties in the risk assessment of three mycotoxins: aflatoxin, ochratoxin, and zearalenone. Author(s): Kuiper-Goodman T. Source: Canadian Journal of Physiology and Pharmacology. 1990 July; 68(7): 1017-24. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2143430

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Urinary aflatoxin B and effects of preservatives on its detecton. Author(s): Parpia HA, Sreenivasamurthy V, Shantha T, Shankaramurti A, Amla I, Srikantia S. Source: The American Journal of Clinical Nutrition. 1972 January; 25(1): 13-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4621421

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Urinary aflatoxin biomarkers and risk of hepatocellular carcinoma. Author(s): Ross RK, Yuan JM, Yu MC, Wogan GN, Qian GS, Tu JT, Groopman JD, Gao YT, Henderson BE. Source: Lancet. 1992 April 18; 339(8799): 943-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1348796

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Urinary aflatoxin levels, hepatitis-B virus infection and hepatocellular carcinoma in Taiwan. Author(s): Hatch MC, Chen CJ, Levin B, Ji BT, Yang GY, Hsu SW, Wang LW, Hsieh LL, Santella RM. Source: International Journal of Cancer. Journal International Du Cancer. 1993 July 30; 54(6): 931-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8392983

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Urinary excretion of aflatoxin and liver cancer in Karachi. Author(s): Nizami F, Nizami HM, Ahmad M. Source: J Pak Med Assoc. 1986 May; 36(5): 112-4. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3093719

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Use of aflatoxin adducts as intermediate endpoints to assess the efficacy of chemopreventive interventions in animals and man. Author(s): Kensler TW, Groopman JD, Roebuck BD. Source: Mutation Research. 1998 June 18; 402(1-2): 165-72. Review. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9675269

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Use of an improved method for analysis of urinary aflatoxin M1 in a survey of mainland China and Taiwan. Author(s): Cheng Z, Root M, Pan W, Chen J, Campbell TC. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 1997 July; 6(7): 523-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9232340

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Variability in aflatoxin B(1)-macromolecular binding and relationship to biotransformation enzyme expression in human prenatal and adult liver. Author(s): Doi AM, Patterson PE, Gallagher EP. Source: Toxicology and Applied Pharmacology. 2002 May 15; 181(1): 48-59. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12030842

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Variability in aflatoxin-albumin adduct levels and effects of hepatitis B and C virus infection and glutathione S-transferase M1 and T1 genotype. Author(s): Ahsan H, Wang LY, Chen CJ, Tsai WY, Santella RM. Source: Environmental Health Perspectives. 2001 August; 109(8): 833-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11564620

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Variability of aflatoxin and cyclopiazonic acid production by Aspergillus section flavi from different substrates in Argentina. Author(s): Vaamonde G, Patriarca A, Fernandez Pinto V, Comerio R, Degrossi C. Source: International Journal of Food Microbiology. 2003 November 15; 88(1): 79-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14527788

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Vitamin A ameliorates the genotoxicity in mice of aflatoxin B1-containing Aspergillus flavus infested food. Author(s): Sinha SP, Dharmshila K. Source: Cytobios. 1994; 79(317): 85-95. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7835072

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CHAPTER 2. NUTRITION AND AFLATOXIN Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and aflatoxin.

Finding Nutrition Studies on Aflatoxin The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail: [email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “aflatoxin” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.

7 Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.

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The following information is typical of that found when using the “Full IBIDS Database” to search for “aflatoxin” (or a synonym): •

A pilot clinical study examining the ability of a mixture of Lactobacillus and Propionibacterium to remove aflatoxin from the gastrointestinal tract of healthy Egyptian volunteers. Author(s): RMIT University, Melbourne (Australie). Key Centre for Toxicology Source: Ahokas, J.T. El Nezami, H.S. Kankaanpaeae, P. Mykkaenen, H. Salminen, S. Revue-de-Medecine-Veterinaire (France). (June 1998). volume 146(6) page 568.

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Study on the ability of esterified glucomannans (EGM) to prevent the gastrointestinal absorption of mycotoxins in laying hens. Author(s): Bologna Univ. (Italy). Dipartimento di Sanita Pubblica Veterinaria e Patologia Animale Bologna Univ. (Italy). Dipartimento di Morfofisiologia Veterinaria e Produzioni Animali Source: Zaghini, A. Altafini, A. Rizzi, L. Simioli, M. Proceedings-of-the-ASPA-CongressRecent-Progress-in-Animal-Production-Science (Italy). (2001). volume 2 page 442-444.

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Trials for restoring the toxicity of aflatoxin. Author(s): Tanta Univ., Kafr El-Sheikh (Egypt). Faculty of Veterinary Medicine Source: Abdel Aziz, M.I. kamel, F.M. Hegazi, S. Alexandria-Journal-of-VeterinaryScience (Egypt). (April 1995). volume 11 (1) page 19-26. Received 1999.

Additional physician-oriented references include: •

A rationale for the control of aflatoxin in human foods. Source: Stoloff, L. Bioactive-Mol. Amsterdam : Elsevier Science Publishers, B.V. 1986. volume 1 page 457-471.

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Aflatoxin and aflatoxicosis. IV. The effect of dietary aflatoxins on adult fertile male and female rabbits at various reproductive conditons. Source: Hafez, A.H. Gomma, A. Mousa, S.A. Megalla, S.E. Mycopathologia. The Hague : W. Junk. November 25, 1983. volume 83 (3) page 183-186. 0301-486X

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Aflatoxin B1 induces apoptosis in rat liver: protective effect of melatonin. Author(s): Biochemistry Department, Faculty of Medicine, Assiut University, Assiut, Egypt. [email protected]. Source: Meki, A R Abdel Ghaffar, S K El Gibaly, I Neuroendocrinol-Lett. 2001 December; 22(6): 417-26 0172-780X

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Aflatoxin B1 production in orange (Citrus reticulata) juice by isolates of Aspergillus flavus Link. Source: Varma, S K Verma, R A Mycopathologia. 1987 February; 97(2): 101-4 0301-486X

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Aflatoxin excretion in children with kwashiorkor or marasmic kwashiorkor--a clinical investigation. Author(s): St Mary's Hospital Mumias, Kakamega district, Kenya. Source: de Vries, H R Maxwell, S M Hendrickse, R G Mycopathologia. 1990 April; 110(1): 1-9 0301-486X

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Aflatoxin in the Philippines. Source: Garcia, R.P. Ilag, L.L. Aflatoxin in maize : proceedings of the workshop, El Batan, Mexico, April 7-11, 1986 / sponspored by CIMMYT, UNDP and USAID. Mexico, D.F. : CIMMYT, [1986]. page 365-372. ISBN: 9686127127

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Aflatoxin production in supplemental feeders provided for northern bobwhite in Texas and Oklahoma. Author(s): Department of Range, Wildlife, and Fisheries Management, Texas Tech University, Lubbock, Texas 79409-2125, USA. Source: Oberheu, D G Dabbert, C B J-Wildl-Dis. 2001 July; 37(3): 475-80 0090-3558

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Aflatoxins in sunflower seeds: effect of zinc in aflatoxin production by two strains of Aspergillus parasiticus. Author(s): Department of Microbiology and Immunology, National University of Rio Cuarto, Argentina. Source: Chulze, S Fusero, S Dalcero, A Etcheverry, M Varsavsky, E Mycopathologia. 1987 August; 99(2): 91-4 0301-486X

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Alteration of aflatoxin B1 metabolic profiles and reduction of aflatoxin B1 mutagenicity by hepatic microsomes of rats fed butylated hydroxyanisole. Author(s): Department of Pharmacology and Toxicology, Inha Medical College, Inchon, Japan. Source: Choi, C Y Park, S H Park, E H Cha, Y N J-Toxicol-Sci. 1991 February; 16 Suppl 1119-32 0388-1350

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Altered DNA mutation spectrum in aflatoxin b1-treated transgenic mice that express the hepatitis B virus x protein. Author(s): Department of Molecular Virology and Microbiology. Department of Pathology, Baylor College of Medicine, Houston, Texas 77030, USA. Source: Madden, C R Finegold, M J Slagle, B L J-Virol. 2002 November; 76(22): 11770-4 0022-538X

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Application of monoclonal antibodies and dietary antioxidant-based animal models to define human exposure to aflatoxin B1. Source: Groopman, J D Roebuck, B D Kensler, T W Prog-Exp-Tumor-Res. 1987; 3152-62 0079-6263

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Combined effect of aflatoxin and vitamin A on clastogeny in mice chromosomes. Source: Kumari, D. Sinha, S.P. Cytologia-Int-J-Cytol. Tokyo : Cytologia. Sept 1990. volume 55 (3) page 387-390. 0011-4545

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Comparative uptake, vascular transport, and cellular internalization of aflatoxin-B1 and benzo(a)pyrene. Author(s): Department of Anatomy, College of Veterinary Medicine, Texas A&M University, College Station 77843. Source: Busbee, D L Norman, J O Ziprin, R L Arch-Toxicol. 1990; 64(4): 285-90 0340-5761

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Conservation of structure and function of the aflatoxin regulatory gene aflR from Aspergillus nidulans and A. flavus. Source: Yu, J.H. Butchko, R.A.E. Fernandes, M. Keller, N.P. Leonard, T.J. Adams, T.H. Curr-genet. Berlin; New York : Springer-Verlag, 1979-. 1996. volume 29 (6) page 549-555. 0172-8083

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Contaminated diet of Oreochromis niloticus genotoxic and pathological effects of aflatoxin. Author(s): Alexandria Univ. (Egypt). Faculty of Veterinary Medicine Source: El Fiky, S.A. Zaki, V.H. Alexandria-Journal-of-Veterinary-Science (Egypt). (1997). volume 13(3) page 159-170. Received 1998. oreochromis niloticus mycotoxins pathology aflatoxins 1110-3047

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Decontamination of groundnut meal containing aflatoxin by treatment with calcium hydroxide and paraformaldehyde. Source: Piva, G. Pietri, A. Carini, E. Amerio, M. Gatti, S. New strategies for improving animal production for human welfare : proceedings / the Fifth World Conference on Animal Production, August 14-19, 1983. Tokyo, Japan : Japanese Society of Zootechnical Science, 1983. volume 2 page 563-564.

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Detection of aflatoxin B1 guanine adducts in human urine samples from Kenya. Source: Dragsted, L.O. Wakhisi, J. Autrup, H. Environmental epidemiology / [edited by] Frederick C. Kopfler, Gunther F. Craun. Chelsea, Mich. : Lewis Publishers, c1986. page 1-15. ISBN: 0873710738

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Determinants of formation of aflatoxin-albumin adducts: a seven-township study in Taiwan. Author(s): School of Public Health, National Defense Medical Center, School of Public Health, No. 161, Section 6, Min-Chuan East Road, Taipei 114, Taiwan, Republic of China. [email protected] Source: Sun, C A Wu, D M Wang, L Y Chen, C J You, S L Santella, R M Br-J-Cancer. 2002 October 21; 87(9): 966-70 0007-0920

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Effect of (+)-catechin, dimethyl sulfoxide and ethanol on the microsome-mediated metabolism of two hepatocarcinogens, N-nitrosodimethylamine and aflatoxin B1. Author(s): Fels Research Institute, Philadelphia, PA. Source: Prasanna, H R Lotlikar, P D Hacobian, N Ho, L L Magee, P N IARC-Sci-Publ. 1987; (84): 175-7 0300-5038

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Effect of aflatoxin B1 on the delayed type hypersensitivity and phagocytic activity of reticuloendothelial system in chickens. Author(s): Department of Veterinary Microbiology, Haryana Agricultural University, Hisar, India. Source: Kadian, S K Monga, D P Goel, M C Mycopathologia. 1988 October; 104(1): 33-6 0301-486X

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Effect of alpha-tocopherol supplementation on the impact of aflatoxin B1 on the testes of rats. Author(s): Embryotoxicology section industrial toxicology research centre (ITRC), Lucknow, India. Source: Ibeh, I N Saxena, D K Exp-Toxicol-Pathol. 1998 June; 50(3): 221-4 0940-2993

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Effect of ascorbic acid on some biochemical parameters of rabbits affected by aflatoxin B1. Source: Yousef, M.I. El Demerdash, F.M. El Agamy, E.I. Environ-nutr-interact. Philadelphia, PA : Taylor & Francis. July/Sept 1999. volume 3 (3) page 141-143. 10865683

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Effect of dietary aflatoxin B1 on the growth response and haematologic changes of young Japanese quail. Author(s): Department of Veterinary Pathology, Haryana Agricultural University, Hisar, India. Source: Sadana, J R Asrani, R K Pandita, A Mycopathologia. 1992 June; 118(3): 133-7 0301-486X

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Effect of dietary beta-1,3 glucan on immune responses and disease resistance of healthy and aflatoxin B1-induced immunocompromised rohu (Labeo rohita Hamilton). Author(s): Central Institute of Freshwater Aquaculture, Kausalyaganga, Bhubaneswar, India. [email protected] Source: Sahoo, P K Mukherjee, S C Fish-Shellfish-Immunol. 2001 November; 11(8): 68395 1050-4648

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Effect of long term feeding and withdrawal of aflatoxin B1 and ochratoxin A on kidney cell transformation in albino rats. Author(s): Department of Microbiology & Sanitation, Central Food Technological Research Institute, Mysore, India. Source: Rati, E R Shantha, T Ramesh, H P Indian-J-Exp-Biol. 1991 September; 29(9): 813-7 0019-5189

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Effect of long-term feeding of nivalenol on aflatoxin B1-initiated hepatocarcinogenesis in mice. Author(s): Department of Toxicology and Microbial Chemistry, Faculty of Pharmaceutical Sciences, Science University of Tokyo, Japan. Source: Ueno, Y Kobayashi, T Yamamura, H Kato, T Tashiro, F Nakamura, K Ohtsubo, K IARC-Sci-Publ. 1991; (105): 420-3 0300-5038

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Effect of low level of dietary aflatoxins on baladi rabbits. Author(s): Dept. of Animal and Poultry Production, Fac. of Agriculture, Mansoura University, Egypt. Source: Abdelhamid, A M el Shawaf, I el Ayoty, S A Ali, M M Gamil, T Arch-Tierernahr. 1990 May-June; 40(5-6): 517-37 0003-942X

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Effect of low protein diet on chronic aflatoxin B1-induced liver injury in rhesus monkeys. Author(s): Department of Pathology, All India Institute of Medical Sciences, New Delhi. Source: Mathur, M Rizvi, T A Nayak, N C Mycopathologia. 1991 March; 113(3): 175-9 0301-486X

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Effect of melatonin on the production of microsomal hydrogen peroxide and cytochrome P-450 content in rat treated with aflatoxin B(1). Author(s): Department of Environmental Studies, Institute of Graduate Studies and Research, Alexandria University, 163 Horreya Avenue, Chatby, 21131, Alexandria, Egypt. [email protected] Source: Awney, Hala A Attih, Ahmed M Habib, Sami L Mostafa, Mostafa H Toxicology. 2002 March 20; 172(2): 143-8 0300-483X

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Effect of parboiling and bran removal on aflatoxin levels in Sri Lankan rice. Author(s): Department of Agricultural Biology, University of Peradeniya, Sri Lanka. Source: Bandara, J M Vithanege, A K Bean, G A Mycopathologia. 1991 July; 115(1): 31-5 0301-486X

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Effect of peanut tannin extracts on growth of Aspergillus parasiticus and aflatoxin production. Author(s): Texas A & M University, Department of Plant Pathology, College Station 77843. Source: Azaizeh, H A Pettit, R E Sarr, B A Phillips, T D Mycopathologia. 1990 June; 110(3): 125-32 0301-486X

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Effects of cyclopiazonic acid and aflatoxin singly and in combination on selected clinical, pathological and immunological responses of guinea pigs. Author(s): Department of Veterinary Sciences, University of Wyoming, Laramie 82071. Source: Pier, A C Belden, E L Ellis, J A Nelson, E W Maki, L R Mycopathologia. 1989 March; 105(3): 135-42 0301-486X

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Effects of dietary fat and aflatoxin B1 on microsomal monooxygenase activity. Source: Nyandieka, H S Arch-Toxicol. 1987; 60(1-3): 59-60 0340-5761

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Effects of prolonged oral administration of fumonisin B1 and aflatoxin B1 in rats. Source: Pozzi, C.R. Correa, B. Xavier, J.G. Direito, G.M. Orsi, R.B. Matarazzo, S.V. Mycopathologia. Dordrecht : Kluwer Academic Publishers. 2001. volume 151 (1) page 21-27. 0301-486X

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Effects of various inducers on the activities of cytochrome P-450-mixed function oxidases and aflatoxin B1 activation in microsomes of hamster livers. Author(s): Division of Pharmacology, National Institute of Hygienic Sciences, Tokyo, Japan. Source: Sunouchi, M Fukuhara, M Ohno, Y Takanaka, A J-Toxicol-Sci. 1988 November; 13(4): 193-204 0388-1350

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Fungal contamination, natural occurrence of mycotoxins and resistance for aflatoxin accumulation of some broad bean (Vicia faba L.) cultivars. Author(s): Botany Department, Faculty of Science, Assiut University, Sohag, Egypt. Source: Saber, S M J-Basic-Microbiol. 1992; 32(4): 249-58 0233-111X

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Genetic selection for aflatoxin B1 resistance influences chicken T-cell and thymocyte proliferation. Author(s): Department of Poultry Science, Clemson University, SC 29634. Source: Scott, T R Rowland, S M Rodgers, R S Bodine, A B Dev-Comp-Immunol. 1991 Fall; 15(4): 383-91 0145-305X

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In vivo effect of selenium on the mutagenic activity of aflatoxin B1. Author(s): Institute of Hygiene and Epidemiology, Prague, Czechoslovakia. Source: Petr, T Barta, I Turek, B J-Hyg-Epidemiol-Microbiol-Immunol. 1990; 34(2): 123-8 0022-1732

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Influence of dietary aflatoxin on certain serum enzyme levels in broiler chickens. Author(s): Department of Pathology, Madras Veterinary College, India. Source: Balachandran, C Ramarkrishnan, R Mycopathologia. 1988 February; 101(2): 65-7 0301-486X

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Influence of gamma-irradiation and maize lipids on the production of aflatoxin B1 by Aspergillus flavus. Author(s): National Center for Radiation Research and Technology, Microbiology Department, P.O. Box 29, Nasr City, Cairo, Egypt. Source: Aziz, N H el Zeany, S A Moussa, L A Nahrung. 2002 October; 46(5): 327-31 0027769X

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Inhibition by the bioflavonoid ternatin of aflatoxin B1-induced lipid peroxidation in rat liver. Author(s): Department of Physiology and Pharmacology, Faculty of Medicine, Federal University of Ceara, Fortaleza, Brazil. Source: Souza, M F Tome, A R Rao, V S J-Pharm-Pharmacol. 1999 February; 51(2): 125-9 0022-3573

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Inhibition of aflatoxin production & growth of Aspergillus flavus by eugenol & onion & garlic extracts. Author(s): University Department of Botany, Bhagalpur University. Source: Bilgrami, K S Sinha, K K Sinha, A K Indian-J-Med-Res. 1992 June; 96171-5 09715916

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Initial characterization of a type I fatty acid synthase and polyketide synthase multienzyme complex NorS in the biosynthesis of aflatoxin B(1). Author(s): Department of Chemistry, The Johns Hopkins University, 3400 N. Charles Street, Baltimore, MD 21218, USA. Source: Watanabe, C M Townsend, C A Chem-Biol. 2002 September; 9(9): 981-8 10745521

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Interaction of fumonisin B(1) and aflatoxin B(1) in a short-term carcinogenesis model in rat liver. Author(s): PROMEC Unit, Medical Research Council, P.O. Box 19070, 7505, Tygerberg, South Africa. [email protected] Source: Gelderblom, W C A Marasas, W F O Lebepe Mazur, S Swanevelder, S Vessey, C J Hall, P de la M Toxicology. 2002 February 28; 171(2-3): 161-73 0300-483X

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Interrelationship of kernel water activity, soil temperature, maturity, and phytoalexin production in preharvest aflatoxin contamination of drought-stressed peanuts. Author(s): USDA, ARS, National Peanut Research Laboratory, Dawson, Georgia, 31742. Source: Dorner, J W Cole, R J Sanders, T H Blankenship, P D Mycopathologia. 1989 February; 105(2): 117-28 0301-486X

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Liver fibrosis in guinea pigs experimentally induced by combined copper and aflatoxin application. Author(s): Federal Environmental Agency, Institute for Water-, Soil- and Air-Hygiene, Berlin, Germany. Source: Schiller, F Lippold, U Heinze, R Hoffmann, A Seffner, W Exp-Toxicol-Pathol. 1998 September; 50(4-6): 519-27 0940-2993

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Long-term immune dysfunction in rainbow trout (Oncorhynchus mykiss) exposed as embryos to aflatoxin B1. Author(s): Department of Environmental Sciences, School of Marine Science, Virginia Institute of Marine Science, College of William and Mary, Gloucester Point 23062, USA. Source: Ottinger, C A Kaattari, S L Fish-Shellfish-Immunol. 2000 January; 10(1): 101-6 1050-4648

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Mechanism of biochemical action of substituted 4-methylbenzopyran-2-ones. Part II: Mechanism-based inhibition of rat liver microsome-mediated aflatoxin B1-DNA binding by the candidate antimutagen 7,8-diacetoxy-4-methylcoumarin. Author(s): Department of Biochemistry, V. P. Chest Institute, University of Delhi, India. Source: Raj, H G ParMarch, V S Jain, S C Goel, S Singh, A Gupta, K Rohil, V Tyagi, Y K Jha, H N Olsen, C E Wengel, J Bioorg-Med-Chem. 1998 October; 6(10): 1895-904 09680896

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Metabolism of aflatoxin B1 by Petroselinum crispum (parsley). Author(s): Department of Biochemistry, University of Natal, South Africa. Source: Howes, A W Dutton, M F Chuturgoon, A A Mycopathologia. 1991 January; 113(1): 25-9 0301-486X

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Modulating role of Semecarpus anacardium L. nut milk extract on aflatoxin B(1) biotransformation. Author(s): Department of Medical Biochemistry, Dr. A.L.M. Post-Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, 600 113, India. Source: Premalatha, B Sachdanandam, P Pharmacol-Res. 2000 January; 41(1): 19-24 10436618

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On the effect of aflatoxin on lipid metabolism in three strains of broiler chickens. Author(s): PCSIR Labs., Karachi (Pakistan) Source: Khan, B.A. Husain, S.S. Ahmed, M.A. Sultana, L. Khalid, Q. Pakistan-Journal-ofScientific-and-Industrial-Research (Pakistan). (August 1989). volume 32(8) page 528-530. broiler chickens aflatoxins lipid metabolism weight cholesterol 0030-9885

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Potential natural exposure of Mississippi sandhill cranes to aflatoxin B1. Author(s): College of Veterinary Medicine, Mississippi State University, Mississippi State 39762. Source: Couvillion, C E Jackson, J R Ingram, R P Bennett, L W McCoy, C P J-Wildl-Dis. 1991 October; 27(4): 650-6 0090-3558

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Protective effect of Cochlospermum tinctorium A. Rich extract versus aflatoxin B1induced liver damage in rats. Source: Dalvi, R.R. Sere, A. Int-J-Crude-Drug-Res. Lisse : Swets & Zeitlinger. June 1988. volume 26 (2) page 117-120. 0167-7314

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Quantitative risk analysis of aflatoxin toxicity for the consumers of 'kenkey'-- a fermented maize product. Source: Nickelsen, L. Jakobsen, M. Food-control. Oxford, UK : Elsevier Science Ltd. June 1997. volume 8 (13) page 149-159. 0956-7135

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Reduction of aflatoxin content of infected cowpea seeds during processing into food. Author(s): Department of Chemistry, University of Ibadan, Nigeria. Source: Ogunsanwo, B M Faboya, O O Idowu, O R Ikotun, T Nahrung. 1989; 33(6): 595-7 0027-769X

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Reliability of a short-term test for hepatocarcinogenesis induced by aflatoxin B1. Author(s): Department of Pathology, Guangxi Cancer Institute, Nanning, China. Source: Li, Y Yan, R Q Qin, G Z Qin, L L Duan, X X IARC-Sci-Publ. 1991; (105): 431-3 0300-5038

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Selection pressure and altered hepatocellular islands after a single injection of aflatoxin B1. Author(s): Department of Experimental Pathology, Cancer Institute, Tokyo. Source: Moore, M A Nakagawa, K Ishikawa, T Jpn-J-Cancer-Res. 1988 February; 79(2): 187-94 0910-5050

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Short-term moderate aflatoxin B1 exposure has only minor effects on the gutassociated lymphoid tissue of Brown Norway rats. Author(s): Institute of Nutritional Physiology, Federal Research Centre for Nutrition, Karlsruhe, Germany. [email protected] Source: Watzl, B Neudecker, C Hansch, G M Rechkemmer, G Pool Zobel, B L Toxicology. 1999 November 5; 138(2): 93-102 0300-483X

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Studies of aflatoxins in Chiang Mai, Thailand. Author(s): Department of Clinical Microbiology, Faculty of Associated Medical Sciences, Chiang Mai University, Thailand.

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Source: Sutabhaha, S Suttajit, M Niyomca, P Kitasato-Arch-Exp-Med. 1992 April; 65(1): 45-52 0023-1924 •

Studies on the toxicity of shrimp (Penaeus vannamei) fed diets dosed with aflatoxin B1 to humans. Source: Divakaran, S. Tacon, A.G.J. J-aquat-food-prod-technol. Binghamton, NY : Food Products Press, 1992-. 2000. volume 9 (3) page 115-120. 1049-8850

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The determination of ultra-trace amounts of aflatoxin M1 in human urine in the Czech Republic. Author(s): National Institute of Public Health Prague, Brno (Republique Tcheque). Centre for the Hygiene of Food Chains Source: Ostry, V. Ruprich, J. Cerna, M. Revue-de-Medecine-Veterinaire (France). (June 1998). volume 149(6) page 712. mankind urine aflatoxins analytical methods surveys czech republic 0035-1555

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The effect of diet on carcinogenicity of aflatoxin B1 in animals: a review. Source: Nyathi, C.B. Hasler, J.A. Chetsanga, C.J. Zimbabwe-Vet-J. Causeway : Zimbabwe Veterinary Association. June 1985. volume 16 (1/2) page 18-22.

Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •

healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0

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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov

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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov

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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/

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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/

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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/

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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/

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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/

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Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •

AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats

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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html

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Google: http://directory.google.com/Top/Health/Nutrition/

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Healthnotes: http://www.healthnotes.com/

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Open Directory Project: http://dmoz.org/Health/Nutrition/

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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/

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WebMDHealth: http://my.webmd.com/nutrition

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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html

The following is a specific Web list relating to aflatoxin; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •

Food and Diet Peanuts Source: Healthnotes, Inc.; www.healthnotes.com

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CHAPTER 3. ALTERNATIVE MEDICINE AND AFLATOXIN Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to aflatoxin. At the conclusion of this chapter, we will provide additional sources.

National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to aflatoxin and complementary medicine. To search the database, go to the following Web site: http://www.nlm.nih.gov/nccam/camonpubmed.html. Select “CAM on PubMed.” Enter “aflatoxin” (or synonyms) into the search box. Click “Go.” The following references provide information on particular aspects of complementary and alternative medicine that are related to aflatoxin: •

A UK retail survey of aflatoxins in herbs and spices and their fate during cooking. Author(s): MacDonald S, Castle L. Source: Food Additives and Contaminants. 1996 January; 13(1): 121-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8647302

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Aflatoxin - induced alteration in the levels of membrane chemical of subcellular organelles isolated from excised, incubated glycine max, cv. “Essex” roots. I. Nonenriched organelles. Author(s): Danley JM, Staggers S, Walker S, Varner A, Llewellyn GC, Dashek WV. Source: Mycopathologia. 1981 June 5; 74(3): 149-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6166863

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Aflatoxin B1 degradation by flavobacterium aurantiacum in the presence of reducing conditions and seryl and sulfhydryl group inhibitors. Author(s): D'Souza DH, Brackett RE.

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Source: J Food Prot. 2001 February; 64(2): 268-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11271780 •

Aflatoxin B1 in common Egyptian foods. Author(s): Selim MI, Popendorf W, Ibrahim MS, el Sharkawy S, el Kashory ES. Source: J Aoac Int. 1996 September-October; 79(5): 1124-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8823921

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Aflatoxin B1-induced micronuclei and cell cycle alterations in lung and bone marrow cells and their modulation by Piper argyrophyllum extract. Author(s): Raj HG, Gupta K, Rohil V, Bose M, Biswas G, Singh SK, Jain SC, Parmar VS, Olsen CE, Wengel J. Source: Teratogenesis, Carcinogenesis, and Mutagenesis. 1998; 18(5): 249-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9876014

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Aflatoxin contamination in foods and foodstuffs in Tokyo: 1986-1990. Author(s): Tabata S, Kamimura H, Ibe A, Hashimoto H, Iida M, Tamura Y, Nishima T. Source: J Aoac Int. 1993 January-February; 76(1): 32-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8448440

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Aflatoxin contamination of some common drug plants. Author(s): Roy AK, Sinha KK, Chourasia HK. Source: Applied and Environmental Microbiology. 1988 March; 54(3): 842-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3132102

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Aflatoxin exposure is higher in vegetarians than nonvegetarians in Thailand. Author(s): Vinitketkumnuen U, Chewonarin T, Kongtawelert P, Lertjanyarak A, Peerakhom S, Wild CP. Source: Natural Toxins. 1997; 5(4): 168-71. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9407561

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Aflatoxin exposure, hepatitis B virus infection and liver cancer in Swaziland. Author(s): Peers F, Bosch X, Kaldor J, Linsell A, Pluijmen M. Source: International Journal of Cancer. Journal International Du Cancer. 1987 May 15; 39(5): 545-53. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3570547

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Aflatoxin formation and varietal difference of cow pea (Vigna unguiculata (L.) Walp.) and garden pea (Pisum sativum L.) cultivars. Author(s): El-Kady IA, El-Maraghy SS, Zohri AA.

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Source: Mycopathologia. 1996; 133(3): 185-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8927121 •

Aflatoxin in betel nut and its control by use of food preservatives. Author(s): Raisuddin S, Misra JK. Source: Food Additives and Contaminants. 1991 November-December; 8(6): 707-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1812017

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Aflatoxin production in supplemental feeders provided for northern bobwhite in Texas and Oklahoma. Author(s): Oberheu DG, Dabbert CB. Source: J Wildl Dis. 2001 July; 37(3): 475-80. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11504221

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Aflatoxin-albumin adduct formation after single and multiple doses of aflatoxin B(1) in rats treated with Thai medicinal plants. Author(s): Vinitketkumnuen U, Chewonarin T, Dhumtanom P, Lertprasertsuk N, Wild CP. Source: Mutation Research. 1999 July 16; 428(1-2): 345-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10518006

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Aflatoxins and fungal flora in lentil (Lens esculenta L.). Author(s): el-Maraghy SS. Source: Mycopathologia. 1988 April; 102(1): 31-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3419482

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Aflatoxins B1 in different grades of chillies (Capsicum annum L.) in India as determined by indirect competitive-ELISA. Author(s): Reddy SV, Mayi DK, Reddy MU, Thirumala-Devi K, Reddy DV. Source: Food Additives and Contaminants. 2001 June; 18(6): 553-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11407753

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Aflatoxins in Egyptian foodstuffs. Author(s): Girgis AN, el-Sherif S, Rofael N, Nesheim S. Source: J Assoc Off Anal Chem. 1977 May; 60(3): 746-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=858708

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Aflatoxins in spices marketed in Portugal. Author(s): Martins ML, Martins HM, Bernardo F. Source: Food Additives and Contaminants. 2001 April; 18(4): 315-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11339266

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Aflatoxins: production of the toxins on rice-corn steep medium according to some cultural conditions. Author(s): Mabrouk SS, el-Shayeb NM. Source: Zentralbl Bakteriol Naturwiss. 1981; 136(4): 330-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6795852

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Anticancer potency of the milk extract of Semecarpus anacardium Linn. nuts against aflatoxin B1 mediated hepatocellular carcinoma bearing Wistar rats with reference to tumour marker enzymes. Author(s): Premalatha B, Muthulakshmi V, Sachdanandam P. Source: Phytotherapy Research : Ptr. 1999 May; 13(3): 183-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10353153

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Antioxidants and radical scavenging properties of vegetable extracts in rats fed aflatoxin-contaminated diet. Author(s): Abdel-Wahhab MA, Aly SE. Source: Journal of Agricultural and Food Chemistry. 2003 April 9; 51(8): 2409-14. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12670189

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Application of a minicolumn detection method for screening spices for aflatoxin. Author(s): Seenappa M, Kempton AG. Source: Journal of Environmental Science and Health. Part. B, Pesticides, Food Contaminants, and Agricultural Wastes. 1980; 15(3): 219-31. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6769994

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Aspergillus infection and aflatoxin production in some cowpea (Vigna unguiculata (L.) Walp) lines in Tanzania. Author(s): Seenappa M, Keswani CL, Kundya TM. Source: Mycopathologia. 1983 November 21; 83(2): 103-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6422301

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Atmospheric pressure photo-ionization liquid chromatography/mass spectrometric determination of aflatoxins in food. Author(s): Takino M, Tanaka T, Yamaguchi K, Nakahara T. Source: Food Additives and Contaminants. 2004 January; 21(1): 76-84. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14744683

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Binding of aflatoxin B1 to DNA inhibited by ajoene and diallyl sulfide. Author(s): Tadi PP, Lau BH, Teel RW, Herrmann CE. Source: Anticancer Res. 1991 November-December; 11(6): 2037-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1776837


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Bioactivation of aflatoxin B1 by human liver microsomes: role of cytochrome P450 IIIA enzymes. Author(s): Ramsdell HS, Parkinson A, Eddy AC, Eaton DL. Source: Toxicology and Applied Pharmacology. 1991 May; 108(3): 436-47. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1902334

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Chemoprevention of aflatoxin B1-initiated and carbon tetrachloride-promoted hepatocarcinogenesis in the rat by green tea. Author(s): Qin G, Ning Y, Lotlikar PD. Source: Nutrition and Cancer. 2000; 38(2): 215-22. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11525600

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Chinese medicinal herbs modulate mutagenesis, DNA binding and metabolism of aflatoxin B1. Author(s): Wong BY, Lau BH, Tadi PP, Teel RW. Source: Mutation Research. 1992 June 1; 279(3): 209-16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1377337

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Chromosome aberrations induced by aflatoxin B1 in rat bone marrow cells in vivo and their suppression by green tea. Author(s): Ito Y, Ohnishi S, Fujie K. Source: Mutation Research. 1989 March; 222(3): 253-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2922009

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Comparative effect of dietary butylated hydroxyanisole and beta-naphthoflavone on aflatoxin B1 metabolism, DNA adduct formation, and carcinogenesis in rainbow trout. Author(s): Goeger DE, Shelton DW, Hendricks JD, Pereira C, Bailey GS. Source: Carcinogenesis. 1988 October; 9(10): 1793-800. Erratum In: Carcinogenesis 1988 November; 9(11): 2146. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3139317

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Comparison of the effects of dietary selenium, zinc, and selenium and zinc supplementation on growth and immune response between chick groups that were inoculated with Salmonella and aflatoxin or Salmonella. Author(s): Hegazy SM, Adachi Y. Source: Poultry Science. 2000 March; 79(3): 331-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10735198

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Comparison of the prevention of aflatoxin b(1)-induced genotoxicity by quercetin and quercetin pentaacetate. Author(s): Kohli E, Raj HG, Kumari R, Rohil V, Kaushik NK, Prasad AK, Parmar VS.

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Source: Bioorganic & Medicinal Chemistry Letters. 2002 September 16; 12(18): 2579-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12182864 •

Comparison of the profiles of seedborne fungi and the occurrence of aflatoxins in mould-damaged beans and soybeans. Author(s): Tseng TC, Tu JC, Soo LC. Source: Microbios. 1995; 84(339): 105-16. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8628121

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Comparison of three methods for determining aflatoxins in sunflower seed meals. Author(s): Trucksess MW, Stoloff L. Source: J Assoc Off Anal Chem. 1980 November; 63(6): 1357-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7451399

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Dependence of aflatoxin in almonds on the type and amount of insect damage. Author(s): Schatzki TF, Ong MS. Source: Journal of Agricultural and Food Chemistry. 2001 September; 49(9): 4513-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11559163

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Dietary exposure to aflatoxin in Benin City, Nigeria: a possible public health concern. Author(s): Ibeh IN, Uraih N, Ogonor JI. Source: International Journal of Food Microbiology. 1991 November; 14(2): 171-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1777386

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Diminution of aflatoxin toxicity to growing lambs by dietary supplementation with hydrated sodium calcium aluminosilicate. Author(s): Harvey RB, Kubena LF, Phillips TD, Corrier DE, Elissalde MH, Huff WE. Source: Am J Vet Res. 1991 January; 52(1): 152-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1850585

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DNA binding and mutagenicity of aflatoxin B1 catalyzed by isolated rabbit lung cells. Author(s): Daniels JM, Matula TI, Massey TE. Source: Carcinogenesis. 1993 July; 14(7): 1429-34. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8330361

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Drug resistance patterns and susceptibility to aflatoxin B1 of strains of Escherichia coli and Staphylococcus aureus. Author(s): Tiwari RP, Singh G, Vadehra DV. Source: Journal of Medical Microbiology. 1986 September; 22(2): 115-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3091837


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Effect of a lignan-enriched extract of Schisandra chinensis on aflatoxin B1 and cadmium chloride-induced hepatotoxicity in rats. Author(s): Ip SP, Mak DH, Li PC, Poon MK, Ko KM. Source: Pharmacology & Toxicology. 1996 June; 78(6): 413-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8829203

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Effect of aflatoxin G1 on germination, growth and metabolic activities of some crop plants. Author(s): el-Naghy MA, Fadl-Allah EM, Samhan M. Source: Cytobios. 1999; 97(385): 87-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10418120

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Effect of aflatoxin in growing lambs fed ruminally degradable or escape protein sources. Author(s): Edrington TS, Harvey RB, Kubena LF. Source: Journal of Animal Science. 1994 May; 72(5): 1274-81. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8056674

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Effect of allixin, a phytoalexin produced by garlic, on mutagenesis, DNA-binding and metabolism of aflatoxin B1. Author(s): Yamasaki T, Teel RW, Lau BH. Source: Cancer Letters. 1991 August; 59(2): 89-94. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1909211

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Effect of alpha-tocopherol supplementation on the impact of aflatoxin B1 on the testes of rats. Author(s): Ibeh IN, Saxena DK. Source: Experimental and Toxicologic Pathology : Official Journal of the Gesellschaft Fur Toxikologische Pathologie. 1998 June; 50(3): 221-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9681652

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Effect of an extract of the root of Scutellaria baicalensis and its flavonoids on aflatoxin B1 oxidizing cytochrome P450 enzymes. Author(s): Kim BR, Kim DH, Park R, Kwon KB, Ryu DG, Kim YC, Kim NY, Jeong S, Kang BK, Kim KS. Source: Planta Medica. 2001 July; 67(5): 396-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11488450

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Effect of C6 to C9 alkenals on aflatoxin production in corn, cottonseed, and peanuts. Author(s): Zeringue HJ Jr. Source: Applied and Environmental Microbiology. 1991 August; 57(8): 2433-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1768117

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Effect of cyclopropenoid fatty acids on the hepatic microsomal mixed-functionoxidase system and aflatoxin metabolism in rabbits. Author(s): Eisele TA, Loveland PM, Kruk DL, Meyers TR, Sinnhuber RO, Nixon JE. Source: Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association. 1982 August; 20(4): 407-12. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6813208

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Effect of diallyl sulfide and diallyl disulfide, the active principles of garlic, on the aflatoxin B(1)-induced DNA damage in primary rat hepatocytes. Author(s): Sheen LY, Wu CC, Lii CK, Tsai SJ. Source: Toxicology Letters. 2001 May 31; 122(1): 45-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11397556

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Effect of different inhibitors of sterol biosynthesis on both fungal growth and aflatoxin production. Author(s): Fanelli C, Fabbri AA, Brasini S, De Luca C, Passi S. Source: Natural Toxins. 1995; 3(2): 109-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7613735

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Effect of herba artemisiae scopariae on cytogenetic damage induced by aflatoxin B1. Author(s): Hong Z, Ye T, Chen S, Liu L, Lin L. Source: J Tradit Chin Med. 1996 March; 16(1): 51-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8758712

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Effect of Piper betle L. and its extracts on the growth and aflatoxin production by Aspergillus parasiticus. Author(s): Chou CC, Yu RC. Source: Proc Natl Sci Counc Repub China B. 1984 January; 8(1): 30-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6531413

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Effect of Salvia miltiorrhiza on aflatoxin B1-induced oxidative stress in cultured rat hepatocytes. Author(s): Liu J, Yang CF, Lee BL, Shen HM, Ang SG, Ong CN. Source: Free Radical Research. 1999 December; 31(6): 559-68. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10630680

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Effects of capsaicin on rat liver S9-mediated metabolism and DNA binding of aflatoxin. Author(s): Teel RW. Source: Nutrition and Cancer. 1991; 15(1): 27-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1901992


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Effects of saturated and unsaturated dietary fat on aflatoxin B1 metabolism. Author(s): Marzuki A, Norred WP. Source: Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association. 1984 May; 22(5): 383-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6427082

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Ergosterol oxidation may be considered a signal for fungal growth and aflatoxin production in Aspergillus parasiticus. Author(s): De Luca C, Passi S, Fabbri AA, Fanelli C. Source: Food Additives and Contaminants. 1995 May-June; 12(3): 445-50. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7664941

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Failure of plant tissues to metabolize aflatoxin B1? Author(s): Reiss J. Source: Mycopathologia. 1984 March 15; 85(1-2): 43-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6427615

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Failure of vitamin supplementation to alter the fatty liver syndrome caused by aflatoxin. Author(s): Hamilton PB, Garlich JD. Source: Poultry Science. 1972 March; 51(2): 688-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4629962

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Fungal contamination, natural occurrence of mycotoxins and resistance for aflatoxin accumulation of some broad bean (Vicia faba L.) cultivars. Author(s): Saber SM. Source: Journal of Basic Microbiology. 1992; 32(4): 249-58. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1460568

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Fungi and aflatoxins associated with spices in the Sultanate of Oman. Author(s): Elshafie AE, Al-Rashdi TA, Al-Bahry SN, Bakheit CS. Source: Mycopathologia. 2002; 155(3): 155-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12617502

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Hepatocurative effect of picroliv and silymarin against aflatoxin B1 induced hepatotoxicity in rats. Author(s): Rastogi R, Srivastava AK, Srivastava M, Rastogi AK. Source: Planta Medica. 2000 December; 66(8): 709-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11199126

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High pressure liquid chromatographic determination of aflatoxins in spices. Author(s): Awe MJ, Schranz JL.

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Immunoaffinity column cleanup with liquid chromatography using post-column bromination for determination of aflatoxins in peanut butter, pistachio paste, fig paste, and paprika powder: collaborative study. Author(s): Stroka J, Anklam E, Jorissen U, Gilbert J. Source: J Aoac Int. 2000 March-April; 83(2): 320-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10772170

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In vitro cytochrome P450 monooxygenase and prostaglandin H-synthase mediated aflatoxin B1 biotransformation in guinea pig tissues: effects of beta-naphthoflavone treatment. Author(s): Liu L, Nakatsu K, Massey TE. Source: Archives of Toxicology. 1993; 67(6): 379-85. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8215906

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In vitro inhibition of dihydropyridine oxidation and aflatoxin B1 activation in human liver microsomes by naringenin and other flavonoids. Author(s): Guengerich FP, Kim DH. Source: Carcinogenesis. 1990 December; 11(12): 2275-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2265479

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In vivo effect of dietary factors on the molecular action of aflatoxin B1: role of nonnutrient phenolic compounds on the catalytic activity of liver fractions. Author(s): Aboobaker VS, Balgi AD, Bhattacharya RK. Source: In Vivo. 1994 November-December; 8(6): 1095-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7772744

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Incidence of aflatoxin B1 in the Egyptian cured meat basterma and control by gammairradiation. Author(s): Refai MK, Niazi ZM, Aziz NH, Khafaga NE. Source: Die Nahrung. 2003 December; 47(6): 377-82. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=14727763

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Incidence of aflatoxin-potential contamination in Spanish sausages. Author(s): Guergue J, Ramirez C. Source: Ann Nutr Aliment. 1977; 31(4-6): 485-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=613913

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Incidence of seed-borne fungi and aflatoxins in Sudanese lentil seeds. Author(s): el-Nagerabi SA, Elshafie AE.


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Increase in glucuronide conjugation of aflatoxin P1 after pretreatment with microsomal enzyme inducers. Author(s): Ehrich M, Huckle WR, Larsen C. Source: Toxicology. 1984 August; 32(2): 145-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6464026

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Indole-3-carbinol and beta-naphthoflavone induction of aflatoxin B1 metabolism and cytochromes P-450 associated with bioactivation and detoxication of aflatoxin B1 in the rat. Author(s): Stresser DM, Bailey GS, Williams DE. Source: Drug Metabolism and Disposition: the Biological Fate of Chemicals. 1994 MayJune; 22(3): 383-91. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8070314

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Indole-3-carbinol induces a rat liver glutathione transferase subunit (Yc2) with high activity toward aflatoxin B1 exo-epoxide. Association with reduced levels of hepatic aflatoxin-DNA adducts in vivo. Author(s): Stresser DM, Williams DE, McLellan LI, Harris TM, Bailey GS. Source: Drug Metabolism and Disposition: the Biological Fate of Chemicals. 1994 MayJune; 22(3): 392-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8070315

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Influence of ascorbic acid supplementation on the haematological and clinical biochemistry parameters of male rabbits exposed to aflatoxin B1. Author(s): Yousef MI, Salem MH, Kamel KI, Hassan GA, El-Nouty FD. Source: Journal of Environmental Science and Health. Part. B, Pesticides, Food Contaminants, and Agricultural Wastes. 2003 March; 38(2): 193-209. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12617557

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Influence of sundrying on the chemical composition, aflatoxin content and fungal counts of two pepper varieties--Capsicum annum and Capsicum frutescens. Author(s): Adegoke GO, Allamu AE, Akingbala JO, Akanni AO. Source: Plant Foods for Human Nutrition (Dordrecht, Netherlands). 1996 February; 49(2): 113-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8811723

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Inhibition by the bioflavonoid ternatin of aflatoxin B1-induced lipid peroxidation in rat liver. Author(s): Souza MF, Tome AR, Rao VS.

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Inhibition of aflatoxin B1 carcinogenesis in rainbow trout by flavone and indole compounds. Author(s): Nixon JE, Hendricks JD, Pawlowski NE, Pereira CB, Sinnhuber RO, Bailey GS. Source: Carcinogenesis. 1984 May; 5(5): 615-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6426808

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Inhibition of aflatoxin B1 genotoxicity in human liver-derived HepG2 cells by kolaviron biflavonoids and molecular mechanisms of action. Author(s): Nwankwo JO, Tahnteng JG, Emerole GO. Source: European Journal of Cancer Prevention : the Official Journal of the European Cancer Prevention Organisation (Ecp). 2000 October; 9(5): 351-61. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11075889

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Inhibition of aflatoxin B1-hepatocarcinogenesis in rats by beta-naphthoflavone. Author(s): Gurtoo HL, Koser PL, Bansal SK, Fox HW, Sharma SD, Mulhern AI, Pavelic ZP. Source: Carcinogenesis. 1985 May; 6(5): 675-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3924427

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Inhibition of aflatoxin B1-induced initiation of hepatocarcinogenesis in the rat by green tea. Author(s): Qin G, Gopalan-Kriczky P, Su J, Ning Y, Lotlikar PD. Source: Cancer Letters. 1997 January 30; 112(2): 149-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9066721

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Inhibition of aflatoxin formation by some spices. Author(s): Mabrouk SS, El-Shayeb NM. Source: Z Lebensm Unters Forsch. 1980; 171(5): 344-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6778016

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Inhibition of aflatoxin production & growth of Aspergillus flavus by eugenol & onion & garlic extracts. Author(s): Bilgrami KS, Sinha KK, Sinha AK. Source: The Indian Journal of Medical Research. 1992 June; 96: 171-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1512040

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Inhibition of Aspergillus growth and aflatoxin release by derivatives of benzoic acid. Author(s): Chipley JR, Uraih N.


Source: Applied and Environmental Microbiology. 1980 August; 40(2): 352-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6781406 •

Inhibition of dexamethasone-induced cytochrome P450-mediated mutagenicity and metabolism of aflatoxin B1 by Chinese medicinal herbs. Author(s): Wong BY, Lau BH, Yamasaki T, Teel RW. Source: European Journal of Cancer Prevention : the Official Journal of the European Cancer Prevention Organisation (Ecp). 1993 July; 2(4): 351-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8358288

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Inhibition of growth and aflatoxin production in Aspergillus parasiticus by essential oils of selected plant materials. Author(s): Tantaoui-Elaraki A, Beraoud L. Source: Journal of Environmental Pathology, Toxicology and Oncology : Official Organ of the International Society for Environmental Toxicology and Cancer. 1994; 13(1): 67-72. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7823297

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Inhibition of growth and aflatoxin production of Aspergillus parasiticus by citrus oils. Author(s): Alderman GG, Marth EH. Source: Z Lebensm Unters Forsch. 1976 April 28; 160(4): 353-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=973437

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Interaction of aflatoxin B 1 metabolite with rat liver RNA. Author(s): Gurtoo HL, Dave C. Source: Res Commun Chem Pathol Pharmacol. 1973 May; 5(3): 635-45. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4144818

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Investigation of various extractants for the analysis of aflatoxin B1 in different food and feed matrices. Author(s): Stroka J, Petz M, Joerissen U, Anklam E. Source: Food Additives and Contaminants. 1999 August; 16(8): 331-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10645347

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Isolation of aflatoxin from Acacia and the incidence of Aspergillus flavus in the Sudan. Author(s): Abdalla MH. Source: Mycopathologia. 1988 December; 104(3): 143-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3148862

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Isolation, purification and characterization of enzyme(s) responsible for conversion of sterigmatocystin to aflatoxin B1. Author(s): Mashaly RI, Habib SL, el-Deeb SA, Salem MH, Safwat MM. Source: Z Lebensm Unters Forsch. 1988 February; 186(2): 118-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3128018

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Long term effect of aflatoxin B(1) on lipid peroxidation in rat liver and kidney: effect of picroliv and silymarin. Author(s): Rastogi R, Srivastava AK, Rastogi AK. Source: Phytotherapy Research : Ptr. 2001 June; 15(4): 307-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11406853

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Malonate as a precursor in the biosynthesis of aflatoxins. Author(s): Gupta SR, Prasanna HR, Viswanathan L, Venkitasurbramanian TA. Source: J Gen Microbiol. 1975 June; 88(2): 317-20. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=239093

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Mechanism of action of aflatoxin B1 in Bacillus megaterium. Author(s): Tiwari RP, Dham CK, Bhalla TC, Saini SS, Vadehra DV. Source: Applied and Environmental Microbiology. 1985 April; 49(4): 904-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3923926

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Mechanism of action of dietary chemoprotective agents in rat liver: induction of phase I and II drug metabolizing enzymes and aflatoxin B1 metabolism. Author(s): Manson MM, Ball HW, Barrett MC, Clark HL, Judah DJ, Williamson G, Neal GE. Source: Carcinogenesis. 1997 September; 18(9): 1729-38. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9328168

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Mechanisms of protection against aflatoxin B(1) genotoxicity in rats treated by organosulfur compounds from garlic. Author(s): Guyonnet D, Belloir C, Suschetet M, Siess MH, Le Bon AM. Source: Carcinogenesis. 2002 August; 23(8): 1335-41. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12151352

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Medicinal herb, Thonningia sanguinea protects against aflatoxin B1 acute hepatotoxicity in Fischer 344 rats. Author(s): Gyamfi MA, Aniya Y. Source: Human & Experimental Toxicology. 1998 August; 17(8): 418-23. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9756133


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Modifying role of dietary factors on the mutagenicity of aflatoxin B1: in vitro effect of plant flavonoids. Author(s): Francis AR, Shetty TK, Bhattacharya RK. Source: Mutation Research. 1989 April; 222(4): 393-401. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2495440

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Modulating effect of Semecarpus anacardium Linn. nut extract on glucose metabolizing enzymes in aflatoxin B1-induced experimental hepatocellular carcinoma. Author(s): Premalatha B, Sujatha V, Sachdanandam P. Source: Pharmacological Research : the Official Journal of the Italian Pharmacological Society. 1997 September; 36(3): 187-92. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9367662

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Modulating role of Semecarpus anacardium L. nut milk extract on aflatoxin B(1) biotransformation. Author(s): Premalatha B, Sachdanandam P. Source: Pharmacological Research : the Official Journal of the Italian Pharmacological Society. 2000 January; 41(1): 19-24. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10600265

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Modulation of aflatoxin B1 activated protein kinase C by phenolic compounds. Author(s): Mistry KJ, Krishna M, Bhattacharya RK. Source: Cancer Letters. 1997 December 16; 121(1): 99-104. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9459180

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Modulation of aflatoxin B1 biotransformation by beta-naphthoflavone in isolated rabbit lung cells. Author(s): Im SH, Bolt MW, Stewart RK, Massey TE. Source: Archives of Toxicology. 1996; 71(1-2): 72-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9010588

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Modulation of aflatoxin B1 biotransformation in rabbit pulmonary and hepatic microsomes. Author(s): Daniels JM, Massey TE. Source: Toxicology. 1992 August; 74(1): 19-32. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1514185

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Modulatory effects of essential oils from spices on the formation of DNA adduct by aflatoxin B1 in vitro. Author(s): Hashim S, Aboobaker VS, Madhubala R, Bhattacharya RK, Rao AR.

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Mutation of Chinese Hamster V79 cells and transformation and mutation of mouse fibroblast C3H/10T1/2 clone 8 cells by aflatoxin B1 and four other furocoumarins isolated from two Nigerian medicinal plants. Author(s): Uwaifo AO, Billings PC, Heidelberger C. Source: Cancer Research. 1983 March; 43(3): 1054-8. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6402296

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Negative ion chemical ionization mass spectrometric method for confirmation of identity of aflatoxin B1: collaborative study. Author(s): Park DL, Diprossimo V, Abdel-Malek E, Trucksess MW, Nesheim S, Brumley WC, Sphon JA, Barry TL, Petzinger G. Source: J Assoc Off Anal Chem. 1985 July-August; 68(4): 636-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3928591

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Organosulfur compounds of garlic modulate mutagenesis, metabolism, and DNA binding of aflatoxin B1. Author(s): Tadi PP, Teel RW, Lau BH. Source: Nutrition and Cancer. 1991; 15(2): 87-95. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1903884

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Oxidative metabolism of aflatoxin B1 by rat liver microsomes in vitro and its effect on lipid peroxidation. Author(s): Raj HG, Santhanam K, Gupta RP, Venkitasubramanian TA. Source: Res Commun Chem Pathol Pharmacol. 1974 August; 8(4): 703-6. No Abstract Available. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4153624

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Piperine inhibits aflatoxin B1-induced cytotoxicity and genotoxicity in V79 Chinese hamster cells genetically engineered to express rat cytochrome P4502B1. Author(s): Reen RK, Wiebel FJ, Singh J. Source: Journal of Ethnopharmacology. 1997 November; 58(3): 165-73. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9421252

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Potency of Semecarpus anacardium Linn. nut milk extract against aflatoxin B(1)induced hepatocarcinogenesis: reflection on microsomal biotransformation enzymes. Author(s): Premalatha B, Sachdanandam P. Source: Pharmacological Research : the Official Journal of the Italian Pharmacological Society. 2000 August; 42(2): 161-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10887046


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Potential mold growth, aflatoxin production, and antimycotic activity of selected natural spices and herbs. Author(s): Llewellyn GC, Burkett ML, Eadie T. Source: J Assoc Off Anal Chem. 1981 July; 64(4): 955-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7275911

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Preventive action of garlic on aflatoxin B1-induced carcinogenesis in the toad Bufo regularis. Author(s): el-Mofty MM, Sakr SA, Essawy A, Abdel Gawad HS. Source: Nutrition and Cancer. 1994; 21(1): 95-100. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8183725

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Protection of salvia miltiorrhiza against aflatoxin-B1-induced hepatocarcinogenesis in Fischer 344 rats dual mechanisms involved. Author(s): Liu J, Yang CF, Wasser S, Shen HM, Tan CE, Ong CN. Source: Life Sciences. 2001 June 8; 69(3): 309-26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11441922

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Protective effect of food additives on aflatoxin-induced mutagenicity and hepatocarcinogenicity. Author(s): Soni KB, Lahiri M, Chackradeo P, Bhide SV, Kuttan R. Source: Cancer Letters. 1997 May 19; 115(2): 129-33. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9149115

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Protective effect of soybean saponins and major antioxidants against aflatoxin B1induced mutagenicity and DNA-adduct formation. Author(s): Jun HS, Kim SE, Sung MK. Source: Journal of Medicinal Food. 2002 Winter; 5(4): 235-40. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12639399

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Protective effects of baicalein and wogonin against benzo[a]pyrene- and aflatoxin B(1)-induced genotoxicities. Author(s): Ueng YF, Shyu CC, Liu TY, Oda Y, Lin YL, Liao JF, Chen CF. Source: Biochemical Pharmacology. 2001 December 15; 62(12): 1653-60. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11755119

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Purification and characterization of the esterases involved in aflatoxin biosynthesis in Aspergillus parasiticus. Author(s): Kusumoto K, Hsieh DP. Source: Canadian Journal of Microbiology. 1996 August; 42(8): 804-10. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8776851

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Quantification of the copy number of nor-1, a gene of the aflatoxin biosynthetic pathway by real-time PCR, and its correlation to the cfu of Aspergillus flavus in foods. Author(s): Mayer Z, Bagnara A, Farber P, Geisen R. Source: International Journal of Food Microbiology. 2003 April 25; 82(2): 143-51. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=12568754

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Reduction of aflatoxin content of infected cowpea seeds during processing into food. Author(s): Ogunsanwo BM, Faboya OO, Idowu OR, Ikotun T. Source: Die Nahrung. 1989; 33(6): 595-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2797118

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Reliability of a short-term test for hepatocarcinogenesis induced by aflatoxin B1. Author(s): Li Y, Yan RQ, Qin GZ, Qin LL, Duan XX. Source: Iarc Sci Publ. 1991; (105): 431-3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1677348

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Reversal of aflatoxin induced liver damage by turmeric and curcumin. Author(s): Soni KB, Rajan A, Kuttan R. Source: Cancer Letters. 1992 September 30; 66(2): 115-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1394115

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Screening of aflatoxins in Shiro and ground red pepper in Addis Ababa. Author(s): Fufa H, Urga K. Source: Ethiop Med J. 1996 October; 34(4): 243-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9164040

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Semecarpus anacardium L. nut extract administration induces the in vivo antioxidant defence system in aflatoxin B1 mediated hepatocellular carcinoma. Author(s): Premalatha B, Sachdanandam P. Source: Journal of Ethnopharmacology. 1999 August; 66(2): 131-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10433469

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Some factors regulating [1-14C] acetate incorporation into aflatoxins by spheroplasts and spheroplast lysates from Aspergillus. Author(s): Tyagi JS, Tyagi AK, Venkitasubramanian TA. Source: Toxicon : Official Journal of the International Society on Toxinology. 1981; 19(4): 445-54. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6800068

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Studies of aflatoxins in Chiang Mai, Thailand. Author(s): Sutabhaha S, Suttajit M, Niyomca P.


Source: Kitasato Arch Exp Med. 1992 April; 65(1): 45-52. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1479782 •

Suppressive effect of penta-acetyl geniposide on the development of gammaglutamyl transpeptidase foci-induced by aflatoxin B(1) in rats. Author(s): Lin YL, Hsu JD, Chou FP, Lee MJ, Shiow SJ, Wang CJ. Source: Chemico-Biological Interactions. 2000 October 16; 128(2): 115-26. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=11024451

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Survey of some cereal grains and legume seeds for aflatoxin contamination in the Sudan. Author(s): Abdel-Rahim AM, Osman NA, Idris MO. Source: Zentralbl Mikrobiol. 1989; 144(2): 115-21. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2501947

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The effects of selected cotton-leaf volatiles on growth, development and aflatoxin production of Aspergillus parasiticus. Author(s): Greene-McDowelle DM, Ingber B, Wright MS, Zeringue HJ Jr, Bhatnagar D, Cleveland TE. Source: Toxicon : Official Journal of the International Society on Toxinology. 1999 June; 37(6): 883-93. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10340828

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The influence of divalent cations and chelators on aflatoxin B1 degradation by Flavobacterium aurantiacum. Author(s): D'Souza DH, Brackett RE. Source: J Food Prot. 2000 January; 63(1): 102-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=10643777

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The model Ah-receptor agonist beta-naphthoflavone inhibits aflatoxin B1-DNA binding in vivo in rainbow trout at dietary levels that do not induce CYP1A enzymes. Author(s): Takahashi N, Harttig U, Williams DE, Bailey GS. Source: Carcinogenesis. 1996 January; 17(1): 79-87. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8565141

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The occurrence of aflatoxins in mustard and mustard products. Author(s): Sahay SS, Prasad T. Source: Food Additives and Contaminants. 1990 July-August; 7(4): 509-13. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=2118457

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The purity of aflatoxin G1 and use of antioxidant and chelating agent on the purification of the toxin by thin-layer chromatography. Author(s): Kwon TW, Ayres JC.

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Source: Journal of Chromatography. 1967 December; 31(2): 420-6. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=4967407 •

The response of Bobwhite quail chicks to dietary ammonium and an antibioticvitamin supplement when fed B1 aflatoxin. Author(s): Wilson HR, Manley JG, Harms RH, Damron BL. Source: Poultry Science. 1978 March; 57(2): 403-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=674026

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The role of trace metal ions in aflatoxin B1 degradation by Flavobacterium aurantiacum. Author(s): D'Souza DH, Brackett RE. Source: J Food Prot. 1998 December; 61(12): 1666-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=9874346

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The use of EDTA-permeabilized E. coli cells as indicators of aflatoxin B1-induced differential lethality in the DNA repair host-mediated assay. Author(s): Zeilmaker MJ, van Teylingen CM, van Helten JB, Mohn GR. Source: Mutation Research. 1991 July; 263(3): 137-42. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1906132

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Thin layer chromatographic determination of aflatoxins in dry ginger root and ginger oleoresin. Author(s): Trucksess MW, Stoloff L. Source: J Assoc Off Anal Chem. 1980 September; 63(5): 1052-4. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=7410297

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Toxic effects of aflatoxin B1 in chickens given feed contaminated with Aspergillus flavus and reduction of the toxicity by activated charcoal and some chemical agents. Author(s): Dalvi RR, Ademoyero AA. Source: Avian Dis. 1984 January-March; 28(1): 61-9. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=6426455

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Toxigenic Aspergillus flavus and aflatoxins in Sri Lankan medicinal plant material. Author(s): Abeywickrama K, Bean GA. Source: Mycopathologia. 1991 March; 113(3): 187-90. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=1906136

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Ursolic acid inhibits aflatoxin B1-induced mutagenicity in a Salmonella assay system. Author(s): Young HS, Chung HY, Lee CK, Park KY, Yokozawa T, Oura H.


Source: Biological & Pharmaceutical Bulletin. 1994 July; 17(7): 990-2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=8000393 •

Winged bean (Psophocarpus tetragonolobus (L.) DC) as a substrate for growth and aflatoxin production by aflatoxigenic strains of Aspergillus spp. Author(s): Bean G, Fernando T. Source: Mycopathologia. 1986 January; 93(1): 3-7. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3083261

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Winged bean (Psophocarpus tetragonolobus (L.) DC) as a substrate for growth and aflatoxin production by aflatoxigenic strains of Aspergillus spp. Author(s): Bean G, Fernando T. Source: Mycopathologia. 1985 June; 90(3): 141-5. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=A bstract&list_uids=3929093

Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •

Alternative Medicine Foundation, Inc.: http://www.herbmed.org/

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Chinese Medicine: http://www.newcenturynutrition.com/

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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html

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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm

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Google: http://directory.google.com/Top/Health/Alternative/

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Healthnotes: http://www.healthnotes.com/

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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine

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Open Directory Project: http://dmoz.org/Health/Alternative/

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HealthGate: http://www.tnp.com/

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WebMDHealth: http://my.webmd.com/drugs_and_herbs

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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,00.html

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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/

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The following is a specific Web list relating to aflatoxin; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation: •

Herbs and Supplements Cinnamomum Alternative names: Cinnamon; Cinnamomum zeylanicum Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Curcuma Alternative names: Turmeric; Curcuma longa L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Eugenia Clove Alternative names: Cloves; Eugenia sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Foeniculum Alternative names: Fennel; Foeniculum vulgare Mill Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Humulus Alternative names: Hops; Humulus lupulus L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Illicium Alternative names: Star Anise; Illicium verum (Hook, F.) Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Indole-3-carbinol Source: Healthnotes, Inc.; www.healthnotes.com NAC (N-Acetyl Cysteine) Source: WholeHealthMD.com, LLC.; www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,809,00.html Oregano/Wild Marjoram Alternative names: Origanum vulgare Source: Healthnotes, Inc.; www.healthnotes.com Origanum Alternative names: Oregano; Origanum vulgare Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Picrorhiza Alternative names: Picrorhiza kurroa Source: Healthnotes, Inc.; www.healthnotes.com


Pimpinella Alternative names: Anise; Pimpinella anisum (L) Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Piper Nigrum Alternative names: Black Pepper Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Rosmarinus Alternative names: Rosemary; Rosmarinus officinalis L. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Thymus Alternative names: Thyme; Thymus vulgaris Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Zanthoxylum Alternative names: Prickly Ash; Zanthoxylum sp. Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org Zingiber Alternative names: Ginger; Zingiber officinale Roscoe Source: Alternative Medicine Foundation, Inc.; www.amfoundation.org

General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.

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CHAPTER 4. DISSERTATIONS ON AFLATOXIN Overview In this chapter, we will give you a bibliography on recent dissertations relating to aflatoxin. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “aflatoxin” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on aflatoxin, we have not necessarily excluded non-medical dissertations in this bibliography.

Dissertations on Aflatoxin ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to aflatoxin. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •

Aflatoxin B(1) metabolism and DNA adduct formation in the proliferating mouse liver by Shupe, Thomas David; PhD from Albany Medical College of Union University, 2003, 103 pages http://wwwlib.umi.com/dissertations/fullcit/3082963

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Assessing the binding specificity of aflatoxin B(1) and deoxynivalenol by lactic acid bacteria by Kahler, Andrea Joan; MS from Truman State University, 2003, 33 pages http://wwwlib.umi.com/dissertations/fullcit/1416309

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Dietary clay (HSCAS) reduces urinary aflatoxin metabolites in dogs by Bingham, Allen Kunz; PhD from Texas A&M University, 2003, 206 pages http://wwwlib.umi.com/dissertations/fullcit/3088118

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Effect of interaction between Streptococcus lactis and Aspergillus flavus on the production of aflatoxin by Coallier-Ascah, Jose; PhD from Mcgill University (Canada), 1982 http://wwwlib.umi.com/dissertations/fullcit/NK58070

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Investigations of interesting enzymes in the early and late stages of aflatoxin biosynthesis by Udwary, Daniel W.; PhD from The Johns Hopkins University, 2003, 158 pages http://wwwlib.umi.com/dissertations/fullcit/3080784

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The conversion of versicolorin to sterigmatocystin in aflatoxin biosynthesis by Henry, Kevin Michael; PhD from The Johns Hopkins University, 2003, 207 pages http://wwwlib.umi.com/dissertations/fullcit/3068167

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Transcriptional regulation of the Aspergillus parasiticus aflatoxin biosynthetic pathway gene nor-1 by Miller, Michael Joseph; PhD from Michigan State University, 2003, 155 pages http://wwwlib.umi.com/dissertations/fullcit/3100470

Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.

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CHAPTER 5. PATENTS ON AFLATOXIN Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.8 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “aflatoxin” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on aflatoxin, we have not necessarily excluded non-medical patents in this bibliography.

Patents on Aflatoxin By performing a patent search focusing on aflatoxin, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We

8Adapted from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.

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will tell you how to obtain this information later in the chapter. The following is an example of the type of information that you can expect to obtain from a patent search on aflatoxin: •

Analysis of aflatoxins in peanuts by high pressure liquid chromatograph Inventor(s): Dunmire; David L. (St. Louis, MO), Otto; Susan E. (Fenton, MO) Assignee(s): Peanut Research & Testing Laboratories, Inc. (edenton, Nc) Patent Number: 4,285,698 Date filed: April 28, 1980 Abstract: A method is disclosed for quickly and easily determining the presence and concentration of aflatoxins in peanuts. Aflatoxins are extracted from ground peanuts with a methanol-water solution using a tissuemizer. The extracted sample is filtered and an aliquot of the filtrate is transferred to a separatory funnel. A salt solution is added to remove interferences. The combined aqueous solution is then extracted with dichloromethane. The dichloromethane extract is evaporated to dryness, trifluoroacetic acid is then added and the resulting residue taken up in the mobile phase. The solution is then passed through a minicolumn for filtration and final cleanup. An aliquot is then injected into a high pressure liquid chromatograph system for separation of the four aflatoxin components, B1, B2, G1 and G2. Quantitation is done using a filter fluorescence detector. Excerpt(s): This invention relates generally to the quantitative and qualitative detection of aflatoxins in peanuts and more particularly is directed towards a new and improved method for analyzing aflatoxins in peanuts by means of high pressure liquid chromatography. Aflatoxin is a known carcinogen that enters food as a consequence of the manner in which foods are grown, handled or stored. Aflatoxin is not a deliverate food additive but occurs as a natural contaminant in such common foods as peanuts and corn. Aflatoxin is a generic term referring to a group of highly toxic compounds produced by the fungus Aspergillus flavus/parasiticus. In additional to the original recognition of aflatoxins B1, B2, G1 and G2, there also have been a large number of metabolites whose structures have been examined. These are mostly produced in mammalian tissue upon ingestion by the mammal of the parent compound B1, although some may also be produced by the fungus or by chemical treatment of B1. Of the four original aflatoxins, B1 is the most common, usually comprising about 90% of the aflatoxin residue observed on contaminated foodstuffs and it is also the most toxic. The biological activity of aflatoxin B1 is relatively similar to the other aflatoxins. Web site: http://www.delphion.com/details?pn=US04285698__

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Animal feed containing selected montmorillonite clay as additive and method for selecting the clay Inventor(s): Taylor; Dennis R. (Houston, TX) Assignee(s): Engelhard Corporation (iselin, Nj) Patent Number: 5,192,547 Date filed: October 1, 1990 Abstract: A correlation is established between aflatoxin B1 binding on raw montmorillonite clays and the ratio of their surface acidities divided by their porosities for surface acid sites whose pKa values fall in the range 5.0-6.8 (i.e. weakly acidic) and

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porosities for pores whose diameters fall in the region 50-600 A. This information provides a method for preselecting clay additives for animal feeds which have enhanced toxin binding capacity. Excerpt(s): This application is related to U.S. Ser. No. 07/552,715, filed Jul. 16, 1990. This invention relates to a method for inactivating mycotoxins which may be present as contaminants in dry animal feeds by adding a selected type of montmorillonite clay. More specifically, the selected clay is a calcium montmorillonite clay in which the ratio of surface acidity (as determined by Hammett indicators in the 5.0-6.8 pKa range) to pore volume (in the 50-600 Angstrom range) is above 5 and is preferably above 10. Mycotoxins, chemical substances produced by ubiquitous fungi, can make the difference between profit and loss to the poultry and livestock industries. Animals are extremely vulnerable to mycotoxins due to the common practice of diversion of mycotoxin contaminated agricultural commodities to animal feed. Thus, mycotoxicoses, or mycotoxin-induced diseases, frequently occur in animals. Web site: http://www.delphion.com/details?pn=US05192547__ •

Apparatus and method for fumigation and detoxification of plant seed Inventor(s): Enos; Quentin M. (Chandler, AZ) Assignee(s): Toltec Corporation (phoenix, Az) Patent Number: 4,780,279 Date filed: April 14, 1987 Abstract: The present invention relates to a method of fumigation and detoxification of plant seed and to an pneumatic apparatus having a positive pressure air source, seed feed, a vacuum wheel air lock, fumigant and detoxicant source, a spraying apparatus for introducing the fumigant and/or the detoxicant and an exit cyclone having an optional air return for returning fumigant and/or detoxicant saturated air to the apparatus. The inventive apparatus and method have been found effective for aflatoxin B.sub.1 and B.sub.2 suppression as well as for insect extermination in infested plant seed. Excerpt(s): The present invention relates generally to an apparatus and method for the fumigation and detoxification of plant seed such as rice, corn, cottonseed, soybeans, peanuts, wheat, barley and other seeds. More particularly, the present invention relates to a pneumatic apparatus having a positive pressure air source, seed feed, a vacuum wheel air lock, fumigant and detoxicant source, a spraying apparatus for introducing the fumigant and/or the detoxicant and an exit cyclone having an optional air return for returning fumigant/detoxicant saturated air to the apparatus. Further, the inventive apparatus and method have been found effective for aflatoxin B.sub.1 and B.sub.2 suppression as well as for extermination of pink boll worm and weevils which commonly infest and contaminate the nation's seed supply and food chain. In addition to the efficacious fumigant and detoxicant activity of the present invention, increases in nutrient values of the treated seeds has been noted. At present time conventional means for fumigation and detoxication of the nation's seed supply has been accomplished by employing the highly toxic chemicals phostoxin and methyl bromide. Despite their inherent toxicity these two chemicals are the major fumigants and detoxicants currently employed by growers and/or seed treatment facilities to comport with the U.S. Department of Agricultural (hereinafter "USDA") regulations and requirements for qualification for the Phyto-Sanitary Certificate of Approved Fumigation which is required for interstate transport of treated seed. Current methodology and regulation

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mandates, for example, that cotton planting seed stored for interstate transport must be covered, treated and retained in such state for at least five days before transportation from the storage area. The five day retention period has been found to be the optimum time permissible for insuring safe levels of residual phostoxin or methyl bromide toxicity. This retention period had been tremendously burdensome to cotton gins which do not have endless seed storage capacity and must, at times, abandon or ignore proper storage procedures. Web site: http://www.delphion.com/details?pn=US04780279__ •

Bacillus subtilis strain and prevention of aflatoxin contamination in cereals and nuts Inventor(s): Kimura; Norio (Yokohama, JP) Assignee(s): Morinaga & Co., Ltd. (tokyo, Jp) Patent Number: 4,931,398 Date filed: January 21, 1988 Abstract: A microbiological prevention of aflatoxin contamination in cereals and nuts is provided. Bacillus subtilis NK-330 and NK-C-3 effectively inhibit not only growth of aflatoxin-producing fungi including Aspergillus flavus and Aspergillus parasiticus but also production of aflatoxin by them. Excerpt(s): This invention relates to a microbiological prevention of aflatoxin contamination in cereals and nuts, in particular, to certain strains of Bacillus subtilis capable of inhibiting growth of fungi which produce aflatoxin, hereinafter referred to as "aflatoxin-producing fungi", and moreover of suppressing production of aflatoxin by them. More specifically, the invention relates to Bacillus subtilis strains NK-330 and NKC-3 and their variants. Aflatoxin is one of the most potent carcinogens among those hitherto known. Aflatoxin is a metabolite secreted by the aflatoxin-producing fungi such as Aspergillus flavus and Aspergillus parasiticus, and several homologues thereof including aflatoxin B.sub.1 and aflatoxin G.sub.1 are also known. Among food cereals such as wheat, barley, rice, corn (maize), etc. and food nuts such as hazelnut, almond, Brazil nut, peanut, etc., those contaminated with the aflatoxin have been found (cf. Am. Assoc. Cereal Chemists Inc., 595(1974); Am. Assoc. Cereal Chemists Inc., 603(1975); JAOCS, 980A, December (1981); J. Agric. Food Chem., 26, 249 (1978); Dtsch Lebensm. Rudsch., 76, 47(1980); Lebensm. -Wiss. u. -Technol., 14, 252(1981)), and the aflatoxinproducing fungous microbes are supposed to possibly spread around the areas where these crops are cultivated and yielded. Since such cereals and nuts contaminated with the aflatoxin provide a serious health problem, a lot of countries strictly regulate the importation of the contaminated cereals and nuts so as not to enter their territories. Web site: http://www.delphion.com/details?pn=US04931398__

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Control of mycotoxin production by chemically inhibiting fungal growth Inventor(s): Gueldner; Richard C. (Chula, GA), Wilson, Jr.; David M. (Tifton, GA) Assignee(s): The United States of America AS Represented by the Secretary of (washington, Dc) Patent Number: 4,474,816 Date filed: October 4, 1983

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Abstract: An effective method to control aflatoxin produced by toxic strains of Aspergillus parasiticus fungi is disclosed. An effective amount of Beta-ionone is applied to said fungi to inhibit the growth and sporulation of the fungi and thereby control production of aflatoxin from the fungi without killing the fungi. Excerpt(s): This invention relates to the control of mycotoxins by means of chemical treatment. Heretofore, it has been known that "turkey X" disease has been caused by a toxin produced by some strains of the fungi Aspergillus parasiticus. This aflatoxin which is produced by strains of A. parasiticus is acutely toxic as well as carcinogenic. However, much of the research on aflatoxin dealt solely with the detection of aflatoxin and relatively little research has been done on the prevention of formation of aflatoxins. A review of the control or suppression of fungi producing aflatoxin reveals efforts of fumigating with high level dosages of methyl bromide, ethylene dibromide, propane/propene ethylene oxide, sulfur dioxide, and phosphine and did show some effects of fungicidal activity. Ammonia proved to be fungicidal but demonstrated a lack of any residual effect. Propionic, acetic, and isobutyric acids also have antifungal activity. However, all the above chemicals have the definite disadvantage of toxicity to humans and animals, corrosiveness, and lowered nutritional quality. Therefore, they are not acceptable to either humans or animals. Web site: http://www.delphion.com/details?pn=US04474816__ •

Extraction of gossypol from cottonseed Inventor(s): Abraham; George (Metairie, LA), Fisher; Gordon S. (Metairie, LA), Hron, Sr.; Robert J. (New Orleans, LA), Kuk; Myong S. (Metairie, LA) Assignee(s): The United States of America AS Represented by the Secretary of (washington, Dc) Patent Number: 5,112,637 Date filed: November 5, 1990 Abstract: The present invention is drawn to a process for extraction of gossypol for cottonseed using a solvent solution which includes: (a) a water miscible organic solvent; (b) water; and (c) an acid which is strong enough to prevent binding of gossypol to cottonseed protein but which is not so strong as to hydrolyze a substantial portion of the cottonseed protein. The present invention also includes cotton seed meals of reduced gossypol content (and optionally reduced aflatoxin and/or fat content) produced by the aforementioned extraction. Excerpt(s): This invention relates to a solvent extraction process for removing gossypol (a toxic pigment) from cottonseed. The extraction is conducted with a solvent solution comprised of: a water miscible organic solvent, water and an acid which is strong enough to prevent gossypol from binding to cottonseed protein, but not so strong that it hydrolyses a substantial amount of the cottonseed protein. Unlike other commercial oilseeds, cottonseed contains a toxic pigment, gossypol, which prevents it from being a feed for animals, other than those that have a rumen. That is, while some whole cottonseed is fed to mature ruminants, most of it is separated into oil and meal, typically by solvent extraction using hexane. As used herein, cottonseed meal, or flour, refers to the whole residue remaining after most of the oil has been removed. Before the oil and meal can be used as a food source, the gossypol must be removed or deactivated. In addition, unfavorable growing, harvesting, or storage conditions can cause cottonseed to mold and become contaminated with a mold metabolite aflatoxin, which, because it

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is carcinogenic, must be removed, or destroyed. The presence of such toxic components prevents cottonseed from reaching its full potential as a food source, especially in countries that grow cotton but not soybeans. In the intact cottonseed, the gossypol is concentrated in glands that are covered with a hydrophilic coating, which keeps the gossypol from coming into contact with other components of the seed. Originally, gossypol was deactivated by pressing, or expelling, the oil out of moist seeds at relatively high temperatures, such as at temperatures from about 110.degree. to 130.degree. C. Under these conditions, the glands are ruptured by hot moisture, releasing gossypol. Most of the gossypol reacts with protein, thereby forming bound gossypol, which is insoluble. The rest reacts with phospholipids and other low molecular weight components of the seed to give products that are soluble in oil and other organic solvents, as is any unreacted gossypol. The gossypol in these soluble products is referred to as free gossypol. Total gossypol is the sum of bound gossypol and free gossypol. Total gossypol content of meals made by such a process are typically from about 0.7 to 1.0 wt. %. While binding to protein is advantageous in that it acts to detoxify the gossypol, it is disadvantageous because it reduces the nutritive value of the meal by reducing the available lysine content. Currently, separation is done by expression, or by extraction of the oil from flaked kernels at elevated temperatures with a solvent such as hexane, or a combination of expression and extraction. The most common method used today is solvent extraction, but unless a separate moist heating preconditioning step is included, meals produced by this method will contain unruptured glands and excessive amounts of free gossypol. Furthermore, it is well known that adverse physiological effects can occur with some meals containing high total gossypol, even though free gossypol is within acceptable limits. Web site: http://www.delphion.com/details?pn=US05112637__ •

Flotation separation of aflatoxin-contaminated grain or nuts Inventor(s): Hagen; William R. (Cincinnati, OH), Henderson; James C. (Cincinnati, OH), Kreutzer; Stanley H. (Cincinnati, OH), Schmidt; Arthur A. (Cincinnati, OH), Smith; Charles A. (Cincinnati, OH) Assignee(s): The Procter & Gamble Company (cincinnati, Oh) Patent Number: 4,795,651 Date filed: May 4, 1987 Abstract: Disclosed is a method for separating mycotoxin-contaminated grains, kernels, seeds and nuts, from uncontaminated whole grain seeds, whole or split kernel nuts and seeds to obtain a substantially uncontaminated supply source of these foods. The separate contaminated source can be further processed to lower the mycotoxin contamination. The process involves the separation of the mycotoxin or aflatoxincontaining materials by floating the aflatoxin-contaminated foods in a liquid having a specific gravity of from about 0.9 to about 1.2. A highly preferred process uses dynamic flotation. Excerpt(s): This invention relates to a method for separating mycotoxin-contaminated grains, kernels, seeds and nuts, from uncontaminated whole grain seeds, whole or split kernels, nuts and seeds to obtain a substantially uncontaminated supply source of these foods. The process involves the separation by specific gravity of the mycotoxincontaining materials by floating the mycotoxin-contaminated foods in a liquid. Preferably, the separate contaminated source can be further processed to provide foodstuffs with safe levels of mycotoxin. Mycotoxins are a broad class of toxic materials

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produced by the growth of fungi on foods. Aflatoxin is a specific mycotoxin produced by the action of a fungi belonging to the genus, Aspergillus, on grain, seeds, kernels or nuts. Aflatoxin contamination is particularly a problem in the peanut industry. In addition, aflatoxin can affect grains such as corn and hops, oilseeds, such as cottonseed, soybean, almonds, brazel nuts, pecans, pistachios, etc. The growth of fungi which produce aflatoxin is favored under the same conditions which are good for growing nuts and grains. High levels of aflatoxin in foods presents a threat to animals and humans since aflatoxins at high levels have been shown to cause cancer in laboratory animals. For this reason, the USDA has set limits on the amount of aflatoxin and other mycotoxins that can be in food products. Web site: http://www.delphion.com/details?pn=US04795651__ •

Method and apparatus for sorting agricultural products Inventor(s): Fraenkel; Herbert (London, GB2), Gough; Patrick B. (Wallington, GB2), Maughan; William S. (Burgess Hill, GB2) Assignee(s): Sortex North America, Inc. (lowell, Mi) Patent Number: 4,203,522 Date filed: August 31, 1978 Abstract: A sorting machine for sorting ground nuts affected by a mould which produces aflatoxin comprises detectors for detecting infra-red (or red) and green light respectively reflected from a ground nut being viewed. The infra-red detector produces a first signal indicative of the amount of mould carried by the ground nut. The green detector produces a signal indicative of the extent to which the ground nut is mechanically damaged, and also produces a gating signal. A comparison signal is derived from these first and second signals and is passed by way of a gate and a level detector to an ejector. The gating signal controls the operation of the gate in dependence upon the extent to which the ground nut being viewed is mechanically damaged, so that the ejector is actuated by comparison signals of a predetermined level only when the extent to which the ground nut is mechanically damaged does not exceed a predetermined value. Excerpt(s): This invention concerns a method and an apparatus for effecting relative separation between desired and undesired agricultural products, e.g. between mouldcarrying agricultural products and agricultural products free of such mould. Although the invention is applicable to the sorting of a number of different agricultural products, e.g. maize, it is more particularly applicable to the sorting of oil stock ground nuts which are liable to be contaminated by a toxic mould which produces aflatoxin. After the oil has been extracted from ground nuts, the material remaining may be formed into a cattle cake. However, if the said ground nuts have been contaminated by aflatoxin, the cattle cake made therefrom is similarly contaminated, and since aflatoxin is highly toxic, many countries have legislation which limits the permissible amount of aflatoxin in cattle cake. Attempts have been made to detoxify the cattle cake, e.g. by the use of ammonia, but the cost and the undesirable side effects of such detoxification have so far prevented its use. Web site: http://www.delphion.com/details?pn=US04203522__

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Method and test kit for detecting an aflatoxin B.sub.1 and G.sub.1 using novel monoclonal antibodies Inventor(s): Dixon; Deborah E. (Lansing, MI), Hart; L. Patrick (Lansing, MI), Pestka; James J. (East Lansing, MI) Assignee(s): Neogen Corporation (lansing, Mi) Patent Number: 4,835,100 Date filed: October 31, 1986 Abstract: Novel monoclonal antibodies to an aflatoxin B.sub.1 and G.sub.1 in a test kit and used in a method of testing are described. The method for producing the monoclonal antibodies uses repeated administration of aflatoxin B.sub.1 or the related analog compound as a 1-position polypeptide to a murine and production of a hybridoma to generate the novel monoclonal antibodies. The novel antibodies have limited cross-reactivity to aflatoxins B.sub.2, G.sub.2 and M.sub.1. Aflatoxin B.sub.1 or aflatoxin G.sub.1 are detected in foods and the like using the test kit and method. Excerpt(s): The present invention relates to novel monoclonal antibodies against aflatoxin B.sub.1 and G.sub.1 and to a test kit and a method which uses these monoclonal antibodies to detect the presence of aflatoxin B.sub.1 and G.sub.1 in foods and other materials. In particular the present invention relates to monoclonal antibodies produced (1) by repeated introduction of aflatoxin B.sub.1 as a 1-position polypeptide conjugate into a murine over a period of time so that polyclonal antibodies are released into the blood serum of the murine and then (2) by the production of hybridomas from spleen cells of the murine which generate the monoclonal antibodies and which have substantially the cross-reactivity of the specific monoclonal antibody produced by hybridoma IVI-10108 to aflatoxin B.sub.1 and G.sub.1 and limited cross-reactivity to aflatoxins B.sub.2, G.sub.2 and M.sub.1. Aflatoxins are toxic metabolites produced by the fungal species Aspergillus flavus and Aspergillus parasiticus. The ability of aflatoxin B.sub.1 and its metabolites to act as potent carcinogens, mutagens and teratogens has been described (Butler, W. H. Mycotoxins p. 1-28 (1974); Chu, F. S., Adv. Appl. Microbiol. 22, 83 (1971)). Interest in development of rapid sensitive assays for detection of aflatoxins has been steadily increasing, since the compounds are known to occur naturally in peanuts, corn, milk, wheat, and animal rations (Butler, W. H. Mycotoxins p. 1-28 (1974)). Use of high performance liquid chromatography has been described for quantitation of aflatoxins (Gregory, J. F. and Manley, D. B., J. Assoc. Off. Anal. Chem. 65, 869 (1982); Stubblefield, R. D. and Shotwell, O. L., J. Assoc. Anal. Chem. 60. 4066 (1977)). Several drawbacks to using this procedure as a quick screening method include the high cost of the instrumentation, the need for extensive sample clean up, and only single samples may be analyzed at one time. A number of immunoassays using polyclonal antiserum have been described for detection of aflatoxin B.sub.1 (Chu, F. S. and Ueno, I. Appl. Environ. Microbiol. 33, 1125 (1977); El-Nakib, O., Pestka, J. J. and Chu, F. S., J. Assoc. Off. Anal. Chem. 64, 1077 (1981); Langone, J. L. and Van Vunakis, H., J. Natl. Cancer Inst. 56, 591 (1976); Lawellin, D. W., Grant, D. W. and Joyce, B. K., Appl. Environ. Microbiol. 34, 94 (1977); Pestka, J. J., Gaur, P. K. and Chu, F. S., Appl. Environ. Microbiol. 40, 1027 (1980); and Pestka, J. J. and Chu, F. S., J. Fd. Prot. 47, 305 (1984)). The advantages offered by these assays include a reduction in assay time, simplified extraction procedures, an increase in assay sensitivity, and the ability to routinely screen large numbers of samples. Web site: http://www.delphion.com/details?pn=US04835100__

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Method for detecting aflatoxin in almonds Inventor(s): King, Jr.; A. Douglas (Martinez, CA), Schade; John E. (Walnut Creek, CA) Assignee(s): The United States of America AS Represented by the Secretary of (washington, Dc) Patent Number: 4,535,248 Date filed: August 24, 1984 Abstract: Aflatoxin contamination in almonds is detected by exposing almond kernels to long wave ultraviolet light and detecting the presence of aflatoxin as determined by violet-purple fluorescence. The method is particularly adaptable to automation to detect and sort out aflatoxin contaminated almonds. Excerpt(s): This invention relates to and has among its objects the provision of a novel method for detecting aflatoxin contamination in almonds. Aflatoxins, a group of highly toxic substances produced by certain species of Aspergillus, especially A. flavus, have been found to occur in agricultural products such as corn, cottonseed, a variety of oilseeds, and many varieties of nuts. Experimental studies indicate that aflatoxins are acutely toxic to most animal species. The extreme toxicity of aflatoxin is demonstrated by the fact that the LD.sub.50 of the B.sub.1 component is less than 30 micrograms for day-old ducklings. Animals which consume sublethal quantities of aflatoxin for several days or weeks develop a subacute toxicity syndrome which commonly includes moderate to severe liver damage. Prolonged administration of the toxin at subacute levels leads to formation of cancerous liver tumors. Data accumulated from feeding tests indicate that the effective dose of the B.sub.I component of aflatoxin for the induction of liver tumors in rats is approximately 10 mg per day. When this value is compared with similar estimates for other hepatocarcinogens such as dimethylnitrosamine (750 mg/day) and butteryellow (9,000 mg/day), the relative potency of aflatoxin is readily apparent. Aflatoxins occur at varying concentrations throughout the tissue of contaminated products and can occur at concentrations up to over 1,000,000 parts per billion (ppb) in individual nuts such as peanut kernels. These toxins may remain after the molds that produced them are removed or destroyed. Aflatoxins are fairly resistant to heat and to chemical treatments that do not destroy the nutmeat. conventional food processing, such as roasting nuts, can reduce the aflatoxin level but not sufficiently to solve the problem. Web site: http://www.delphion.com/details?pn=US04535248__

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Method for detoxifying foodstuffs Inventor(s): Chapman; Russell R. (Mesa, AZ) Assignee(s): Aflatoxin Limited Partnership (cave Creek, Az) Patent Number: 5,082,679 Date filed: January 25, 1991 Abstract: An improved method for de-toxifying aflatoxin contaminated foodstuffs is provided by pre-treating the contaminated foodstuff with a wetting agent prior to exposure to the de-toxicant. An aqueous solution of detergent or soap is a suitable wetting agent which can be applied to the foodstuff by spraying or immersion. Ammonia gas is the preferred de-toxicant. Once the wetting agent has been applied, the de-toxification reaction is exothermic so that little or no heat need be added to reach the

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elevated temperatures that facilitate rapid de-toxification. The process runs at atmospheric pressure in low cost vessels and may be accomplished in times of an hour or less without external heat sources. Excerpt(s): This invention concerns an improved method for de-toxifying foodstuffs and, more particularly, an improved method for de-toxifying foodstuffs containing aflatoxins and similar naturally occurring contaminants. There are many foodstuffs that are susceptible to contamination by mold and bacteria and products thereof. For example, grains and feeds that have been exposed to warm humid atmospheres can become contaminated by aflatoxins. Aflatoxins are highly toxic carcinogenic substances produced by the naturally occurring molds Aspergillus flavus and Asgergillus parasiticus. Unless the affected material is de-toxified, the aflatoxins can cause severe damage and death to animals or humans who ingest the affected foodstuffs. Hence, there is an ongoing need for economical processes for de-toxifying aflatoxin contaminated agricultural products intended for human or animal consumption. A number of techniques have already been developed for de-toxifying aflatoxin contaminated foodstuffs. The following patents and article are incorporated herein by reference and describe the results set forth below by way of example. Web site: http://www.delphion.com/details?pn=US05082679__ •

Method for obtaining aflatoxin-free food products Inventor(s): Carmona; Julian Y. (279 Guevara Avenue, San Juan, Rizal, RP), Marasigan; Marcelo P. (6-Legaspi Street, Philamlife Homes, Quezon City, RP) Assignee(s): None Reported Patent Number: 4,035,518 Date filed: October 6, 1975 Abstract: A method for obtaining food products substantially free of aflatoxin in the form of particles, kernels, and the like, is disclosed wherein a food product such as whole grain seeds or whole kernel nuts are subjected to a weakly alkaline aqueous solution maintained at elevated temperatures for a short period of time, washing the thusly treated food product with water until the wash effluent indicates that it is pH neutral and separating the aflatoxin-contaminated food product from the uncontaminated food product. The uncontaminated food product sources can then be further processed to obtain a food product ready for consumption. Excerpt(s): This invention relates to a method for separating aflatoxin contaminated kernels, seeds, nuts, and the like, from uncontaminated whole grain seeds, whole or split kernels nuts, and the like, to obtain an uncontaminated supply source for a food product. Aflatoxin is produced by the action of a fungi belonging to the genus, Asperigillus, on exposed grain seeds or nuts. Aflatoxin affects certain grains such as corn, hops, cottonseed, soybean, and the like, as well as such nuts as almonds, Brazil nuts, pecans, pistachios, peanuts, and the like, and is particularly active and dominant when such grains and nuts are grown and cultivated in wet climates. Due to the toxic threat that aflatoxin-contaminated food sources present to animals, there have been many attempts to treat grains and nuts in meal form so as to either detoxify these food sources or lower the level of their aflatoxin-contamination. Representative of such attempts are the use of photochemical means to detoxify the aflatoxin-contaminated food sources (U.S. Pat. No. 3,506,452), mixing the food source product with methylamine at elevated temperatures (U.S. Pat. No. 3,585,041), contacting the food

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source product with ozone (U.S. Pat. No. 3,592,641), treating suspension of the food product with peroxide (British Pat. No. 1,117,573), treating the food products with various aromatic solvents such as aqueous isopropanol (E. T. Raynor et al., J. Amer. Oil. Chem. Soc., 1968, 45 (9) pp. 622-4), aqueous ethanol (E. T. Raynor et al., J. Amer. Oil Chem. Soc., 1970, 47 (1), 26 Chem. Abstracts, 72:6847z), an actone-hexane-waterazeotrope mixture (U.S. Pat. No. 3,515,736), and aqueous acetone followed by hexane extraction (U.S. Pat. No. 3,557,168). Web site: http://www.delphion.com/details?pn=US04035518__ •

Method for the removal of aflatoxin from cereals, oil seeds and feedstuffs Inventor(s): Fukinbara; Itaru (Tokyo, JA), Korenaga; Tokiyoshi (Sakaimachi, JA), Yano; Nobumitsu (Tokyo, JA), Yoshida; Koji (Sakaimachi, JA) Assignee(s): Asahi Kasei Kogyo Kabushiki Kaisha (osaka, Ja) Patent Number: 4,055,674 Date filed: June 14, 1976 Abstract: A method for the removal of Aflatoxin from materials including cereals, oil seeds and feedstuffs contaminated therewith comprising contacting said materials with a mixed solvent system of liquid dimethyl ether and water. The water is employed in an amount of 2 to 8 % by weight with respect to the liquid dimethyl ether. Such method which can reduce the Aflatoxin content to 15 ppb or less, can be conducted at low temperatures so that no proteins contained therein are denaturated. Further, the spent solvent system containing Aflatoxin can be easily regenerated by contacting it with activated carbon and recycled. Excerpt(s): This invention relates to a method for the removal of Aflatoxin from cereals, oil seeds and feedstuffs which are contaminated therewith, by the use of a mixed solvent system comprising liquid dimethyl ether and water. More particularly, this invention relates to a method for the complete removal or elimination of a carcinogenic poisonous substance produced by a mold, which is named "Aflatoxin", from those cereals, oil seeds and feedstuffs contaminated with said substance through extraction in an extraction system containing liquid dimethyl ether and water. The term "cereal" as used herein means to refer to any cereals, which are normally ingestable orally in any optional form of raw or processed grains and meals such as rice and so on. The term "oil seed" as used herein means to refer to any oil seeds, which are normally edible in any optional form of raw or processed grains, meals and cakes, such as peanut, peanut meal, cotton seed, cotton seed meal, cotton seed cakes and so on. The term "feedstuff" as used herein refers to any other materials which may be employed for preparing a feed of domestic animals. It is well-known in the art of Aflatoxin is one sort of those toxins produced by a variety of molds, of an extremely high carcinogenicity and a typical one produced by a microbe belonging to Aspergillus flavus and growing on foodstuffs such as grains. It is generally realized that such materials as peanuts, cotton seeds, rice and the like are easily susceptible to contamination with this toxin and thus badly damaged thereby. Web site: http://www.delphion.com/details?pn=US04055674__

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Method of inhibiting mycotoxin production in seed crops by modifying lipoxygenase pathway genes Inventor(s): Keller; Nancy P. (College Station, TX) Assignee(s): The Texas a & M University System (college Station, Tx) Patent Number: 5,844,121 Date filed: January 19, 1996 Abstract: A method of inhibiting the production of mycotoxins of fungus, such as aflatoxin-producing and sterigmatocystin-producing fungi, in plants susceptible to contamination by such mycotoxins consists of introducing into the susceptible plant a gene encoding for lipoxygenase pathway enzyme of the mycotoxin. Exemplary of the lipoxygenase pathway enzymes are soybean lipoxygenase, allene oxidase, hydroperoxide lyase and hydroperoxide dehydratase. The resulting transgenic plant demonstrates substantial resistance to mycotoxin contamination of such fungus. Plants which are substantially resistant to mycotoxin contamination of Aspergillus spp. are further obtained by incorporating into mycotoxin susceptible plant antisense genes for the 9-hydroperoxide fatty acid producing lipoxygenases. Excerpt(s): The invention is drawn to a method of eliminating or substantially reducing toxicity in seed crops caused by colonization of fungi which produce toxic fungal metabolites called mycotoxins. In particular, the invention relates to a method of eliminating or substantially reducing toxicity in seed crops caused by colonization of aflatoxin-producing or sterigmatocystin-producing fungi. Colonization by aflatoxinproducing or sterigmatocystin-producing fungi, such as Aspergillus spp., leads to contamination of food and feed crops by aflatoxin/sterigmatocystin. In addition, the invention is drawn to novel genetically enhanced crops containing the "anti-fungus aflatoxin or sterigmatocystin" gene which masks the detrimental effects caused by aflatoxin and sterigmatocystin. According to the invention, a mycotoxin-inhibiting agent within the lipoxygenase pathway is transferred by genetic engineering techniques to crops susceptible to the mycotoxin. In particular, the invention is drawn to the transfer of an inhibiting agent of aflatoxin or sterigmatocystin to such aflatoxin/sterigmatocystin susceptible crops as corn, peanuts, treenuts, cottonseed, etc. Alternatively, the genes encoding lipoxygenase may be modified in-situ to render a product which masks the detrimental effects caused by aflatoxin and sterigmatocystin. Still, the invention is drawn to a method of blocking the transcription of the 9hydroperoxy producing lipoxygenase genes by anti-sense genes. Still further, the invention is drawn to the creation of an "anti-Aspergillus aflatoxin or sterigmatocystin" gene (e.g. by altering lipoxygenase pathway enzyme production) and its incorporation into aflatoxin/sterigmatocystin susceptible crops. Web site: http://www.delphion.com/details?pn=US05844121__

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Non-aflatoxigenic aspergillus parasiticus strains and their use in controlling aflatoxin contamination Inventor(s): Blankenship; Paul D. (Preston, GA), Cole; Richard J. (Albany, GA), Dorner; Joe W. (Albany, GA) Assignee(s): The United States of America AS Represented by the Secretary of (washington, Dc) Patent Number: 5,292,661 Date filed: August 7, 1991 Abstract: A process for biologically controlling the preharvest accumulation of aflatoxin in soil-borne crops. Non-aflatoxigenic strains of Aspergillus parasiticus having all of the relevant identifying characteristics of NRRL 18786 and NRRL 18991 are shown to inhibit aflatoxin production by native toxigenic strains of Aspergillus flavus or Aspergillus parasiticus in the soil environment. Excerpt(s): This invention relates to a method for the preharvest control of aflatoxin in crops. This is accomplished by inoculating either the crop or the soil in which it is grown with non-aflatoxigenic strains of Aspergillus parasiticus (A. parasiticus), deposited and designated as NRRL 18786 and NRRL 18991. Aflatoxins are potent hepatotoxic, carcinogenic compounds produced by fungi, particularly Aspergillus flavus (A. flavus) and A. parasiticus [Cast, (1989) Mycotoxins: economic and health risks. Report 116. Council for Agricultural Science and Technology). When these fungi invade and grow in agricultural commodities such as peanuts, corn, and cottonseed, the resulting contamination with the aflatoxins often makes the commodity unfit for consumption. They are a serious threat to humans and animals [Cast, Counc. Agric. Sci. Technol. Rep., Vol. 80, (1979), Ames, IA., 56 pp.]. The four naturally-occurring aflatoxins are designated B.sub.1,B.sub.2,G.sub.1, and G.sub.2 and will hereafter be collectively referred to as aflatoxin. The United States peanut industry has identified aflatoxin contamination of peanuts as the number one problem for which a solution is needed [Consensus Report of the National Peanut Council Quality Task Force (1987) National Peanut Council]. Web site: http://www.delphion.com/details?pn=US05292661__

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Non-toxigenic strain of Aspergillus oryzae and Aspergillus sojae for biocontrol of toxigenic fungi Inventor(s): Cole; Richard J. (Albany, GA), Dorner; Joe W. (Albany, GA), Horn; Bruce W. (Albany, GA) Assignee(s): The United States of America, AS Represented by the Secretary of (washington, Dc) Patent Number: 6,027,724 Date filed: July 6, 1998 Abstract: Non-toxigenic strains of Aspergillus such as from the species Aspirgillus oryzae and Aspergillus sojae are useful fungal biocontrol agents for preventing toxin contamination in agricultural commodities, especially those for human consumption such as peanuts and corn. These strains do not produce aflatoxin, any bis-furan ringcontaining intermediates of the aflatoxin biosynthetic pathway and cyclopiazonic acid. They are also useful for controlling toxin damage to crops such as cotton. The strains

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include Aspergillus strains NRRL 21368, NRRL 21369, NRRL 21882, NRRL 30038, NRRL 30039 and mixtures thereof. Excerpt(s): The present invention relates to novel non-toxigenic strains of Aspergillus including Aspergillus flavus (A. flavus), Aspergillus parasiticus (A. parasiticus), Aspergillus oryzae (A. oryzae), and Aspergillus sojae (A. sojae); agricultural compositions containing non-toxigenic strains of Aspergillus flavus (A. flavus), Aspergillus parasiticus (A. parasiticus), Aspergillus oryzae (A. oryzae), and Aspergillus sojae (A. sojae) on agriculturally acceptable carriers; and to methods for the control of toxin contamination in agricultural commodities using non-toxigenic strains of A. flavus, A. parasiticus, A. oryzae, and A. sojae. Aflatoxins are potent hepatotoxic, carcinogenic compounds produced by A. flavus Link:Fr. and A. parasiticus Speare (CAST, In: Mycotoxins: Economic and Health Risks. Report 116, 99 pp., Council for Agricultural Science and Technology, 137 Lynn Avenue, Ames, IA 50010). Cyclopiazonic acid (CPA) is another potent mycotoxin that is produced by A. flavus, but not by A. parasiticus. When these fungi invade and grow in commodities such as peanuts, corn, cottonseed, and tree nuts, the resulting contamination with the aflatoxins and CPA often makes the commodity unfit for consumption. The United States peanut industry has identified aflatoxin contamination of peanuts as the number one problem for which a solution is needed (Consensus Report of the National Peanut Council Quality Task Force, 1987, National Peanut Council, Alexandria, Va. 22314). Because peanuts are used primarily for food, strict regulatory limits for the amount of aflatoxin allowable in finished peanut products have been established. Although the United States Food and Drug Administration has an action level of 20 ppb of total aflatoxins in food products, international tolerances for aflatoxin are much lower, typically in the range of 0-4 ppb, and are important because U.S. companies compete internationally in the market to export peanuts and peanut products. For this reason the United States peanut industry has a goal to ensure the delivery of aflatoxin-free peanut products by the year 2000. Although aflatoxin contamination of peanuts can occur during postharvest curing and storage, the most significant contamination usually occurs prior to harvest during periods of late-season drought stress as peanuts are maturing. The only known method for controlling preharvest aflatoxin contamination in peanuts is irrigation, an option that is unavailable to the majority of peanut growers. Cyclopiazonic acid is an indole-tetramic acid that was first isolated from cultures of Penicillium cyclopium Westling in 1968 (Holzapfel, Tetrahedrom, Volume 24, 2101-2119, 1968). CPA is now know to be produced by a variety of fungi including P. patulum, P. viridicatum, P. puberulum, P. crustosum, P. camemberti, A. flavus, A. versicolor and A. oryzae. In addition, CPA has been found as a natural contaminant of corn and peanuts, often occurring together with aflatoxin (Lansden and Davidson, Applied and Environmental Microbiology, Volume 45, 766-769,1983; Urano et al., Journal of AOAC International, Volume 75, 838-841, 1992). It was also implicated as the causative agent in a human intoxication involving consumption of contaminated millet (Rao and Husain, Mycopathologia, Volume 89, 177-180, 1985). With the discovery of CPA production by A. flavus, 54 isolates of A. flavus were investigated for production of CPA and aflatoxin (Gallagher et al., Mycopathologia, Volume 66, 31-36, 1978). It was found that 28 of the 54 (52%) produced CPA whereas only 18 (33%) produced aflatoxin. Regulatory limits for CPA have not been established; however, because of the co-occurrence of aflatoxin and CPA in commodities, efforts to attain biological control of aflatoxin also need to attain control of CPA. Web site: http://www.delphion.com/details?pn=US06027724__

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Optical inspection of food products Inventor(s): Hill, Jr.; Ralph H. (San Antonio, TX) Assignee(s): Southwest Research Institute (san Antonio, Tx) Patent Number: 4,866,283 Date filed: August 12, 1988 Abstract: An optical inspection system for using laser-induced luminescence to detect the quality of organic materials, such as peanuts. The inspection system comprises an excitation means for illuminating a specimen to cause it to produce fluorescent radiation. The spectral representation of the fluorescence produced by the specimen is compared to a reference spectrum to obtain an indication of the physical characteristics of the specimen. In a preferred embodiment, the system identifies and removes peanuts contaminated with aflatoxin from a stream of peanuts by determining fluorescence at a predetermined wavelength. Excerpt(s): The present invention relates generally to the field of optical inspection of materials. More specifically, the present invention provides a method and apparatus for utilizing laser-induced fluorescence techniques to determine the quality of organic materials, such as foods. The laser-induced fluorescence techniques of the present invention can be used to detect the existence of contaminants in a stream of materials containing desired food products, such as peanuts. A common method of sorting food products is based on colorimetry. Food and biological samples have rather different light scattering properties than simple solids. The detection of slight variations in color, either by visual or by optical/electrical methods, can thus be used to sort the food products. One of the primary difficulties with such methods, however, is the inability to detect slight variations in color which represent different grades of the material or which represent undesired material. For example, in the case of food products such as peanuts, sorting systems which are based on colorimetry techniques often are not able to differentiate between a desired peanut and a rock or stem which may have the approximate color and size as a desired peanut. In addition to the basic problem of differentiating between a desired peanut and a contaminant, such as a rock or stem, it is important to be able to locate and remove contaminated peanuts. One of the contaminanants which food processors fear most is aflatoxin. This pervasive material, which is produced by the Aspergillus flavus fungus when food is improperly stored, costs the food industry millions of dollars per year. Current methods for detection of aflatoxin are time consuming and cumbersome. Web site: http://www.delphion.com/details?pn=US04866283__

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Primers for identifying aflatoxinogenic aspergilli and an improved method thereof Inventor(s): Chandrashekar; Arun (Mysore, IN), Manonmani; Haravey Krishnan (Mysore, IN), Rao; Eddiya Rati (Mysore, IN) Assignee(s): Council of Scientific and Industrial Research (in) Patent Number: 6,623,932 Date filed: March 27, 2002 Abstract: The present invention relates to three sets of novel primers of SEQ ID Nos. 1-6, wherein said three sets of primer are designed from three genes omt, ord, and afl R respectively of aflatoxin biosynthesis pathway of fungi Aspergillus flavus and an

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improved method of identifying aflatoxinogenic aspergilli using said three sets of primers. Excerpt(s): Aflatoxins are potent carcinogenic, mutagenic and teratogenic metabolites produced primarily by the fungal species of Aspergillus flavus and Aspergillus parasiticus. Foods and feeds, especially in warm climates are susceptible to invasion by aflatoxigenic Aspergillus sp. And subsequent production of Aflatoxins during preharvesting, processing, transportation or storage. Over the last few years, means for mycotoxin detection have been simplified, by the adoption of immunological methods. The level of mold infestation and identification of the governing species are important parameters which could give an indication of the quality of the material and future potential for the presence of mycotoxins. Mold counts are a part of quality control assurance for foods. This method is time consuming, labour intensive, costly requires facilities and mycological expertise and do not allow the specification of mycotoxegenic fungi. Web site: http://www.delphion.com/details?pn=US06623932__ •

Process of sparing poultry from the effect of toxins Inventor(s): Taylor; Gregg W. (Murrayville, GA) Assignee(s): A.h.p., Inc. (gainesville, Ga) Patent Number: 4,126,701 Date filed: July 8, 1977 Abstract: A process of feeding animals and poultry a complete feed consisting only of (i) between 0.00077 and 0.005 percent by weight, based on the weight of the feed, of gentian violet and (ii) the remainder medically inert ingredients, such inert ingredients not having a sparing effect for poultry and animals from the toxic and/or lethal effects of aflatoxin. The gentian violet has the effect of sparing animals and poultry from the toxic effects of aflatoxins in feeds. The inert ingredients include all of the inert ingredients normally in a complete or basal animal or poultry feed. Excerpt(s): This invention relates to animal and poultry feed which contains a medicinal agent that is a selective fungicidal mold inhibitor of Candida albicans. This invention also relates to the use of such feed to spare animals and poultry from the toxic effects of aflatoxins and other mycotoxins in feed. It is known that a given strain of mold may gain or lose its ability to produce toxins without known reason. Several reasons for this phenomenon have been advanced, namely, change of substrate, genetics, stage of growth, accumulation and metabolism of the toxin, and actual stability of the toxin. Facial eczema of sheep in New Zealand has been caused by Pithomyces chartarus -- the toxin caused liver damage and skin disorders. A malady in horses, cattle, and poultry has been caused by a toxin from a mold called Stachybotrys atra. A field outbreak in Georgia of mold toxicosis in swine resulted from corn left in the field -- the toxic molds were Aspergillus flavus and Penicillium rubrum. A massive outbreak of toxicity from moldy ground nut meal (peanut) occurred in England -- the toxin producing mold was a strain of Aspergillus flavus. The common name applied to the disease is "Turkey X" disease, and the poisonous material has been designated as "Aflatoxin." Aflatoxin has carcinogenic properties. Hemorrhagic disease in chicks occurred -- toxins from certain molds will cause lesions indistinguishable from field hemorrhagic disease. Bovine hyperkeratosis has been caused by Aspergillus clavatus. A toxicosis from moldy feed at Texas Agricultural Experimental Station was caused by unidentified molds. The mold

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brought on acute lysine deficiency. Arginine was similarly affected. These amino acids alleviated most of the problem in poults. Web site: http://www.delphion.com/details?pn=US04126701__ •

Production aflastatin A from streptomyces sp., a pharmaceutical composition and methods of use Inventor(s): Isogai; Akira (Chiba, JP), Ono; Makoto (Kawasaki, JP), Sakuda; Shouhei (Chiba, JP), Suzuki; Akinori (Chigasaki, JP) Assignee(s): Morinaga & Co., Ltd. (tokyo, Jp) Patent Number: 5,773,263 Date filed: March 3, 1997 Abstract: The antibiotic aflastatin A or its salt and its production by Streptomyces sp. MRI 142, FERM BP-5841 is presented. Aflastatin A is incorporated into a pharmaceutical composition and is employed as an aflatoxin contamination inhibitor, antimicrobial agent, antifungal agent and antitumor agent. Excerpt(s): The present invention relates to an antibiotic aflastatin A or its salt; an aflatoxin contamination inhibitor, an antimicrobial agent, an antifungus agent and an antitumor agent containing it; aflatoxin contamination inhibiting method and tumorinhibiting method employing it; and a process for preparing it. Aflatoxin produced from some mildew belonging to Aspergillus sp. has been known to have a potent carcinogenicity. Further, such aflatoxin producing-mildew have been known to infect agricultural commodities such as corn or peanuts and produce the aflatoxin, resulting in contamination of these agricultural commodities. As pharmaceuticals intended to prevent the aflatoxin contamination, dichlorovos and antibiotic Iturin A have heretofore been known. However, these pharmaceuticals have not been practiced until now. Web site: http://www.delphion.com/details?pn=US05773263__

•

Pure culture of Bacillus subtilis FERM BP-3418 Inventor(s): Kubo; Kazuhiro (Maebashi, JP) Assignee(s): Ahc Inc. (maebashi, Jp) Patent Number: 5,364,788 Date filed: June 30, 1992 Abstract: A bacterium belonging to Bacillus subtilis. The bacterium being identified as Bacillus subtilis FERM BP-3418. In addition the bacterium possesses the capability of decomposing aflatoxin. It is useful as an active ingredient in products such as a fungal growth inhibitor, fermentation promoter, and livestock fattening agent. Excerpt(s): This invention relates to a novel bacterium belonging to Bacillus subtilis and also to its usage. In a wide range of agricultural businesses, various microbial activities take place with some sort of relevance to the agricultural businesses. This relevance may be advantageous or disadvantageous to the agriculture. For example, fungi are microorganisms generally called "molds" and can be classified roughly into Phycomycetes, Ascomycetes, Basidiomycetes and imperfect fungi. They include many useful fungi, led by yeast.

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Web site: http://www.delphion.com/details?pn=US05364788__ •

Reduction of aflatoxin content in peanuts Inventor(s): Gross; David R. (Orrville, OH), Kragt; Marvin (Orrville, OH), Valenzky, Jr.; Robert J. (Akron, OH) Assignee(s): The J. M. Smucker Company (orrville, Oh) Patent Number: 5,230,160 Date filed: August 24, 1992 Abstract: Peanuts with a moisture content of from 6% to 15% are subjected to vacuum drying and/or roasting in a chamber using microwave energy to ensure penetration of the kernel. Aflatoxin compounds are destroyed and/or driven off with the vapors exiting the vacuum chamber. Excerpt(s): This invention relates to the art of removal of aflatoxin from cereals, oil seeds and feedstuffs which are contaminated therewith and, more particularly, to an improved method for the removal of aflatoxin from cereals, oil seeds and feedstuffs. It is of course well known that aflatoxin is a specific mycotoxin produced by the action of a fungi belonging to the genus, aspergillus, on grain, seeds, kernels or nuts. Aflatoxins are a group of related, complex, hetercyclic chemical compounds. These compounds are very slightly soluble in water and in the crystalline form melt (and decompose) at temperatures in the 240.degree. C. to 280.degree. C. range. Aflatoxin contamination is particularly problematic in the peanut industry and, in addition, can affect grains such as corn and rice, other oil seeds such as cotton seed, and meals of such grains and seeds which are often used as feed for domestic animals. The growth of fungi which produce aflatoxin is favored under the same conditions which are good for growing nuts and grains. High levels of aflatoxin in foods and feeds presents a threat to humans and animals in that aflatoxins have been shown to cause cancer in laboratory animals. Accordingly, the U.S. Food & Drug Administration has set limits on the amount of aflatoxin that can be in food products, namely less than 20 ppb. The production of aflatoxin results from unfavorable conditions of harvesting and storage, namely high humidity and moisture content. Web site: http://www.delphion.com/details?pn=US05230160__

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Removal of aflatoxin from peanuts Inventor(s): Lindquist; Robert H. (Berkeley, CA) Assignee(s): Chevron Research Company (san Francisco, Ca) Patent Number: 4,062,984 Date filed: August 29, 1975 Abstract: Aflatoxin is removed from seeds or nuts such as peanuts by extraction with methoxymethane. Excerpt(s): The present invention relates to removal of aflatoxin from seeds or nuts. More particularly, the invention pertains to the removal of aflatoxin from peanuts by extraction with methoxymethane. Aflatoxin in seeds or nuts is a poisonous product of metabolic activity of a living organism, probably a fungus. Such poison infects a substantial amount of the peanut crop of the world. The infected peanuts are unsuitable

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for human or animal consumption. Meat from animals fed on the poisonous peanuts is also contaminated and unfit for human consumption. Aflatoxin in ground nuts in general and the problems of detoxification have been studied. Ground nut meal has been exposed to ultraviolet radiation, but shows no change in aflatoxin level. Solvents such as acetone, benzene and chloroform have been used. Likewise, ground nut meal has been treated with sulfur dioxide. Since no treatment was completely successful, it was concluded that successful detoxification seemed to have little potentiality and emphasis should be placed on prevention of contamination. See, for instance, Chemical Abstracts 93565(p), Vol. 66, 1967. Web site: http://www.delphion.com/details?pn=US04062984__ •

Selective removal of aflatoxin from azadirachtin containing compositions Inventor(s): Ellenberger; Suzanne R. (Salem, UT), Ellenberger; William P. (Salem, UT) Assignee(s): Agridyne Technologies, Inc. (salt Lake City, Ut) Patent Number: 5,229,007 Date filed: April 17, 1992 Abstract: A method for the selective removal of contaminants, including aflatoxin, from azadirachtin-containing materials comprising contacting said materials with a binding agent capable of selectively binding contaminants compared to azadirachtin. Excerpt(s): The present invention relates to a method for the selective removal of contaminants, including aflatoxins, from azadirachtin-containing materials. More particularly, this invention relates to a method of reducing the aflatoxin content of azadirachtin-containing materials through the selective binding of aflatoxin by charcoal. Charcoal is defined as a black form of carbon produced by partially burning wood, coal, lignin, bone or other organic matter in a kiln from which air is excluded. Some of the synonyms for charcoal include carbon, activated carbon, and activated charcoal. Charcoal may be prewashed with acid or base with or without subsequent neutralization and may be in powder, granular or pelletized forms. Extracts of the neem (Azadirachta indica) and the chinaberry (Melia azedarach) trees have long been known to have insecticidal activity (Natural Pesticides from the Neem Tree, Proc. 1st Int'l Neem Conf., Rottach-Egern, 1980 (H. Schmutterer, et al. eds. 1982); Natural Pesticides from the Neem Tree and Other Tropical Plants, Proc. 2nd Int'l Neem Conf., Rauisch holzhausen, 1983 (H. Schmutterer and K.R.S. Asher eds. 1984); Natural Pesticides from the Neem Tree and Other Tropical Plants, Proc. 3rd Int'l Neem Conf., Nairobi, 1986 (H. Schmutterer and K.R.S. Asher eds. 1987)). These extracts have generated intense academic research interest including the isolation and identification of at least sixty different chemical entities from various parts of the neem tree (P. Jones, et al., "The Chemistry of the Neem Tree," in Phytochemical Pesticides, Vol. 1 (M. Jacobson ed., CRC Press, 1988). The active ingredient of the neem and chinaberry extracts, azadirachtin, is a limonoid of the tetranortriterpenoid type. This compound has been shown to be a potent insect growth regulator and feeding deterrent (Yamasaki, R. B., et al. (1987) J. Agric. Food Chem. 35:467-471). Several synthetic analogs of azadirachtin have been prepared (Yamasaki, R. B., et al. (1987) suora); Ley, S. V., et al. (1989) Tetrahedron 45:5175) and organic synthesis of the molecule has been accomplished (Ley, S. V., et al. (1987) Tetrahedron Lett. 28:221; Brasca, M. G., et al. (1988) Tetrahedron Lett. 29:1853; Ley, S. V., et al. (1989) Tetrahedron 45:2143; Nishikimi, Y., et al. (1989) J. Org. Chem 54:3354). Due to the complexity of the azadirachtin molecule, however, the economic synthesis and

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commercialization of a synthetic product is highly unlikely and therefore any salable product will require extraction from an azadirachtin-containing plant source. Web site: http://www.delphion.com/details?pn=US05229007__ •

Shelf stable insect repellent, insect growth regulator and insecticidal formulations prepared from technical azadirachtin isolated from the kernel extract of Azadirachta indica Inventor(s): Kumar; Annam Dilip (Secunderabad, IN), Moorty; Sistla Ramchandra (Hyderabad, IN) Assignee(s): Fortune Biotech Limited (secunderabad, In) Patent Number: 5,827,521 Date filed: March 9, 1995 Abstract: Storage stable azadirachtin, an insect repellent and insect growth regulator, and insecticidal formulations (emulsifiable concentrate) thereof, are prepared from purified neem kernel extract, with an active ingredient content of 0.3% to 4% and characterized by the absence of gums and aflatoxin spores, for example. The aforementioned formulations contain solvents belonging to the class of aliphatic dihydroxylated alcohols of more than 80% by volume and optionally containing sunscreens and antioxidants. Excerpt(s): The invention relates to shelf life stable, insect repellent, insect growth regulator and insecticidal formulations having an azadirachtin content ranging between 0.3 to 4%, technical azadirachtin composition of high purity and methods for preparing same. The insect repellent, insect growth regulator and insecticidal azadirachtin, and associated molecules thereof, isolated from the kernels of Azadirachta indica are well documented. "Neem, A Tree For Solving Global Problems" (1992) National Research Council, National Academy Press, Washington D.C. Various methods for extracting azadirachtin from neem kernels using protic as well as aprotic solvents are published. Those processes generally relate to the use of one solvent, concentration to remove the solvent and water and finally formulating the azadirachtin to the desired percentage, depending on the purity and concentration of azadirachtin. Web site: http://www.delphion.com/details?pn=US05827521__

•

Small peptides with antipathogenic activity, treated plants and methods for treating same Inventor(s): Cleveland; Thomas E. (Mandeville, LA), Moyne; Anne-Laure (Auburn, AL), Tuzun; Sadik (Auburn, AL) Assignee(s): Auburn University (auburn University, Al), Usda/ars Southern Regional Research Center (new Orleans, La) Patent Number: 6,183,736 Date filed: April 7, 1999 Abstract: The invention relates to two lipopeptides a1 and a2 produced by Bacillus subtilis and their use as an anitfungal agent against Aspergillus flavus. Both peptides are cyclic, acidic and have broad range of antifungal and antimicrobial activity. Both peptides belong to the Bacillomycin D family. A method and composition for controlling

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aflatoxin contamination in plants susceptible to alflatoxin-producing fungi, like Aspergillus flavus or Aspergillus parasiticus is also disclosed. Excerpt(s): The present invention relates to the control of pathogenic microorganisms, particularly pathogenic fungi and certain bacteria. The invention also relates to lipopeptides having such antipathogenic activity i.e. high antifungal particularly against the Aspergillus genus and antibacterial activity. The invention also relates to the plants which have been treated with the lipopeptides or the microorganisms that synthesize and produce the lipopeptides. The invention also relates to other aspects further described herein. An important objective of the invention is to address and to contribute to solve the aflatoxin problem that is caused by the aflatoxin-producing fungi, Aspergillus flavus and Aspergillus parasiticus. Bacillus ssp is known to produce a variety of peptide antibiotics that are antibacterial and/or antifungal. Although the peptides antibiotics are composed of amino acids, they often differed from geneencoded polypeptides in their structure and mechanism of biosynthesis. Some are geneencoded and synthesized ribosomally, but these often undergo posttranslational processing and modifications. Antibiotics produced non ribosomally are composed of 2 to 20 amino acids organized in a linear, cyclic or branched cyclic structure. Bacillus subtilis produced gene-encoded antibiotics and a variety of small antibiotic peptides with a molecular weight less than 2000 daltons, synthesized non-ribosomally. Subtilin is one gene-encoded lantibiotic peptide synthesized by B. subtilis as a prepropeptide that undergoes posttranslational processing (1). Among the antibiotics synthesized non ribosomally are two family: the lipopeptides including iturin, surfactin, fengycin, plistatin and the small hydrophilic di- and tripeptides. Iturin is a group of cyclic lipopeptides produced by Bacillus subtilis including iturin A, C, D and E (2,3), bacillomycin D, F and L (4), Bacillopeptin (5) and mycosubtlin (6). All contains a.beta.amino fatty acid linked by amide bonds to the constituent amino acid residues of the iturin group. Iturin lipopeptide share a common sequence [.beta.-hydroxy fatty acidAsx-Tyr-Asx] and show variation at the other four positions. Surfactin is also a cyclic lipopeptide containing seven residues of D- and L-amino acids and one residue of a.beta.-hydroxy fatty acid (7) with an amino acid sequence completely different from the iturin group. It is a powerful surfactant and has been described as an antifungal agent. Fengycin (8) and plipastatin (9) are lipopeptide with ten amino acid and a lipid attached to the N-terminal end of the molecule. They differed from iturin and surfactin by the presence of unusual amino acid such as ornithine and allo-threonine. Web site: http://www.delphion.com/details?pn=US06183736__ •

Trapping of aflatoxins and phytoestrogens Inventor(s): Kuan; Shia S. (Metarie, LA), Umrigar; Pesi P. (Kenner, LA) Assignee(s): The United States of America AS Represented by the Secreatry of the (washington, Dc) Patent Number: 5,487,998 Date filed: January 6, 1993 Abstract: Halo, azido, and amino cyclodextrin/epichlorohydrin copolymers, methods of preparing the copolymers, and the use of the copolymers for removing aflatoxins and phytoestrogens from a sample, for detecting the presence of aflatoxins and phytoestrogens, and for quantifying aflatoxin and phytoestrogen levels.

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Excerpt(s): The present invention relates to new derivatives of a cyclodextrin/epichlorohydrin copolymer and the use of such compounds for removing aflatoxins and phytoestrogens from a sample, for detecting the presence of aflatoxins and phytoestrogens, and for quantifying aflatoxin and phytoestrogen levels. It has long been recognized that limiting the exposure of both humans and animals to toxic or carcinogenic substances in food, water, and air is critical to our survival. Of all the toxic or carcinogenic substances that can be encountered in the environment, aflatoxins are especially important, since the presence of even minute quantities of these fungal metabolites constitute a serious health hazard. Aflatoxins are polycyclic aromatic compounds that are found in foods such as grain and peanuts as a consequence of the manner in which the foods were grown, handled, or stored. A variety of aflatoxins, including B.sub.1, B.sub.2, G.sub.1, G.sub.2, M.sub.1, and M.sub.2, have been isolated and characterized. Aflatoxin B.sub.1 is the most biologically potent of these compounds, and, as well as being a potent toxin, is also a mutagen and carcinogen. Since aflatoxins endanger public health, it is a common practice to run regular tests for aflatoxins on samples of certain foodstuffs. Such tests are typically conducted by extracting samples with an appropriate solvent, and then using standard techniques such as high pressure liquid chromatography (HPLC) to detect and quantitate aflatoxins. For example, the use of HPLC for analysis of aflatoxins in peanuts is described in U.S. Pat. No. 4,285,698. Web site: http://www.delphion.com/details?pn=US05487998__ •

Use of native Aspergillus flavus strains to prevent aflatoxin contamination Inventor(s): Cotty; Peter J. (New Orleans, LA) Assignee(s): The United States of America AS Represented by the United States (washington, Dc) Patent Number: 5,171,686 Date filed: November 29, 1989 Abstract: Methods and compositions are provided for the control or prevention of aflatoxin contamination of agricultural commodities. Non-toxigenic strains of Aspergillus flavus are shown to inhibit aflatoxin production by toxigenic strains. Additionally, the non-toxigenic strains produce a factor in culture that alone inhibits aflatoxin production by toxigenic strains. Excerpt(s): This invention relates to a method for the control or prevention of aflatoxin contamination of commodities using non-toxigenic strains of Aspergillus flavus (A. flavus). Aflatoxins are toxic compounds produced by fungi, particularly A. flavus and Aspergillus parasiticus (A. parasiticus), and are potent carcinogens that frequently contaminate agricultural commodities, especially during drought conditions, and are a serious threat to humans and animals [Cast, Counc. Agric. Sci. Technol. Rep., Vol. 80, (1979), Ames, IA., 56 pp]. The United States and most other countries prohibit aflatoxin levels in foods and feeds above 0.02.mu.g/g (20 parts per billion) Schuller, et al., Proceedings of the International Symposium on Mycotoxins, 1983, pp. 111-129, Naguib, et al. (eds.), National Research Centre, Cairo. A. flavus produces aflatoxins B.sub.1 and B.sub.2 and is the primary cause of aflatoxin contamination of corn, cottonseed, and tree nuts [Diener, et al., Annu. Rev. Phytopathol., Vol. 25, (1987), pp. 249-270]. There are several instances where a plant disease problem can be prevented by forms of the organism that incites the problem. Frost injury to plants results from ice formation caused by ice nucleation-active strains of Pseudomonas syringae and Erwinia herbicola; strains of these bacteria that are not ice nucleation active can be used to competitively

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exclude ice nucleation active strains and thereby prevent frost injury (Lindow, S.E., Appl. Environ. Microbiol., Vol. 53, pp. 2520-2527). Several viral diseases of plants are managed by infecting the plants with mild strains of the inciting viruses; through cross protection, plants infected with the mild strains are protected from infection by more severe strains [Yeh, et al., Plant Dis., Vol. 72, (1988), pp. 369-460]. Nonpathogenic strains of Fusarium oxysporum can prevent infection of celery by pathogenic strains through competitive exclusion [Schneider, R. W., Phytopathology, Vol. 74, (1984), pp. 646-653]. Web site: http://www.delphion.com/details?pn=US05171686__

Patent Applications on Aflatoxin As of December 2000, U.S. patent applications are open to public viewing.9 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to aflatoxin: •

Device for the detecting of aflatoxins Inventor(s): Stroka, Jorg; (Duisburg, DE) Correspondence: Nath & Associates, Pllc; Sixth Floor; 1030 15th Street, N.W.; Washington; DC; 20005; US Patent Application Number: 20030025086 Date filed: September 18, 2002 Abstract: A compact and portable analytical instrument dedicated to aflatoxin determination under minimum electrical power conditions employs a light emitting diode (LED) as light source with a peak output wavelength of 370 nm in addition to a 418 nm cut-off filter and a photodiode with a peak sensitivity of 140 nm. Thus, the relative amount of transmitted fluorescence energy at a wavelength of greater than 418 nm incident upon the aflatoxin is separated from the excitation light of 370 nm. In addition to the LED and the photodiode, the instrument preferably comprises amplifying, digital conversion, data storage, data transfer, display and power supply means and a graphical data output. The power supply regulator is a integrated circuit. As a result, current consumption is minimised, and thus battery life and instrument accuracy is maximised. The LED is powered by a constant current regulator, which minimises errors due to fluctuations in illumination intensity. Excerpt(s): The present invention relates to a device for the detection of aflatoxins, especially for the quantification of aflatoxins on a thin layer chromatogram (TLC). Aflatoxin determination is recognised as one of the most crucial parameters in food control, particularly for the detection of aflatoxin B1. Such measurements are today generally carried out by the use of high-pressure liquid chromatography (HPLC). However in those cases where HPLC equipment is not available or appropriate, the determination by thin layer chromatography (TLC) is commonly used. Commercial TLC scanners are available for the purpose of aflatoxin determination after TLC separation of the aflatoxins. These commercially available products TLC scanners use mercury lamps with an emission wave-length of 366 nm as a light source, while the detector consists of photo-multiers. It is clear that due to the high power consumption of these components,

9

This has been a common practice outside the United States prior to December 2000.

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these scanners are unsuitable for use where no constant electrical power is available. Furthermore these TLC scanners are quite unwieldy and therefore not suitable for infield analysis. The object of the present invention is to provide a compact device for the detection of aflatoxins, which is well suited for in-field analysis. In order to overcome the abovementioned problems, the present invention proposes a device for the detection of aflatoxin, comprising a sample holder, an excitation unit and a detection unit, wherein said excitation unit comprises an light emitting diode, said light emitting diode for emitting an excitation radiation having an excitation wavelength in the ultraviolet spectrum, wherein said detection unit comprises a cut-off filter and a photodiode, said cut-off filter having a cut-off wavelength which is higher than said excitation wavelength of said light emitting diode and said photodiode having a sensitivity at a sensing wavelength which is higher than said cut-off wavelength, and wherein said sample holder, said excitation unit and said detection unit are arranged so that said excitation radiation is emitted towards a sample placed in said sample holder and that said cut-off filter and said photodiode are positioned in the direction of emission of a fluorescence radiation emitted from said sample. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Human aflatoxin B1 aldehyde reductase Inventor(s): Bandman, Olga; (Mountain View, CA), Corley, Neil C.; (Mountain View, CA), Guegler, Karl J.; (Menlo Park, CA), Shah, Purvi; (Sunnyvale, CA) Correspondence: Incyte Genomics, INC.; 3160 Porter Drive; Palo Alto; CA; 94304; US Patent Application Number: 20030013853 Date filed: May 16, 2000 Abstract: The invention provides a human aflatoxin B1 aldehyde reductase (AFB1-hAR) and polynucleotides which identify and encode AFB1-hAR. The invention also provides expression vectors, host cells, agonists, antibodies and antagonists. The invention also provides methods for treating disorders associated with expression of AFB1-hAR. Excerpt(s): This application is a divisional application of U.S. application Ser. No. 09/391,959, filed Sep. 8, 1999, which is a divisional application of U.S. application Ser. No. 09/215,087, filed Dec. 18, 1998, now U.S. Pat. No 5,981,244, which is a divisional application of U.S. application Ser. No. 08/907,674, filed Aug. 8, 1997, now U.S. Pat. No 5,919,685. This invention relates to nucleic acid and amino acid sequences of a human aflatoxin B1 aldehyde reductase and to the use of these sequences in the diagnosis, prevention, and treatment of gastrointestinal and neoplastic disorders. Aflatoxin B1 (AFB1) is a potent environmental carcinogen produced by the common molds Aspergillus flavus, A. parasiticus, and A. nominus. Human exposure results principally from the ingestion of stored foodstuffs contaminated with these molds. Carcinogenicity is associated with the conversion of AFB1 to its 8,9-oxide by the hepatic cytochrome P450-dependent monooxygenase system. Ingestion of food contaminated with fungal aflatoxins is believed to contribute to the high incidence of hepatoma and chronic liver disease in subtropical regions. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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•

Radioimmunoassay testing kit for detecting aflatoxin-albumin adduct Inventor(s): Huang, Henton; (Tau Yen, TW), Lee, Te-Wei; (Taipei, TW), Ting, Gann; (Taipei, TW), Wang, Mei-Hui; (Hsin Chu, TW), Wu, Chang-Yi; (Taipei, TW) Correspondence: Rosenberg, Klein & Lee; Suite 105; 3444 Ellicott Center Drive; Ellicott City; MD; 21043; US Patent Application Number: 20020115125 Date filed: January 10, 2002 Abstract: The invention discloses one radioimmunoassay testing kit and method for detecting aflatoxin-albumin adducts. The radioimmunoassay testing kit combining with competitive inhibition radioimmunometric assay, could be used to quantitate the aflatoxin-albumin adducts in serum. The invention also discloses their clinical uses in rapid mass detection of the doses of aflatoxin exposure, which is one of risk factors of liver cancer. Excerpt(s): The present invention relates to a radioimmunoassay testing kit and a method, which is used to quantitate the aflatoxin-albumin adduct. In particular the present invention relates to routine uses in serum. The present invention also relates to a method to determine if there is aflatoxin exposure or not. The normal cutoff value is also discloses. Aflatoxins are toxic metabolites produced by the fungal species Aspergillus flavus and Aspergillus parasiticus. Aflatoxin B1 (AFB 1) is the most toxic group. Experimental normal evidence that aflatoxin is carcinogenic, especially in hepatotoxicity. Using the TD50 values for rats developed by Gold et al (Cancer Res. 1993, 53: 9-11). AFB1, which TD50-9.3.times.10.sup.-4 mg/kg per day, is 1000 times more potent a carcinogen than benzo(a)pyrene. Recently, the International Agency for Research on Cancer (IARC) reported that there is sufficient evidence to classify aflatoxin B1 and mixtures of aflatoxins as Group 1 carcinogens in humans. AFB1 requires microsomal oxidation to the reactive AFB1-8,9-epoxide (AFBO) to exert its hepatocarcinogenic effects, and the extent of covalent binding of AFBO to cellular RNA, DNA, protein or other macromolecules (IARC 1993;56:303). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

Keeping Current In order to stay informed about patents and patent applications dealing with aflatoxin, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “aflatoxin” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on aflatoxin. You can also use this procedure to view pending patent applications concerning aflatoxin. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.

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CHAPTER 6. BOOKS ON AFLATOXIN Overview This chapter provides bibliographic book references relating to aflatoxin. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on aflatoxin include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.

Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “aflatoxin” at online booksellers’ Web sites, you may discover non-medical books that use the generic term “aflatoxin” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “aflatoxin” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com): •

Aflatoxin in Maize: A Proceedings of the Workshop El Batan Mexico, April 7-11, 1986; ISBN: 9686127127; http://www.amazon.com/exec/obidos/ASIN/9686127127/icongroupinterna

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Aflatoxins & Human Health by Ivana Dvorackova (Editor), et al; ISBN: 0849346282; http://www.amazon.com/exec/obidos/ASIN/0849346282/icongroupinterna

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Aflatoxins in Nuts, Nut Products, Dried Figs and Fried Fig Products Regulations (Northern Ireland) 1993: Food (Statutory Rule: 1993: 31); ISBN: 0337905312; http://www.amazon.com/exec/obidos/ASIN/0337905312/icongroupinterna

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Destruction of Aflatoxins IARC 37 by M. Castegnaro (Editor); ISBN: 0197230377; http://www.amazon.com/exec/obidos/ASIN/0197230377/icongroupinterna

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Elimination of Aflatoxin Contamination in Peanut (ACIAR Proceedings) by Ralf G. Dietzgen; ISBN: 1863202706; http://www.amazon.com/exec/obidos/ASIN/1863202706/icongroupinterna

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Food safety and quality existing detection and control programs minimize aflatoxin : report to the Chairman, Subcommittee on Wheat, Soybeans, and Feed Grains, Committee on Agriculture, House of Representatives (SuDoc GA 1.13:RCED-91-109) by U.S. General Accounting Office; ISBN: B000107P5M; http://www.amazon.com/exec/obidos/ASIN/B000107P5M/icongroupinterna

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Human Exposure to Aflatoxins; ISBN: 0631184031; http://www.amazon.com/exec/obidos/ASIN/0631184031/icongroupinterna

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Identification of selected trichothecenes, aflatoxins, and related mycotoxins; ISBN: 9514694651; http://www.amazon.com/exec/obidos/ASIN/9514694651/icongroupinterna

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Laboratory decontamination and destruction of aflatoxins B1, B2, G1, G2 in laboratory wastes; ISBN: 9283211375; http://www.amazon.com/exec/obidos/ASIN/9283211375/icongroupinterna

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Metabolism of Aflatoxins and Other Mycotoxins by O. Bassir; ISBN: 9781211970; http://www.amazon.com/exec/obidos/ASIN/9781211970/icongroupinterna

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Mycotoxins in Grain: Compounds Other Than Aflatoxin by J. David Miller (Editor), et al; ISBN: 0962440752; http://www.amazon.com/exec/obidos/ASIN/0962440752/icongroupinterna

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Review the Impact of Aflatoxin in Southeastern Peanuts: Hearing Before the Committee on Agriculture, U.S. House of Representatives by Thomas W. Ewing (Editor); ISBN: 0788179365; http://www.amazon.com/exec/obidos/ASIN/0788179365/icongroupinterna

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Sampling Plans for Aflatoxin Analysis in Peanuts and Corn: Report of an FAO Technical Consultation Rome, 3-6 May 1993 (FAO Food and Nutrition Paper); ISBN: 9251033951; http://www.amazon.com/exec/obidos/ASIN/9251033951/icongroupinterna

•

The Aflatoxins: Chemical and Biological Aspects by John Godfrey Heathcote; ISBN: 0444416862; http://www.amazon.com/exec/obidos/ASIN/0444416862/icongroupinterna

•

Toxicology of Aflatoxins: Human Health, Veterinary, and Agricultural Significance by David Eaton (Author), John Groopman (Author); ISBN: 0122282558; http://www.amazon.com/exec/obidos/ASIN/0122282558/icongroupinterna

Chapters on Aflatoxin In order to find chapters that specifically relate to aflatoxin, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and aflatoxin using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “aflatoxin” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on aflatoxin:

Books

•

155

Hepatocellular Carcinoma Source: in Textbook of Gastroenterology. 4th ed. [2-volume set]. Hagerstown, MD: Lippincott Williams and Wilkins. 2003. p. 2491-2512. Contact: Available from Lippincott Williams and Wilkins. P.O. Box 1600, Hagerstown, MD 21741. (800) 638-6423. Fax: (301) 223-2400. Website: www.lww.com. PRICE: $289.00. ISBN: 781728614. Summary: Hepatocellular carcinoma (HCC, liver cancer) is the fifth most common cancer and the third most frequent cause of cancer death worldwide, with an estimated 560,000 new cases per year. There are strong etiologic (causative) associations with chronic hepatitis B virus, chronic hepatitis C virus, alcoholic cirrhosis, other causes of chronic liver disease, and dietary aflatoxin exposure. This chapter on HCC is from a comprehensive gastroenterology textbook that provides an encyclopedic discussion of virtually all the disease states encountered in a gastroenterology practice. In this chapter, the authors cover epidemiology, etiology and risk factors, pathogenesis, surveillance, differential diagnosis, diagnosis, staging, locoregional therapies, and systemic therapy. The authors conclude that the selection of an appropriate treatment strategy for patients with HCC depends on careful tumor staging and assessment of the underlying liver disease. All patients with localized HCC should be evaluated for the potentially curative therapy options of partial hepatectomy or liver transplantation. Given the lack of efficacy data, there are no proven systemic chemotherapy regimens, immunotherapy approaches, or hormonal therapies that can be recommended at this time. The chapter is illustrated with black-and-white graphs and drawings. 9 figures. 4 tables. 165 references.

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APPENDICES

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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.

NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute10: •

Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm

•

National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/

•

National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html

•

National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25

•

National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm

•

National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm

•

National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375

•

National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/

10

These publications are typically written by one or more of the various NIH Institutes.

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National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm

•

National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/

•

National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm

•

National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm

•

National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/

•

National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/

•

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm

•

National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html

•

National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm

•

National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm

•

National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm

•

National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html

•

National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm

•

Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp

•

National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/

•

National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp

•

Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html

•

Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm

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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.11 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:12 •

Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html

•

HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html

•

NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html

•

Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/

•

Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html

•

Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html

•

Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/

•

Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html

•

Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html

•

Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html

•

MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html

11 Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 12 See http://www.nlm.nih.gov/databases/databases.html.

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Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html

•

Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html

The NLM Gateway13 The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.14 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “aflatoxin” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category. Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total

Items Found 16074 57 20 0 66 16217

HSTAT15 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.16 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.17 Simply search by “aflatoxin” (or synonyms) at the following Web site: http://text.nlm.nih.gov.

13

Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.

14

The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 15 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 16 17

The HSTAT URL is http://hstat.nlm.nih.gov/.

Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations.

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Coffee Break: Tutorials for Biologists18 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.19 Each report is about 400 words and is usually based on a discovery reported in one or more articles from recently published, peer-reviewed literature.20 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.

Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •

CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.

•

Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.

18 Adapted 19

from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html.

The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story. 20 After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process.

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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on aflatoxin can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internet-based services that post them.

Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to aflatoxin. Due to space limitations, these sources are listed in a concise manner. Do not hesitate to consult the following sources by either using the Internet hyperlink provided, or, in cases where the contact information is provided, contacting the publisher or author directly. The National Institutes of Health The NIH gateway to patients is located at http://health.nih.gov/. From this site, you can search across various sources and institutes, a number of which are summarized below. Topic Pages: MEDLINEplus The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are “health topic pages” which list links to available materials relevant to aflatoxin. To access this system, log on to http://www.nlm.nih.gov/medlineplus/healthtopics.html. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus listed the following when searched for “aflatoxin”:

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Fungal Infections http://www.nlm.nih.gov/medlineplus/fungalinfections.html Liver Cancer http://www.nlm.nih.gov/medlineplus/livercancer.html Molds http://www.nlm.nih.gov/medlineplus/molds.html You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. The NIH Search Utility The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to aflatoxin. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •


•

Family Village: http://www.familyvillage.wisc.edu/specific.htm

•

Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/

•

Med Help International: http://www.medhelp.org/HealthTopics/A.html

•

Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/

•

Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/

•

WebMDHealth: http://my.webmd.com/health_topics

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Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to aflatoxin. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with aflatoxin. The National Health Information Center (NHIC) The National Health Information Center (NHIC) offers a free referral service to help people find organizations that provide information about aflatoxin. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797. Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “aflatoxin” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “aflatoxin”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “aflatoxin” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months.

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The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “aflatoxin” (or a synonym) into the search box, and click “Submit Query.”

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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.

Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.21

Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.

Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of

21

Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.

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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)22: •

Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/

•

Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)

•

Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm

•

California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html

•

California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html

•

California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html

•

California: Gateway Health Library (Sutter Gould Medical Foundation)

•

California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/

•

California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp

•

California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html

•

California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/

•

California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/

•

California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/

•

California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html

•

California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/

•

Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/

•

Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/

•

Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/

22

Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.

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•

Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml

•

Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm

•

Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html

•

Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm

•

Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp

•

Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/

•

Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm

•

Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html

•

Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/

•

Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm

•

Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/

•

Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/

•

Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/

•

Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm

•

Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html

•

Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm

•

Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/

•

Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/

•

Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10

•

Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/

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Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html

•

Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp

•

Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp

•

Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/

•

Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html

•

Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm

•

Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp

•

Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/

•

Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html

•

Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/

•

Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm

•

Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/

•

Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html

•

Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm

•

Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330

•

Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)

•

National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html

•

National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/

•

National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/

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Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm

•

New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/

•

New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm

•

New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm

•

New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/

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New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html

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New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/

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New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html

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New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/

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Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm

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Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp

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Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/

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Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/

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Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml

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Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html

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Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html

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Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml

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Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp

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Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm

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Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/

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South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp

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Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/

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Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/

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Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72

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ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •

ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html

•

MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp

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Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/

•

Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html

•

On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/

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Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp

•

Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm

Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a). The NIH suggests the following Web sites in the ADAM Medical Encyclopedia when searching for information on aflatoxin: •

Basic Guidelines for Aflatoxin Aflatoxin Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002429.htm

•

Background Topics for Aflatoxin Toxins Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002331.htm

Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •

Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical

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•

MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html

•

Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/

•

Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine

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AFLATOXIN DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Absolute risk: The observed or calculated probability of an event in a population under study, as contrasted with the relative risk. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Acetaldehyde: A colorless, flammable liquid used in the manufacture of acetic acid, perfumes, and flavors. It is also an intermediate in the metabolism of alcohol. It has a general narcotic action and also causes irritation of mucous membranes. Large doses may cause death from respiratory paralysis. [NIH] Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak antiinflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage. [NIH] Acetone: A colorless liquid used as a solvent and an antiseptic. It is one of the ketone bodies produced during ketoacidosis. [NIH] Acne: A disorder of the skin marked by inflammation of oil glands and hair glands. [NIH] Acyl: Chemical signal used by bacteria to communicate. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adduct: Complex formed when a carcinogen combines with DNA or a protein. [NIH] Adduction: The rotation of an eye toward the midline (nasally). [NIH] Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH] Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH]

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Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Affinity Chromatography: In affinity chromatography, a ligand attached to a column binds specifically to the molecule to be purified. [NIH] Aflatoxin B1: A potent hepatotoxic and hepatocarcinogenic mycotoxin produced by the Aspergillus flavus group of fungi. It is also mutagenic, teratogenic, and causes immunosuppression in animals. It is found as a contaminant in peanuts, cottonseed meal, corn, and other grains. The mycotoxin requires epoxidation to aflatoxin B1 2,3-oxide for activation. Microsomal monooxygenases biotransform the toxin to the less toxic metabolites aflatoxin M1 and Q1. [NIH] Aflatoxins: A group of closely related toxic metabolites that are designated mycotoxins. They are produced by Aspergillus flavus and A. parasiticus. Members of the group include aflatoxin B1, aflatoxin B2, aflatoxin G1, aflatoxin G2, aflatoxin M1, and aflatoxin M2. [NIH] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]

Age-Adjusted: Summary measures of rates of morbidity or mortality in a population using statistical procedures to remove the effect of age differences in populations that are being compared. Age is probably the most important and the most common variable in determining the risk of morbidity and mortality. [NIH] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Alcohol Dehydrogenase: An enzyme that catalyzes reversibly the final step of alcoholic fermentation by reducing an aldehyde to an alcohol. In the case of ethanol, acetaldehyde is reduced to ethanol in the presence of NADH and hydrogen. The enzyme is a zinc protein which acts on primary and secondary alcohols or hemiacetals. EC 1.1.1.1. [NIH]

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Aldehyde Reductase: An enzyme that catalyzes reversibly the oxidation of an aldose to an alditol. It possesses broad specificity for many aldoses. EC 1.1.1.21. [NIH] Aldehydes: Organic compounds containing a carbonyl group in the form -CHO. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] Alkaline: Having the reactions of an alkali. [EU] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alkylating Agents: Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases. [NIH]

Alkylation: The covalent bonding of an alkyl group to an organic compound. It can occur by a simple addition reaction or by substitution of another functional group. [NIH] Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allo: A female hormone. [NIH] Allylamine: Possesses an unusual and selective cytotoxicity for vascular smooth muscle cells in dogs and rats. Useful for experiments dealing with arterial injury, myocardial fibrosis or cardiac decompensation. [NIH] Alpha Particles: Positively charged particles composed of two protons and two neutrons, i.e., helium nuclei, emitted during disintegration of very heavy isotopes; a beam of alpha particles or an alpha ray has very strong ionizing power, but weak penetrability. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH] Amino Acids: Organic compounds that generally contain an amino (-NH2) and a carboxyl (COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins. [NIH]

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Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Amphetamines: Analogs or derivatives of amphetamine. Many are sympathomimetics and central nervous system stimulators causing excitation, vasopression, bronchodilation, and to varying degrees, anorexia, analepsis, nasal decongestion, and some smooth muscle relaxation. [NIH] Amplification: The production of additional copies of a chromosomal DNA sequence, found as either intrachromosomal or extrachromosomal DNA. [NIH] Anabolic: Relating to, characterized by, or promoting anabolism. [EU] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH] Analgesic: An agent that alleviates pain without causing loss of consciousness. [EU] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Anginal: Pertaining to or characteristic of angina. [EU] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Anomalies: Birth defects; abnormalities. [NIH] Anthraquinones: An anthracene ring which contains two ketone moieties in any position. Can be substituted in any position except on the ketone groups. [NIH] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]

Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Antibody Affinity: A measure of the binding strength between antibody and a simple hapten or antigen determinant. It depends on the closeness of stereochemical fit between

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antibody combining sites and antigen determinants, on the size of the area of contact between them, and on the distribution of charged and hydrophobic groups. It includes the concept of "avidity," which refers to the strength of the antigen-antibody bond after formation of reversible complexes. [NIH] Anticarcinogenic: Pertaining to something that prevents or delays the development of cancer. [NIH] Antidepressant: A drug used to treat depression. [NIH] Antifungal: Destructive to fungi, or suppressing their reproduction or growth; effective against fungal infections. [EU] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Anti-infective: An agent that so acts. [EU] Anti-Infective Agents: Substances that prevent infectious agents or organisms from spreading or kill infectious agents in order to prevent the spread of infection. [NIH] Anti-inflammatory: Having to do with reducing inflammation. [NIH] Antimicrobial: Killing microorganisms, or suppressing their multiplication or growth. [EU] Antimycotic: Suppressing the growth of fungi. [EU] Antineoplastic: Inhibiting or preventing the development of neoplasms, checking the maturation and proliferation of malignant cells. [EU] Antineoplastic Agents: Substances that inhibit or prevent the proliferation of neoplasms. [NIH]

Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antipyretic: An agent that relieves or reduces fever. Called also antifebrile, antithermic and febrifuge. [EU] Antiseptic: A substance that inhibits the growth and development of microorganisms without necessarily killing them. [EU] Antiserum: The blood serum obtained from an animal after it has been immunized with a particular antigen. It will contain antibodies which are specific for that antigen as well as antibodies specific for any other antigen with which the animal has previously been immunized. [NIH] Antiviral: Destroying viruses or suppressing their replication. [EU] Anus: The opening of the rectum to the outside of the body. [NIH] Apoptosis: One of the two mechanisms by which cell pathological process of necrosis). Apoptosis is the physiological deletion of cells and appears to be characterized by distinctive morphologic changes in the

death occurs (the other being the mechanism responsible for the intrinsically programmed. It is nucleus and cytoplasm, chromatin

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cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. [NIH] Approximate: Approximal [EU] Aqueous: Having to do with water. [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arginine: An essential amino acid that is physiologically active in the L-form. [NIH] Arterial: Pertaining to an artery or to the arteries. [EU] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant. [NIH] Aspergillosis: Infections with fungi of the genus Aspergillus. [NIH] Aspergillus: A genus of mitosporic fungi containing about 100 species and eleven different teleomorphs in the family Trichocomaceae. [NIH] Aspergillus flavus: A species of imperfect fungi which grows on peanuts and other plants and produces the carcinogenic substance aflatoxin. It is also used in the production of the antibiotic flavicin. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astringents: Agents, usually topical, that cause the contraction of tissues for the control of bleeding or secretions. [NIH] Asymptomatic: Having no signs or symptoms of disease. [NIH] Atmospheric Pressure: The pressure at any point in an atmosphere due solely to the weight of the atmospheric gases above the point concerned. [NIH] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Attenuation: Reduction of transmitted sound energy or its electrical equivalent. [NIH] Avian: A plasmodial infection in birds. [NIH] Avidity: The strength of the interaction of an antiserum with a multivalent antigen. [NIH] Baclofen: A GABA derivative that is a specific agonist at GABA-B receptors. It is used in the treatment of spasticity, especially that due to spinal cord damage. Its therapeutic effects result from actions at spinal and supraspinal sites, generally the reduction of excitatory transmission. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or

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bacillary, and spiral or spirochetal. [NIH] Bacterial Physiology: Physiological processes and activities of bacteria. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Base Sequence: The sequence of purines and pyrimidines in nucleic acids and polynucleotides. It is also called nucleotide or nucleoside sequence. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]

Benzo(a)pyrene: A potent mutagen and carcinogen. It is a public health concern because of its possible effects on industrial workers, as an environmental pollutant, an as a component of tobacco smoke. [NIH] Benzoic Acid: A fungistatic compound that is widely used as a food preservative. It is conjugated to glycine in the liver and excreted as hippuric acid. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bilirubin: A bile pigment that is a degradation product of heme. [NIH] Binding agent: A substance that makes a loose mixture stick together. For example, binding agents can be used to make solid pills from loose powders. [NIH] Bioassay: Determination of the relative effective strength of a substance (as a vitamin, hormone, or drug) by comparing its effect on a test organism with that of a standard preparation. [NIH] Bioavailability: The degree to which a drug or other substance becomes available to the target tissue after administration. [EU] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biogenesis: The origin of life. It includes studies of the potential basis for life in organic compounds but excludes studies of the development of altered forms of life through mutation and natural selection, which is evolution. [NIH] Biological response modifier: BRM. A substance that stimulates the body's response to infection and disease. [NIH] Bioluminescence: The emission of light by living organisms such as the firefly, certain mollusks, beetles, fish, bacteria, fungi and protozoa. [NIH] Biomarkers: Substances sometimes found in an increased amount in the blood, other body fluids, or tissues and that may suggest the presence of some types of cancer. Biomarkers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and GI tract cancers), and PSA (prostate cancer). Also called tumor markers. [NIH] Biosynthesis: The building up of a chemical compound in the physiologic processes of a living organism. [EU] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived

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constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Biotin: Hexahydro-2-oxo-1H-thieno(3,4-d)imidazole-4-pentanoic acid. Growth factor present in minute amounts in every living cell. It occurs mainly bound to proteins or polypeptides and is abundant in liver, kidney, pancreas, yeast, and milk.The biotin content of cancerous tissue is higher than that of normal tissue. [NIH] Biotransformation: The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alteration may be either nonsynthetic (oxidation-reduction, hydrolysis) or synthetic (glucuronide formation, sulfate conjugation, acetylation, methylation). This also includes metabolic detoxication and clearance. [NIH] Bladder: The organ that stores urine. [NIH] Blastocyst: The mammalian embryo in the post-morula stage in which a fluid-filled cavity, enclosed primarily by trophoblast, contains an inner cell mass which becomes the embryonic disc. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blot: To transfer DNA, RNA, or proteins to an immobilizing matrix such as nitrocellulose. [NIH]

Body Fluids: Liquid components of living organisms. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Bone Marrow Cells: Cells contained in the bone marrow including fat cells, stromal cells, megakaryocytes, and the immediate precursors of most blood cells. [NIH] Boron: A trace element with the atomic symbol B, atomic number 5, and atomic weight 10.81. Boron-10, an isotope of boron, is used as a neutron absorber in boron neutron capture therapy. [NIH] Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Brachytherapy: A collective term for interstitial, intracavity, and surface radiotherapy. It uses small sealed or partly-sealed sources that may be placed on or near the body surface or within a natural body cavity or implanted directly into the tissues. [NIH]

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Bronchi: The larger air passages of the lungs arising from the terminal bifurcation of the trachea. [NIH] Bronchial: Pertaining to one or more bronchi. [EU] Buccal: Pertaining to or directed toward the cheek. In dental anatomy, used to refer to the buccal surface of a tooth. [EU] Butylated Hydroxyanisole: Mixture of 2- and 3-tert-butyl-4-methoxyphenols that is used as an antioxidant in foods, cosmetics, and pharmaceuticals. [NIH] Cadmium: An element with atomic symbol Cd, atomic number 48, and atomic weight 114. It is a metal and ingestion will lead to cadmium poisoning. [NIH] Cadmium Poisoning: Poisoning occurring after exposure to cadmium compounds or fumes. It may cause gastrointestinal syndromes, anemia, or pneumonitis. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calcium Hydroxide: Ca(OH)2. A white powder that has many therapeutic uses. Because of its ability to stimulate mineralization, it is found in many dental formulations. [NIH] Callus: A callosity or hard, thick skin; the bone-like reparative substance that is formed round the edges and fragments of broken bone. [NIH] Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capillary Fragility: The lack of resistance, or susceptibility, of capillaries to damage or disruption under conditions of increased stress. [NIH] Capsaicin: Cytotoxic alkaloid from various species of Capsicum (pepper, paprika), of the Solanaceae. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, polyand heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carcinogen: Any substance that causes cancer. [NIH] Carcinogenesis: The process by which normal cells are transformed into cancer cells. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinogenicity: The ability to cause cancer. [NIH] Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]

Cardiac: Having to do with the heart. [NIH] Cardiopulmonary: Having to do with the heart and lungs. [NIH] Carotenoids: Substance found in yellow and orange fruits and vegetables and in dark green,

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leafy vegetables. May reduce the risk of developing cancer. [NIH] Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Case series: A group or series of case reports involving patients who were given similar treatment. Reports of case series usually contain detailed information about the individual patients. This includes demographic information (for example, age, gender, ethnic origin) and information on diagnosis, treatment, response to treatment, and follow-up after treatment. [NIH] Catechin: Extracted from Uncaria gambier, Acacia catechu and other plants; it stabilizes collagen and is therefore used in tanning and dyeing; it prevents capillary fragility and abnormal permeability, but was formerly used as an antidiarrheal. [NIH] Cathode: An electrode, usually an incandescent filament of tungsten, which emits electrons in an X-ray tube. [NIH] Cations: Postively charged atoms, radicals or groups of atoms which travel to the cathode or negative pole during electrolysis. [NIH] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Cycle: The complex series of phenomena, occurring between the end of one cell division and the end of the next, by which cellular material is divided between daughter cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Division: The fission of a cell. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Centrifugation: A method of separating organelles or large molecules that relies upon differential sedimentation through a preformed density gradient under the influence of a gravitational field generated in a centrifuge. [NIH] Chemical Warfare: Tactical warfare using incendiary mixtures, smokes, or irritant, burning, or asphyxiating gases. [NIH] Chemical Warfare Agents: Chemicals that are used to cause the disturbance, disease, or death of humans during war. [NIH] Chemoprevention: The use of drugs, vitamins, or other agents to try to reduce the risk of, or

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delay the development or recurrence of, cancer. [NIH] Chemopreventive: Natural or synthetic compound used to intervene in the early precancerous stages of carcinogenesis. [NIH] Chemoprotective: A quality of some drugs used in cancer treatment. Chemoprotective agents protect healthy tissue from the toxic effects of anticancer drugs. [NIH] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chemotherapy: Treatment with anticancer drugs. [NIH] Chloroform: A commonly used laboratory solvent. It was previously used as an anesthetic, but was banned from use in the U.S. due to its suspected carcinogenecity. [NIH] Chlorophyll: Porphyrin derivatives containing magnesium that act to convert light energy in photosynthetic organisms. [NIH] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Cirrhosis: A type of chronic, progressive liver disease. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]

Clinical study: A research study in which patients receive treatment in a clinic or other medical facility. Reports of clinical studies can contain results for single patients (case reports) or many patients (case series or clinical trials). [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH] Coca: Any of several South American shrubs of the Erythroxylon genus (and family) that yield cocaine; the leaves are chewed with alum for CNS stimulation. [NIH] Cocaine: An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake. [NIH] Codon: A set of three nucleotides in a protein coding sequence that specifies individual

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amino acids or a termination signal (codon, terminator). Most codons are universal, but some organisms do not produce the transfer RNAs (RNA, transfer) complementary to all codons. These codons are referred to as unassigned codons (codons, nonsense). [NIH] Coenzyme: An organic nonprotein molecule, frequently a phosphorylated derivative of a water-soluble vitamin, that binds with the protein molecule (apoenzyme) to form the active enzyme (holoenzyme). [EU] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Colloidal: Of the nature of a colloid. [EU] Colon: The long, coiled, tubelike organ that removes water from digested food. The remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [NIH] Colorectal: Having to do with the colon or the rectum. [NIH] Colorectal Cancer: Cancer that occurs in the colon (large intestine) or the rectum (the end of the large intestine). A number of digestive diseases may increase a person's risk of colorectal cancer, including polyposis and Zollinger-Ellison Syndrome. [NIH] Comet Assay: A genotoxicological technique for measuring DNA damage in an individual cell using single-cell gel electrophoresis. Cell DNA fragments assume a "comet with tail" formation on electrophoresis and are detected with an image analysis system. Alkaline assay conditions facilitate sensitive detection of single-strand damage. [NIH] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix 'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU]

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Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementation: The production of a wild-type phenotype when two different mutations are combined in a diploid or a heterokaryon and tested in trans-configuration. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Conjugated: Acting or operating as if joined; simultaneous. [EU] Conjugation: 1. The act of joining together or the state of being conjugated. 2. A sexual process seen in bacteria, ciliate protozoa, and certain fungi in which nuclear material is exchanged during the temporary fusion of two cells (conjugants). In bacterial genetics a form of sexual reproduction in which a donor bacterium (male) contributes some, or all, of its DNA (in the form of a replicated set) to a recipient (female) which then incorporates differing genetic information into its own chromosome by recombination and passes the recombined set on to its progeny by replication. In ciliate protozoa, two conjugants of separate mating types exchange micronuclear material and then separate, each now being a fertilized cell. In certain fungi, the process involves fusion of two gametes, resulting in union of their nuclei and formation of a zygote. 3. In chemistry, the joining together of two compounds to produce another compound, such as the combination of a toxic product with some substance in the body to form a detoxified product, which is then eliminated. [EU] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Contamination: The soiling or pollution by inferior material, as by the introduction of organisms into a wound, or sewage into a stream. [EU] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Cortisol: A steroid hormone secreted by the adrenal cortex as part of the body's response to stress. [NIH] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH] Cost-benefit: A quantitative technique of economic analysis which, when applied to radiation practice, compares the health detriment from the radiation doses concerned with the cost of radiation dose reduction in that practice. [NIH] Coumarin: A fluorescent dye. [NIH]

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Cowpox: A mild, eruptive skin disease of milk cows caused by cowpox virus, with lesions occurring principally on the udder and teats. Human infection may occur while milking an infected animal. [NIH] Cowpox Virus: A species of orthopoxvirus that is the etiologic agent of cowpox. It is closely related to but antigenically different from vaccina virus. [NIH] Crossing-over: The exchange of corresponding segments between chromatids of homologous chromosomes during meiosia, forming a chiasma. [NIH] Cryopreservation: Preservation of cells, tissues, organs, or embryos by freezing. In histological preparations, cryopreservation or cryofixation is used to maintain the existing form, structure, and chemical composition of all the constituent elements of the specimens. [NIH]

Culture Media: Any liquid or solid preparation made specifically for the growth, storage, or transport of microorganisms or other types of cells. The variety of media that exist allow for the culturing of specific microorganisms and cell types, such as differential media, selective media, test media, and defined media. Solid media consist of liquid media that have been solidified with an agent such as agar or gelatin. [NIH] Cultured cells: Animal or human cells that are grown in the laboratory. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Curcumin: A dye obtained from tumeric, the powdered root of Curcuma longa Linn. It is used in the preparation of curcuma paper and the detection of boron. Curcumin appears to possess a spectrum of pharmacological properties, due primarily to its inhibitory effects on metabolic enzymes. [NIH] Cutaneous: Having to do with the skin. [NIH] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cysteine: A thiol-containing non-essential amino acid that is oxidized to form cystine. [NIH] Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, . New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytosine: A pyrimidine base that is a fundamental unit of nucleic acids. [NIH] Cytotoxicity: Quality of being capable of producing a specific toxic action upon cells of special organs. [NIH] Dairy Products: Raw and processed or manufactured milk and milk-derived products. These are usually from cows (bovine) but are also from goats, sheep, reindeer, and water

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buffalo. [NIH] Data Collection: Systematic gathering of data for a particular purpose from various sources, including questionnaires, interviews, observation, existing records, and electronic devices. The process is usually preliminary to statistical analysis of the data. [NIH] Deamination: The removal of an amino group (NH2) from a chemical compound. [NIH] Death Certificates: Official records of individual deaths including the cause of death certified by a physician, and any other required identifying information. [NIH] Decidua: The epithelial lining of the endometrium that is formed before the fertilized ovum reaches the uterus. The fertilized ovum embeds in the decidua. If the ovum is not fertilized, the decidua is shed during menstruation. [NIH] Decontamination: The removal of contaminating material, such as radioactive materials, biological materials, or chemical warfare agents, from a person or object. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Deoxyguanosine: A nucleoside consisting of the base guanine and the sugar deoxyribose. [NIH]

Deoxyribonucleic: A polymer of subunits called deoxyribonucleotides which is the primary genetic material of a cell, the material equivalent to genetic information. [NIH] Deoxyribonucleic acid: A polymer of subunits called deoxyribonucleotides which is the primary genetic material of a cell, the material equivalent to genetic information. [NIH] Deoxyribonucleotides: A purine or pyrimidine base bonded to a deoxyribose containing a bond to a phosphate group. [NIH] Dermatitis: Any inflammation of the skin. [NIH] Detoxification: Treatment designed to free an addict from his drug habit. [EU] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Developed Countries: Countries that have reached a level of economic achievement through an increase of production, per capita income and consumption, and utilization of natural and human resources. [NIH] Developing Countries: Countries in the process of change directed toward economic growth, that is, an increase in production, per capita consumption, and income. The process of economic growth involves better utilization of natural and human resources, which results in a change in the social, political, and economic structures. [NIH] Dexamethasone: (11 beta,16 alpha)-9-Fluoro-11,17,21-trihydroxy-16-methylpregna-1,4diene-3,20-dione. An anti-inflammatory glucocorticoid used either in the free alcohol or esterified form in treatment of conditions that respond generally to cortisone. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Diarrhoea: Abnormal frequency and liquidity of faecal discharges. [EU] Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel

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movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Dihydrotestosterone: Anabolic agent. [NIH] Dihydroxy: AMPA/Kainate antagonist. [NIH] Dimethyl: A volatile metabolite of the amino acid methionine. [NIH] Dimethyl Sulfoxide: A highly polar organic liquid, that is used widely as a chemical solvent. Because of its ability to penetrate biological membranes, it is used as a vehicle for topical application of pharmaceuticals. It is also used to protect tissue during cryopreservation. Dimethyl sulfoxide shows a range of pharmacological activity including analgesia and anti-inflammation. [NIH] Dimethylnitrosamine: A nitrosamine derivative with alkylating, carcinogenic, and mutagenic properties. It causes serious liver damage and is a hepatocarcinogen in rodents. [NIH]

Diploid: Having two sets of chromosomes. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Discrete: Made up of separate parts or characterized by lesions which do not become blended; not running together; separate. [NIH] Disease Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis. [NIH] Disease Vectors: Invertebrates or non-human vertebrates which transmit infective organisms from one host to another. [NIH] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Dissection: Cutting up of an organism for study. [NIH] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU] Dissociative Disorders: Sudden temporary alterations in the normally integrative functions of consciousness. [NIH] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Dosimetry: All the methods either of measuring directly, or of measuring indirectly and computing, absorbed dose, absorbed dose rate, exposure, exposure rate, dose equivalent, and the science associated with these methods. [NIH]

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Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug. [NIH] Drug Resistance: Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from drug tolerance which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Duodenum: The first part of the small intestine. [NIH] Eczema: A pruritic papulovesicular dermatitis occurring as a reaction to many endogenous and exogenous agents (Dorland, 27th ed). [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Elastic: Susceptible of resisting and recovering from stretching, compression or distortion applied by a force. [EU] Electrolysis: Destruction by passage of a galvanic electric current, as in disintegration of a chemical compound in solution. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electrons: Stable elementary particles having the smallest known negative charge, present in all elements; also called negatrons. Positively charged electrons are called positrons. The numbers, energies and arrangement of electrons around atomic nuclei determine the chemical identities of elements. Beams of electrons are called cathode rays or beta rays, the latter being a high-energy biproduct of nuclear decay. [NIH] Electrophoresis: An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current. [NIH]

Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Embryogenesis: The process of embryo or embryoid formation, whether by sexual (zygotic) or asexual means. In asexual embryogenesis embryoids arise directly from the explant or on intermediary callus tissue. In some cases they arise from individual cells (somatic cell embryoge). [NIH] Emesis: Vomiting; an act of vomiting. Also used as a word termination, as in haematemesis. [EU]

Emulsions: Colloids of two immiscible liquids where either phase may be either fatty or aqueous; lipid-in-water emulsions are usually liquid, like milk or lotion and water-in-lipid emulsions tend to be creams. [NIH] Endemic: Present or usually prevalent in a population or geographical area at all times; said of a disease or agent. Called also endemial. [EU] Endocrine Glands: Ductless glands that secrete substances which are released directly into

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the circulation and which influence metabolism and other body functions. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endotoxic: Of, relating to, or acting as an endotoxin (= a heat-stable toxin, associated with the outer membranes of certain gram-negative bacteria. Endotoxins are not secreted and are released only when the cells are disrupted). [EU] Endotoxin: Toxin from cell walls of bacteria. [NIH] Enhancer: Transcriptional element in the virus genome. [NIH] Enterocytes: Terminally differentiated cells comprising the majority of the external surface of the intestinal epithelium (see intestinal mucosa). Unlike goblet cells, they do not produce or secrete mucins, nor do they secrete cryptdins as do the paneth cells. [NIH] Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]

Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed. [NIH] Epichlorohydrin: A chlorinated epoxy compound used as an industrial solvent. It is a strong skin irritant and carcinogen. [NIH] Epidemiological: Relating to, or involving epidemiology. [EU] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelial Cells: Cells that line the inner and outer surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Epitope: A molecule or portion of a molecule capable of binding to the combining site of an antibody. For every given antigenic determinant, the body can construct a variety of antibody-combining sites, some of which fit almost perfectly, and others which barely fit. [NIH]

Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]

Estrogen: One of the two female sex hormones. [NIH] Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH]

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Ether: One of a class of organic compounds in which any two organic radicals are attached directly to a single oxygen atom. [NIH] Ethoxyquin: Antioxidant; also a post-harvest dip to prevent scald on apples and pears. [NIH] Ethylene Dibromide: An effective soil fumigant, insecticide, and nematocide. In humans, it causes severe burning of skin and irritation of the eyes and respiratory tract. Prolonged inhalation may cause liver necrosis. It is also used in gasoline. Members of this group have caused liver and lung cancers in rodents. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), 1,2-dibromoethane may reasonably be anticipated to be a carcinogen. [NIH] Eukaryotic Cells: Cells of the higher organisms, containing a true nucleus bounded by a nuclear membrane. [NIH] Excipients: Usually inert substances added to a prescription in order to provide suitable consistency to the dosage form; a binder, matrix, base or diluent in pills, tablets, creams, salves, etc. [NIH] Excisional: The surgical procedure of removing a tumor by cutting it out. The biopsy is then examined under a microscope. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Excitatory: When cortical neurons are excited, their output increases and each new input they receive while they are still excited raises their output markedly. [NIH] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Exon: The part of the DNA that encodes the information for the actual amino acid sequence of the protein. In many eucaryotic genes, the coding sequences consist of a series of exons alternating with intron sequences. [NIH] External-beam radiation: Radiation therapy that uses a machine to aim high-energy rays at the cancer. Also called external radiation. [NIH] Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extraction: The process or act of pulling or drawing out. [EU] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fasciculation: A small local contraction of muscles, visible through the skin, representing a spontaneous discharge of a number of fibres innervated by a single motor nerve filament. [EU]

Fat: Total lipids including phospholipids. [NIH] Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Fatty Liver: The buildup of fat in liver cells. The most common cause is alcoholism. Other causes include obesity, diabetes, and pregnancy. Also called steatosis. [NIH] Fermentation: An enzyme-induced chemical change in organic compounds that takes place in the absence of oxygen. The change usually results in the production of ethanol or lactic acid, and the production of energy. [NIH]

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Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Filtration: The passage of a liquid through a filter, accomplished by gravity, pressure, or vacuum (suction). [EU] Flatus: Gas passed through the rectum. [NIH] Flavobacterium: A genus of gram-negative, aerobic, rod-shaped bacteria widely distributed in soil and water. Its organisms are also found in raw meats, milk and other foods, hospital environments, and human clinical specimens. Some species are pathogenic in humans. [NIH] Flavoring Agents: Substances added to foods and medicine to improve the quality of taste. [NIH]

Fluorescence: The property of emitting radiation while being irradiated. The radiation emitted is usually of longer wavelength than that incident or absorbed, e.g., a substance can be irradiated with invisible radiation and emit visible light. X-ray fluorescence is used in diagnosis. [NIH] Fold: A plication or doubling of various parts of the body. [NIH] Food Additives: Substances which are of little or no nutritive value, but are used in the processing or storage of foods or animal feed, especially in the developed countries; includes antioxidants, food preservatives, food coloring agents, flavoring agents, anti-infective agents (both plain and local), vehicles, excipients and other similarly used substances. Many of the same substances are pharmaceutic aids when added to pharmaceuticals rather than to foods. [NIH]

Food Chain: The sequence of transfers of matter and energy from organism to organism in the form of food. Food chains intertwine locally into a food web because most organisms consume more than one type of animal or plant. Plants, which convert solar energy to food by photosynthesis, are the primary food source. In a predator chain, a plant-eating animal is eaten by a larger animal. In a parasite chain, a smaller organism consumes part of a larger host and may itself be parasitized by smaller organisms. In a saprophytic chain, microorganisms live on dead organic matter. [NIH] Food Coloring Agents: Natural or synthetic dyes used as coloring agents in processed foods. [NIH] Food Preservatives: Substances capable of inhibiting, retarding or arresting the process of fermentation, acidification or other deterioration of foods. [NIH] Frameshift: A type of mutation which causes out-of-phase transcription of the base sequence; such mutations arise from the addition or delection of nucleotide(s) in numbers other than 3 or multiples of 3. [NIH] Frameshift Mutation: A type of mutation in which a number of nucleotides not divisible by three is deleted from or inserted into a coding sequence, thereby causing an alteration in the reading frame of the entire sequence downstream of the mutation. These mutations may be induced by certain types of mutagens or may occur spontaneously. [NIH] Free Radicals: Highly reactive molecules with an unsatisfied electron valence pair. Free radicals are produced in both normal and pathological processes. They are proven or suspected agents of tissue damage in a wide variety of circumstances including radiation, damage from environment chemicals, and aging. Natural and pharmacological prevention of free radical damage is being actively investigated. [NIH]

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Fumigation: The application of smoke, vapor, or gas for the purpose of disinfecting or destroying pests or microorganisms. [NIH] Fungistatic: Inhibiting the growth of fungi. [EU] Fungus: A general term used to denote a group of eukaryotic protists, including mushrooms, yeasts, rusts, moulds, smuts, etc., which are characterized by the absence of chlorophyll and by the presence of a rigid cell wall composed of chitin, mannans, and sometimes cellulose. They are usually of simple morphological form or show some reversible cellular specialization, such as the formation of pseudoparenchymatous tissue in the fruiting body of a mushroom. The dimorphic fungi grow, according to environmental conditions, as moulds or yeasts. [EU] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gamma Rays: Very powerful and penetrating, high-energy electromagnetic radiation of shorter wavelength than that of x-rays. They are emitted by a decaying nucleus, usually between 0.01 and 10 MeV. They are also called nuclear x-rays. [NIH] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gasoline: Volative flammable fuel (liquid hydrocarbons) derived from crude petroleum by processes such as distillation reforming, polymerization, etc. [NIH] Gastric: Having to do with the stomach. [NIH] Gastroenterology: A subspecialty of internal medicine concerned with the study of the physiology and diseases of the digestive system and related structures (esophagus, liver, gallbladder, and pancreas). [NIH] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]

Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic Techniques: Chromosomal, biochemical, intracellular, and other methods used in the study of genetics. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genomics: The systematic study of the complete DNA sequences (genome) of organisms. [NIH]

Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Gentian Violet: A dye that is a mixture of violet rosanilinis with antibacterial, antifungal, and anthelmentic properties. [NIH]

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Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Ginger: Deciduous plant rich in volatile oil (oils, volatile). It is used as a flavoring agent and has many other uses both internally and topically. [NIH] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucosinolates: Substituted thioglucosides. They are found in rapeseed (Brassica campestris) products and related Cruciferae. They are metabolized to a variety of toxic products which are most likely the cause of hepatocytic necrosis in animals and humans. [NIH]

Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9. [NIH]

Glutathione Transferase: A transferase that catalyzes the addition of aliphatic, aromatic, or heterocyclic radicals as well as epoxides and arene oxides to glutathione. Addition takes place at the sulfur atom. It also catalyzes the reduction of polyol nitrate by glutathione to polyol and nitrite. EC 2.5.1.18. [NIH] Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]

Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine. [NIH] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycoside: Any compound that contains a carbohydrate molecule (sugar), particularly any such natural product in plants, convertible, by hydrolytic cleavage, into sugar and a nonsugar component (aglycone), and named specifically for the sugar contained, as glucoside (glucose), pentoside (pentose), fructoside (fructose) etc. [EU] Goats: Any of numerous agile, hollow-horned ruminants of the genus Capra, closely related to the sheep. [NIH] Goblet Cells: Cells of the epithelial lining that produce and secrete mucins. [NIH] Gonadal: Pertaining to a gonad. [EU] Gossypol: Poisonous pigment found in cottonseed and potentially irritating to gastrointestinal tract. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Graft Rejection: An immune response with both cellular and humoral components, directed against an allogeneic transplant, whose tissue antigens are not compatible with those of the

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recipient. [NIH] Gram-negative: Losing the stain or decolorized by alcohol in Gram's method of staining, a primary characteristic of bacteria having a cell wall composed of a thin layer of peptidoglycan covered by an outer membrane of lipoprotein and lipopolysaccharide. [EU] Grasses: A large family, Gramineae, of narrow-leaved herbaceous monocots. Many grasses produce highly allergenic pollens and are hosts to cattle parasites and toxic fungi. [NIH] Guanine: One of the four DNA bases. [NIH] Haematological: Relating to haematology, that is that branch of medical science which treats of the morphology of the blood and blood-forming tissues. [EU] Haematology: The science of the blood, its nature, functions, and diseases. [NIH] Hair follicles: Shafts or openings on the surface of the skin through which hair grows. [NIH] Haploid: An organism with one basic chromosome set, symbolized by n; the normal condition of gametes in diploids. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Helminths: Commonly known as parasitic worms, this group includes the acanthocephala, nematoda, and platyhelminths. Some authors consider certain species of leeches that can become temporarily parasitic as helminths. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemoglobin A: Normal adult human hemoglobin. The globin moiety consists of two alpha and two beta chains. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hepatic: Refers to the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatitis C: A form of hepatitis, similar to type B post-transfusion hepatitis, but caused by a virus which is serologically distinct from the agents of hepatitis A, B, and E, and which may persist in the blood of chronic asymptomatic carriers. Hepatitis C is parenterally transmitted and associated with transfusions and drug abuse. [NIH] Hepatocellular: Pertaining to or affecting liver cells. [EU] Hepatocellular carcinoma: A type of adenocarcinoma, the most common type of liver tumor. [NIH] Hepatocyte: A liver cell. [NIH] Hepatoma: A liver tumor. [NIH] Hepatotoxic: Toxic to liver cells. [EU] Hepatotoxicity: How much damage a medicine or other substance does to the liver. [NIH]

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Herbicides: Pesticides used to destroy unwanted vegetation, especially various types of weeds, grasses, and woody plants. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH]

Histones: Small chromosomal proteins (approx 12-20 kD) possessing an open, unfolded structure and attached to the DNA in cell nuclei by ionic linkages. Classification into the various types (designated histone I, histone II, etc.) is based on the relative amounts of arginine and lysine in each. [NIH] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Horseradish Peroxidase: An enzyme isolated from horseradish which is able to act as an antigen. It is frequently used as a histochemical tracer for light and electron microscopy. Its antigenicity has permitted its use as a combined antigen and marker in experimental immunology. [NIH] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hybridization: The genetic process of crossbreeding to produce a hybrid. Hybrid nucleic acids can be formed by nucleic acid hybridization of DNA and RNA molecules. Protein hybridization allows for hybrid proteins to be formed from polypeptide chains. [NIH] Hybridoma: A hybrid cell resulting from the fusion of a specific antibody-producing spleen cell with a myeloma cell. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water. [NIH] Hydrophilic: Readily absorbing moisture; hygroscopic; having strongly polar groups that readily interact with water. [EU] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hyperkeratosis: 1. Hypertrophy of the corneous layer of the skin. 2a. Any of various conditions marked by hyperkeratosis. 2b. A disease of cattle marked by thickening and wringling of the hide and formation of papillary outgrowths on the buccal mucous membranes, often accompanied by watery discharge from eyes and nose, diarrhoea, loss of condition, and abortion of pregnant animals, and now believed to result from ingestion of

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the chlorinated naphthalene of various lubricating oils. [EU] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hypertrophy: General increase in bulk of a part or organ, not due to tumor formation, nor to an increase in the number of cells. [NIH] Hypoxanthine: A purine and a reaction intermediate in the metabolism of adenosine and in the formation of nucleic acids by the salvage pathway. [NIH] Imidazole: C3H4N2. The ring is present in polybenzimidazoles. [NIH] Immersion: The placing of a body or a part thereof into a liquid. [NIH] Immune response: The activity of the immune system against foreign substances (antigens). [NIH]

Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunoassay: Immunochemical assay or detection of a substance by serologic or immunologic methods. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance. [NIH] Immunocompromised: Having a weakened immune system caused by certain diseases or treatments. [NIH] Immunodiffusion: Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction. [NIH]

Immunoelectrophoresis: A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera. [NIH] Immunogenic: Producing immunity; evoking an immune response. [EU] Immunologic: The ability of the antibody-forming system to recall a previous experience with an antigen and to respond to a second exposure with the prompt production of large amounts of antibody. [NIH] Immunology: The study of the body's immune system. [NIH] Immunosuppressant: An agent capable of suppressing immune responses. [EU] Immunosuppression: Deliberate prevention or diminution of the host's immune response. It may be nonspecific as in the administration of immunosuppressive agents (drugs or radiation) or by lymphocyte depletion or may be specific as in desensitization or the simultaneous administration of antigen and immunosuppressive drugs. [NIH] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Immunosuppressive therapy: Therapy used to decrease the body's immune response, such as drugs given to prevent transplant rejection. [NIH]

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Immunotherapy: Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH] Implant radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called [NIH] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incubated: Grown in the laboratory under controlled conditions. (For instance, white blood cells can be grown in special conditions so that they attack specific cancer cells when returned to the body.) [NIH] Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]

Infertility: The diminished or absent ability to conceive or produce an offspring while sterility is the complete inability to conceive or produce an offspring. [NIH] Infestation: Parasitic attack or subsistence on the skin and/or its appendages, as by insects, mites, or ticks; sometimes used to denote parasitic invasion of the organs and tissues, as by helminths. [NIH] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Ingestion: Taking into the body by mouth [NIH] Inhalation: The drawing of air or other substances into the lungs. [EU] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH] Initiator: A chemically reactive substance which may cause cell changes if ingested, inhaled or absorbed into the body; the substance may thus initiate a carcinogenic process. [NIH] Inoculum: The spores or tissues of a pathogen that serve to initiate disease in a plant. [NIH] Inorganic: Pertaining to substances not of organic origin. [EU] Insecticides: Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role

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in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Insulin-like: Muscular growth factor. [NIH] Interferon: A biological response modifier (a substance that can improve the body's natural response to disease). Interferons interfere with the division of cancer cells and can slow tumor growth. There are several types of interferons, including interferon-alpha, -beta, and gamma. These substances are normally produced by the body. They are also made in the laboratory for use in treating cancer and other diseases. [NIH] Interferon-alpha: One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells when exposed to live or inactivated virus, double-stranded RNA, or bacterial products. It is the major interferon produced by virus-induced leukocyte cultures and, in addition to its pronounced antiviral activity, it causes activation of NK cells. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Internal Medicine: A medical specialty concerned with the diagnosis and treatment of diseases of the internal organ systems of adults. [NIH] Internal radiation: A procedure in which radioactive material sealed in needles, seeds, wires, or catheters is placed directly into or near the tumor. Also called brachytherapy, implant radiation, or interstitial radiation therapy. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intestinal: Having to do with the intestines. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Invertebrates: Animals that have no spinal column. [NIH] Ionization: 1. Any process by which a neutral atom gains or loses electrons, thus acquiring a net charge, as the dissociation of a substance in solution into ions or ion production by the passage of radioactive particles. 2. Iontophoresis. [EU] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Irradiation: The use of high-energy radiation from x-rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes

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produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Irradiation is also called radiation therapy, radiotherapy, and x-ray therapy. [NIH] Irrigation: The washing of a body cavity or surface by flowing solution which is inserted and then removed. Any drug in the irrigation solution may be absorbed. [NIH] Isocyanates: Organic compounds that contain the -NCO radical. [NIH] Isoenzyme: Different forms of an enzyme, usually occurring in different tissues. The isoenzymes of a particular enzyme catalyze the same reaction but they differ in some of their properties. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH] Keto: It consists of 8 carbon atoms and within the endotoxins, it connects poysaccharide and lipid A. [NIH] Ketoacidosis: Acidosis accompanied by the accumulation of ketone bodies (ketosis) in the body tissues and fluids, as in diabetic acidosis. [EU] Ketone Bodies: Chemicals that the body makes when there is not enough insulin in the blood and it must break down fat for its energy. Ketone bodies can poison and even kill body cells. When the body does not have the help of insulin, the ketones build up in the blood and then "spill" over into the urine so that the body can get rid of them. The body can also rid itself of one type of ketone, called acetone, through the lungs. This gives the breath a fruity odor. Ketones that build up in the body for a long time lead to serious illness and coma. [NIH] Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH] Laxative: An agent that acts to promote evacuation of the bowel; a cathartic or purgative. [EU]

Lesion: An area of abnormal tissue change. [NIH] Lethal: Deadly, fatal. [EU] Leukotrienes: A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system. [NIH] Levo: It is an experimental treatment for heroin addiction that was developed by German scientists around 1948 as an analgesic. Like methadone, it binds with opioid receptors, but it is longer acting. [NIH] Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH]

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Lipid: Fat. [NIH] Lipid A: Lipid A is the biologically active component of lipopolysaccharides. It shows strong endotoxic activity and exhibits immunogenic properties. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipopolysaccharide: Substance consisting of polysaccaride and lipid. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver cancer: A disease in which malignant (cancer) cells are found in the tissues of the liver. [NIH]

Liver Transplantation: The transference of a part of or an entire liver from one human or animal to another. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Locoregional: The characteristic of a disease-producing organism to transfer itself, but typically to the same region of the body (a leg, the lungs, .) [EU] Longitudinal study: Also referred to as a "cohort study" or "prospective study"; the analytic method of epidemiologic study in which subsets of a defined population can be identified who are, have been, or in the future may be exposed or not exposed, or exposed in different degrees, to a factor or factors hypothesized to influence the probability of occurrence of a given disease or other outcome. The main feature of this type of study is to observe large numbers of subjects over an extended time, with comparisons of incidence rates in groups that differ in exposure levels. [NIH] Luminescence: The property of giving off light without emitting a corresponding degree of heat. It includes the luminescence of inorganic matter or the bioluminescence of human matter, invertebrates and other living organisms. For the luminescence of bacteria, bacterial luminescence is available. [NIH] Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphatic system: The tissues and organs that produce, store, and carry white blood cells that fight infection and other diseases. This system includes the bone marrow, spleen, thymus, lymph nodes and a network of thin tubes that carry lymph and white blood cells. These tubes branch, like blood vessels, into all the tissues of the body. [NIH] Lymphocytes: White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each); those with characteristics of neither major class are called null cells. [NIH]

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Lymphocytic: Referring to lymphocytes, a type of white blood cell. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lysine: An essential amino acid. It is often added to animal feed. [NIH] Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]

Malondialdehyde: The dialdehyde of malonic acid. [NIH] Mammary: Pertaining to the mamma, or breast. [EU] Mannans: Polysaccharides consisting of mannose units. [NIH] Meat: The edible portions of any animal used for food including domestic mammals (the major ones being cattle, swine, and sheep) along with poultry, fish, shellfish, and game. [NIH]

Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Megakaryocytes: Very large bone marrow cells which release mature blood platelets. [NIH] Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Lipids: Lipids, predominantly phospholipids, cholesterol and small amounts of glycolipids found in membranes including cellular and intracellular membranes. These lipids may be arranged in bilayers in the membranes with integral proteins between the layers and peripheral proteins attached to the outside. Membrane lipids are required for active transport, several enzymatic activities and membrane formation. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH] Mental Health: The state wherein the person is well adjusted. [NIH] Mental Processes: Conceptual functions or thinking in all its forms. [NIH] Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be

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absorbed through the skin and mucous membranes which leads to mercury poisoning. Because of its toxicity, the clinical use of mercury and mercurials is diminishing. [NIH] Mesenteric: Pertaining to the mesentery : a membranous fold attaching various organs to the body wall. [EU] Meta-Analysis: A quantitative method of combining the results of independent studies (usually drawn from the published literature) and synthesizing summaries and conclusions which may be used to evaluate therapeutic effectiveness, plan new studies, etc., with application chiefly in the areas of research and medicine. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Methanol: A colorless, flammable liquid used in the manufacture of formaldehyde and acetic acid, in chemical synthesis, antifreeze, and as a solvent. Ingestion of methanol is toxic and may cause blindness. [NIH] Methyltransferase: A drug-metabolizing enzyme. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiological: Pertaining to microbiology : the science that deals with microorganisms, including algae, bacteria, fungi, protozoa and viruses. [EU] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Micronuclei: Nuclei, separate from and additional to the main nucleus of a cell, produced during the telophase of mitosis or meiosis by lagging chromosomes or chromosome fragments derived from spontaneous or experimentally induced chromosomal structural changes. This concept also includes the smaller, reproductive nuclei found in multinucleate protozoans. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Microsomal: Of or pertaining to microsomes : vesicular fragments of endoplasmic reticulum formed after disruption and centrifugation of cells. [EU] Microsome: One of the specific metabolic pathways of the liver. [NIH] Milk Thistle: The plant Silybum marianum in the family Asteraceae containing the bioflavonoid complex silymarin. For centuries this has been used traditionally to treat liver disease. [NIH] Mineralization: The action of mineralizing; the state of being mineralized. [EU] Miscible: Susceptible of being mixed. [EU] Mitochondria: Parts of a cell where aerobic production (also known as cell respiration) takes place. [NIH] Mitochondrial Swelling: Increase in volume of mitochondria due to an influx of fluid; it occurs in hypotonic solutions due to osmotic pressure and in isotonic solutions as a result of altered permeability of the membranes of respiring mitochondria. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mitosporic Fungi: A large and heterogenous group of fungi whose common characteristic is the absence of a sexual state. Many of the pathogenic fungi in humans belong to this group. [NIH]

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Mitotic: Cell resulting from mitosis. [NIH] Modeling: A treatment procedure whereby the therapist presents the target behavior which the learner is to imitate and make part of his repertoire. [NIH] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoclonal: An antibody produced by culturing a single type of cell. It therefore consists of a single species of immunoglobulin molecules. [NIH] Monoclonal antibodies: Laboratory-produced substances that can locate and bind to cancer cells wherever they are in the body. Many monoclonal antibodies are used in cancer detection or therapy; each one recognizes a different protein on certain cancer cells. Monoclonal antibodies can be used alone, or they can be used to deliver drugs, toxins, or radioactive material directly to a tumor. [NIH] Monocrotaline: A pyrrolizidine alkaloid and a toxic plant constituent that poisons livestock and humans through the ingestion of contaminated grains and other foods. The alkaloid causes pulmonary artery hypertension, right ventricular hypertrophy, and pathological changes in the pulmonary vasculature. Significant attenuation of the cardiopulmonary changes are noted after oral magnesium treatment. [NIH] Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate bone marrow and released into the blood; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles. [NIH] Mononuclear: A cell with one nucleus. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Mucins: A secretion containing mucopolysaccharides and protein that is the chief constituent of mucus. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] Multidrug resistance: Adaptation of tumor cells to anticancer drugs in ways that make the drugs less effective. [NIH] Muscle Hypertonia: Abnormal increase in skeletal or smooth muscle tone. Skeletal muscle hypertonicity may be associated with pyramidal tract lesions or basal ganglia diseases. [NIH] Mustard Gas: Severe irritant and vesicant of skin, eyes, and lungs. It may cause blindness and lethal lung edema and was formerly used as a war gas. The substance has been proposed as a cytostatic and for treatment of psoriasis. It has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP-85-002, 1985) (Merck, 11th ed). [NIH] Mutagen: Any agent, such as X-rays, gamma rays, mustard gas, TCDD, that can cause abnormal mutation in living cells; having the power to cause mutations. [NIH]

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Mutagenesis: Process of generating genetic mutations. It may occur spontaneously or be induced by mutagens. [NIH] Mutagenic: Inducing genetic mutation. [EU] Mutagenicity: Ability to damage DNA, the genetic material; the power to cause mutations. [NIH]

Mutate: To change the genetic material of a cell. Then changes (mutations) can be harmful, beneficial, or have no effect. [NIH] Mycological: Relating to mycology, that is the science and study of fungi. [EU] Mycotoxins: Toxins derived from bacteria or fungi. [NIH] Myeloma: Cancer that arises in plasma cells, a type of white blood cell. [NIH] Natural selection: A part of the evolutionary process resulting in the survival and reproduction of the best adapted individuals. [NIH] Necrosis: A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH] Nematocide: A chemical used to kill nematodes. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neoplasm: A new growth of benign or malignant tissue. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Diseases: A general term encompassing lower motor neuron disease; peripheral nervous system diseases; and certain muscular diseases. Manifestations include muscle weakness; fasciculation; muscle atrophy; spasm; myokymia; muscle hypertonia, myalgias, and musclehypotonia. [NIH] Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neurotoxic: Poisonous or destructive to nerve tissue. [EU] Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] Neutralization: An act or process of neutralizing. [EU] Neutrons: Electrically neutral elementary particles found in all atomic nuclei except light hydrogen; the mass is equal to that of the proton and electron combined and they are unstable when isolated from the nucleus, undergoing beta decay. Slow, thermal, epithermal, and fast neutrons refer to the energy levels with which the neutrons are ejected from heavier nuclei during their decay. [NIH] Neutrophil: A type of white blood cell. [NIH] Niacin: Water-soluble vitamin of the B complex occurring in various animal and plant tissues. Required by the body for the formation of coenzymes NAD and NADP. Has pellagra-curative, vasodilating, and antilipemic properties. [NIH] Nicotine: Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks

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synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke. [NIH] Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful antianginal agent that also lowers blood pressure. The use of nifedipine as a tocolytic is being investigated. [NIH] Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleic Acid Hybridization: The process whereby two single-stranded polynucleotides form a double-stranded molecule, with hydrogen bonding between the complementary bases in the two strains. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nutritive Value: An indication of the contribution of a food to the nutrient content of the diet. This value depends on the quantity of a food which is digested and absorbed and the amounts of the essential nutrients (protein, fat, carbohydrate, minerals, vitamins) which it contains. This value can be affected by soil and growing conditions, handling and storage, and processing. [NIH] Occupational Exposure: The exposure to potentially harmful chemical, physical, or biological agents that occurs as a result of one's occupation. [NIH] Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases. [NIH] Oligodeoxyribonucleotides: A group of deoxyribonucleotides (up to 12) in which the phosphate residues of each deoxyribonucleotide act as bridges in forming diester linkages between the deoxyribose moieties. [NIH] Oligonucleotide Probes: Synthetic or natural oligonucleotides used in hybridization studies in order to identify and study specific nucleic acid fragments, e.g., DNA segments near or within a specific gene locus or gene. The probe hybridizes with a specific mRNA, if present. Conventional techniques used for testing for the hybridization product include dot blot assays, Southern blot assays, and DNA:RNA hybrid-specific antibody tests. Conventional labels for the probe include the radioisotope labels 32P and 125I and the chemical label biotin. [NIH] Oltipraz: A drug used in cancer prevention. [NIH] Oncogene: A gene that normally directs cell growth. If altered, an oncogene can promote or

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allow the uncontrolled growth of cancer. Alterations can be inherited or caused by an environmental exposure to carcinogens. [NIH] Oncogenic: Chemical, viral, radioactive or other agent that causes cancer; carcinogenic. [NIH] Organelles: Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH] Ornithine: An amino acid produced in the urea cycle by the splitting off of urea from arginine. [NIH] Osmotic: Pertaining to or of the nature of osmosis (= the passage of pure solvent from a solution of lesser to one of greater solute concentration when the two solutions are separated by a membrane which selectively prevents the passage of solute molecules, but is permeable to the solvent). [EU] Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]

Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471). [NIH] Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Oxides: Binary compounds of oxygen containing the anion O(2-). The anion combines with metals to form alkaline oxides and non-metals to form acidic oxides. [NIH] P53 gene: A tumor suppressor gene that normally inhibits the growth of tumors. This gene is altered in many types of cancer. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Paneth Cells: Epithelial cells found in the basal part of the intestinal glands (crypts of Lieberkuhn). Paneth cells synthesize and secrete lysozyme and cryptdins. [NIH] Papillary: Pertaining to or resembling papilla, or nipple. [EU] Parasite: An animal or a plant that lives on or in an organism of another species and gets at least some of its nutrition from that other organism. [NIH] Parasitic: Having to do with or being a parasite. A parasite is an animal or a plant that lives on or in an organism of another species and gets at least some of its nutrients from it. [NIH] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU]

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Pathogen: Any disease-producing microorganism. [EU] Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Perennial: Lasting through the year of for several years. [EU] Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peripheral Nervous System Diseases: Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves. [NIH] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Peroxide: Chemical compound which contains an atom group with two oxygen atoms tied to each other. [NIH] Pesticides: Chemicals used to destroy pests of any sort. The concept includes fungicides (industrial fungicides), insecticides, rodenticides, etc. [NIH] Phagocytosis: The engulfing of microorganisms, other cells, and foreign particles by phagocytic cells. [NIH] Pharmaceutic Aids: Substances which are of little or no therapeutic value, but are necessary in the manufacture, compounding, storage, etc., of pharmaceutical preparations or drug dosage forms. They include solvents, diluting agents, and suspending agents, and emulsifying agents. Also, antioxidants; preservatives, pharmaceutical; dyes (coloring agents); flavoring agents; vehicles; excipients; ointment bases. [NIH] Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipases A: Phosphatide acylhydrolases. Catalyze the hydrolysis of one of the acyl groups of phosphoglycerides or glycerophosphatidates. Phospholipase A1 hydrolyzes the acyl group attached to the 1-position (EC 3.1.1.32) and phospholipase A2 hydrolyzes the

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acyl group attached to the 2-position (EC 3.1.1.4). [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH] Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Photosensitivity: An abnormal cutaneous response involving the interaction between photosensitizing substances and sunlight or filtered or artificial light at wavelengths of 280400 mm. There are two main types : photoallergy and photoxicity. [EU] Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]

Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH] Pigment: A substance that gives color to tissue. Pigments are responsible for the color of skin, eyes, and hair. [NIH] Placenta: A highly vascular fetal organ through which the fetus absorbs oxygen and other nutrients and excretes carbon dioxide and other wastes. It begins to form about the eighth day of gestation when the blastocyst adheres to the decidua. [NIH] Plant Components: The anatomical components of a plant, including seeds. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid and diploid generations. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasma protein: One of the hundreds of different proteins present in blood plasma, including carrier proteins ( such albumin, transferrin, and haptoglobin), fibrinogen and other coagulation factors, complement components, immunoglobulins, enzyme inhibitors, precursors of substances such as angiotension and bradykinin, and many other types of proteins. [EU] Plasmid: An autonomously replicating, extra-chromosomal DNA molecule found in many bacteria. Plasmids are widely used as carriers of cloned genes. [NIH] Plastids: Self-replicating cytoplasmic organelles of plant and algal cells that contain pigments and may synthesize and accumulate various substances. Plastids are used in phylogenetic studies. [NIH] Pneumonia: Inflammation of the lungs. [NIH] Point Mutation: A mutation caused by the substitution of one nucleotide for another. This results in the DNA molecule having a change in a single base pair. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH]

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Pollen: The male fertilizing element of flowering plants analogous to sperm in animals. It is released from the anthers as yellow dust, to be carried by insect or other vectors, including wind, to the ovary (stigma) of other flowers to produce the embryo enclosed by the seed. The pollens of many plants are allergenic. [NIH] Polymerase: An enzyme which catalyses the synthesis of DNA using a single DNA strand as a template. The polymerase copies the template in the 5'-3'direction provided that sufficient quantities of free nucleotides, dATP and dTTP are present. [NIH] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] Polypeptide: A peptide which on hydrolysis yields more than two amino acids; called tripeptides, tetrapeptides, etc. according to the number of amino acids contained. [EU] Polyploid: An organism with more than two chromosome sets in its vegetative cells. [NIH] Polyposis: The development of numerous polyps (growths that protrude from a mucous membrane). [NIH] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Portal Vein: A short thick vein formed by union of the superior mesenteric vein and the splenic vein. [NIH] Post-translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of the effects of each drug taken alone. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Precancerous: A term used to describe a condition that may (or is likely to) become cancer. Also called premalignant. [NIH] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Prenatal: Existing or occurring before birth, with reference to the fetus. [EU] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Primary Prevention: Prevention of disease or mental disorders in susceptible individuals or populations through promotion of health, including mental health, and specific protection, as in immunization, as distinguished from the prevention of complications or after-effects of existing disease. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH]

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Progeny: The offspring produced in any generation. [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Promotor: In an operon, a nucleotide sequence located at the operator end which contains all the signals for the correct initiation of genetic transcription by the RNA polymerase holoenzyme and determines the maximal rate of RNA synthesis. [NIH] Prone: Having the front portion of the body downwards. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane). The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19hydroxy derivatives are found in many organs and tissues. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH]

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Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with formation of smaller polypeptides). [EU] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the animal kingdom. Most are free living. They range in size from submicroscopic to macroscopic. Protozoa are divided into seven phyla: Sarcomastigophora, Labyrinthomorpha, Apicomplexa, Microspora, Ascetospora, Myxozoa, and Ciliophora. [NIH] Pruritic: Pertaining to or characterized by pruritus. [EU] Psoriasis: A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis. [NIH] Psychoactive: Those drugs which alter sensation, mood, consciousness or other psychological or behavioral functions. [NIH] Psychology: The science dealing with the study of mental processes and behavior in man and animals. [NIH] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing. [NIH]

Pulmonary: Relating to the lungs. [NIH] Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]

Pyrimidine Dimers: Dimers found in DNA chains damaged by ultraviolet irradiation. They consist of two adjacent pyrimidine nucleotides, usually thymine nucleotides, in which the pyrimidine residues are covalently joined by a cyclobutane ring. These dimers stop DNA

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replication. [NIH] Quercetin: Aglucon of quercetrin, rutin, and other glycosides. It is widely distributed in the plant kingdom, especially in rinds and barks, clover blossoms, and ragweed pollen. [NIH] Quinoxaline: AMPA/Kainate antagonist. [NIH] Radiation: Emission or propagation of electromagnetic energy (waves/rays), or the waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radiation therapy: The use of high-energy radiation from x-rays, gamma rays, neutrons, and other sources to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy), or it may come from radioactive material placed in the body in the area near cancer cells (internal radiation therapy, implant radiation, or brachytherapy). Systemic radiation therapy uses a radioactive substance, such as a radiolabeled monoclonal antibody, that circulates throughout the body. Also called radiotherapy. [NIH] Radioactive: Giving off radiation. [NIH] Radioimmunoassay: Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Nonimmunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation. [NIH] Radioisotope: An unstable element that releases radiation as it breaks down. Radioisotopes can be used in imaging tests or as a treatment for cancer. [NIH] Radiolabeled: Any compound that has been joined with a radioactive substance. [NIH] Radiotherapy: The use of ionizing radiation to treat malignant neoplasms and other benign conditions. The most common forms of ionizing radiation used as therapy are x-rays, gamma rays, and electrons. A special form of radiotherapy, targeted radiotherapy, links a cytotoxic radionuclide to a molecule that targets the tumor. When this molecule is an antibody or other immunologic molecule, the technique is called radioimmunotherapy. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Ras gene: A gene that has been found to cause cancer when it is altered (mutated). Agents that block its activity may stop the growth of cancer. A ras peptide is a protein fragment produced by the ras gene. [NIH] Reagent: A substance employed to produce a chemical reaction so as to detect, measure, produce, etc., other substances. [EU] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Recurrence: The return of a sign, symptom, or disease after a remission. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called

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erythrocytes. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive error (myopia, hyperopia, or astigmatism). [NIH] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Relative risk: The ratio of the incidence rate of a disease among individuals exposed to a specific risk factor to the incidence rate among unexposed individuals; synonymous with risk ratio. Alternatively, the ratio of the cumulative incidence rate in the exposed to the cumulative incidence rate in the unexposed (cumulative incidence ratio). The term relative risk has also been used synonymously with odds ratio. This is because the odds ratio and relative risk approach each other if the disease is rare ( 5 percent of population) and the number of subjects is large. [NIH] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Respiratory Paralysis: Complete or severe weakness of the muscles of respiration. This condition may be associated with motor neuron diseases; peripheral nerve disorders; neuromuscular junction diseases; spinal cord diseases; injury to the phrenic nerve; and other disorders. [NIH] Response Elements: Nucleotide sequences, usually upstream, which are recognized by specific regulatory transcription factors, thereby causing gene response to various regulatory agents. These elements may be found in both promotor and enhancer regions. [NIH]

Retinoids: Derivatives of vitamin A. Used clinically in the treatment of severe cystic acne, psoriasis, and other disorders of keratinization. Their possible use in the prophylaxis and treatment of cancer is being actively explored. [NIH] Reversion: A return to the original condition, e. g. the reappearance of the normal or wild type in previously mutated cells, tissues, or organisms. [NIH] Ribonucleic acid: RNA. One of the two nucleic acids found in all cells. The other is deoxyribonucleic acid (DNA). Ribonucleic acid transfers genetic information from DNA to proteins produced by the cell. [NIH] Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU] Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Rod: A reception for vision, located in the retina. [NIH] Rodenticides: Substances used to destroy or inhibit the action of rats, mice, or other rodents. [NIH]

Ruminants: A suborder of the order Artiodactyla whose members have the distinguishing feature of a four-chambered stomach. Horns or antlers are usually present, at least in males. [NIH]

Rutin: 3-((6-O-(6-Deoxy-alpha-L-mannopyranosyl)-beta-D-glucopyranosyl)oxy)-2-(3,4dihydroxyphenyl)-5,7-dihydroxy-4H-1-benzopyran-4-one. Found in many plants, including buckwheat, tobacco, forsythia, hydrangea, pansies, etc. It has been used therapeutically to

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decrease capillary fragility. [NIH] Saponins: Sapogenin glycosides. A type of glycoside widely distributed in plants. Each consists of a sapogenin as the aglycon moiety, and a sugar. The sapogenin may be a steroid or a triterpene and the sugar may be glucose, galactose, a pentose, or a methylpentose. Sapogenins are poisonous towards the lower forms of life and are powerful hemolytics when injected into the blood stream able to dissolve red blood cells at even extreme dilutions. [NIH] Saxitoxin: Poison found in certain edible mollusks at certain times; elaborated by Gonyaulax species (Dinoflagellate protozoans) and consumed by mollusks, fishes, etc. without ill effects; it is neurotoxic and causes respiratory paralysis and other effects in mammals, known as paralytic shellfish poisoning. [NIH] Scatter: The extent to which relative success and failure are divergently manifested in qualitatively different tests. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Screening: Checking for disease when there are no symptoms. [NIH] Sebaceous: Gland that secretes sebum. [NIH] Segregation: The separation in meiotic cell division of homologous chromosome pairs and their contained allelomorphic gene pairs. [NIH] Selenium: An element with the atomic symbol Se, atomic number 34, and atomic weight 78.96. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of glutathione peroxidase. [NIH] Sequence Analysis: A multistage process that includes the determination of a sequence (protein, carbohydrate, etc.), its fragmentation and analysis, and the interpretation of the resulting sequence information. [NIH] Serologic: Analysis of a person's serum, especially specific immune or lytic serums. [NIH] Serology: The study of serum, especially of antigen-antibody reactions in vitro. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the broad physiological actions and distribution of this biochemical mediator. [NIH] Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Serum Albumin: A major plasma protein that serves in maintaining the plasma colloidal osmotic pressure and transporting large organic anions. [NIH] Side effect: A consequence other than the one(s) for which an agent or measure is used, as

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the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Silymarin: A mixture of flavonoids extracted from seeds of the milk thistle, Silybum marianum. It consists primarily of three isomers: silicristin, silidianin, and silybin, its major component. Silymarin displays antioxidant and membrane stabilizing activity. It protects various tissues and organs against chemical injury, and shows potential as an antihepatoxic agent. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Smallpox: A generalized virus infection with a vesicular rash. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]

Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Sorbic Acid: Mold and yeast inhibitor. Used as a fungistatic agent for foods, especially cheeses. [NIH] Spasm: An involuntary contraction of a muscle or group of muscles. Spasms may involve skeletal muscle or smooth muscle. [NIH] Spasticity: A state of hypertonicity, or increase over the normal tone of a muscle, with heightened deep tendon reflexes. [EU] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectroscopic: The recognition of elements through their emission spectra. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU]

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Sperm: The fecundating fluid of the male. [NIH] Spheroplasts: Cells, usually bacteria or yeast, which have partially lost their cell wall, lost their characteristic shape and become round. [NIH] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Splenic Vein: Vein formed by the union (at the hilus of the spleen) of several small veins from the stomach, pancreas, spleen and mesentery. [NIH] Spores: The reproductive elements of lower organisms, such as protozoa, fungi, and cryptogamic plants. [NIH] Stabilization: The creation of a stable state. [EU] Staging: Performing exams and tests to learn the extent of the cancer within the body, especially whether the disease has spread from the original site to other parts of the body. [NIH]

Steatosis: Fatty degeneration. [EU] Sterigmatocystin: A carcinogenic mycotoxin produced in high yields by strains of the common molds, Aspergillus versicolor, A. nidulans, and an unidentified species of Bipolaris. It causes necrosis of the liver and kidney and has an inhibitory effect on orotic acid incorporation into nuclear RNA. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Strand: DNA normally exists in the bacterial nucleus in a helix, in which two strands are coiled together. [NIH] Streptomyces: A genus of bacteria that form a nonfragmented aerial mycelium. Many species have been identified with some being pathogenic. This genus is responsible for producing a majority of the antibiotics of practical value. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH] Stromal: Large, veil-like cell in the bone marrow. [NIH] Stromal Cells: Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the

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hematopoietic system and elsewhere. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU] Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]

Substrate: A substance upon which an enzyme acts. [EU] Suction: The removal of secretions, gas or fluid from hollow or tubular organs or cavities by means of a tube and a device that acts on negative pressure. [NIH] Sulfamethazine: A sulfanilamide anti-infective agent. It has a spectrum of antimicrobial action similar to other sulfonamides. [NIH] Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight 32.066. It is found in the amino acids cysteine and methionine. [NIH] Sulfur Dioxide: A highly toxic, colorless, nonflammable gas. It is used as a pharmaceutical aid and antioxidant. It is also an environmental air pollutant. [NIH] Supplementation: Adding nutrients to the diet. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Supraspinal: Above the spinal column or any spine. [NIH] Surfactant: A fat-containing protein in the respiratory passages which reduces the surface tension of pulmonary fluids and contributes to the elastic properties of pulmonary tissue. [NIH]

Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synaptic Transmission: The communication from a neuron to a target (neuron, muscle, or secretory cell) across a synapse. In chemical synaptic transmission, the presynaptic neuron releases a neurotransmitter that diffuses across the synaptic cleft and binds to specific synaptic receptors. These activated receptors modulate ion channels and/or secondmessenger systems to influence the postsynaptic cell. Electrical transmission is less common in the nervous system, and, as in other tissues, is mediated by gap junctions. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Systemic: Affecting the entire body. [NIH] Systemic therapy: Treatment that uses substances that travel through the bloodstream, reaching and affecting cells all over the body. [NIH]

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Telophase: The final phase of cell division, in which two daughter nuclei are formed, the cytoplasm divides, and the chromosomes lose their distinctness and are transformed into chromatin networks. [NIH] Teratogenic: Tending to produce anomalies of formation, or teratism (= anomaly of formation or development : condition of a monster). [EU] Teratogens: An agent that causes the production of physical defects in the developing embryo. [NIH] Terminator: A DNA sequence sited at the end of a transcriptional unit that signals the end of transcription. [NIH] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Tetrahydrocannabinol: A psychoactive compound extracted from the resin of Cannabis sativa (marihuana, hashish). The isomer delta-9-tetrahydrocannabinol (THC) is considered the most active form, producing characteristic mood and perceptual changes associated with this compound. Dronabinol is a synthetic form of delta-9-THC. [NIH] Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH] Thermal: Pertaining to or characterized by heat. [EU] Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. [NIH] Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase. [NIH] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH] Ticks: Blood-sucking arachnids of the order Acarina. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tolnaftate: A synthetic antifungal agent. [NIH] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topical: On the surface of the body. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicokinetics: Study of the absorption, distribution, metabolism, and excretion of test substances. [NIH] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of

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toxic manifestations. [NIH] Toxin: A poison; frequently used to refer specifically to a protein produced by some higher plants, certain animals, and pathogenic bacteria, which is highly toxic for other living organisms. Such substances are differentiated from the simple chemical poisons and the vegetable alkaloids by their high molecular weight and antigenicity. [EU] Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process. [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transferases: Transferases are enzymes transferring a group, for example, the methyl group or a glycosyl group, from one compound (generally regarded as donor) to another compound (generally regarded as acceptor). The classification is based on the scheme "donor:acceptor group transferase". (Enzyme Nomenclature, 1992) EC 2. [NIH] Transfusion: The infusion of components of blood or whole blood into the bloodstream. The blood may be donated from another person, or it may have been taken from the person earlier and stored until needed. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Trees: Woody, usually tall, perennial higher plants (Angiosperms, Gymnosperms, and some Pterophyta) having usually a main stem and numerous branches. [NIH] Trichothecenes: Usually 12,13-epoxytrichothecenes, produced by Fusaria, Stachybotrys, Trichoderma and other fungi, and some higher plants. They may contaminate food or feed grains, induce emesis and hemorrhage in lungs and brain, and damage bone marrow due to protein and DNA synthesis inhibition. [NIH] Trifluoroacetic Acid: A very strong halogenated derivative of acetic acid. It is used in acid catalyzed reactions, especially those where an ester is cleaved in peptide synthesis. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tumor marker: A substance sometimes found in an increased amount in the blood, other body fluids, or tissues and which may mean that a certain type of cancer is in the body. Examples of tumor markers include CA 125 (ovarian cancer), CA 15-3 (breast cancer), CEA (ovarian, lung, breast, pancreas, and gastrointestinal tract cancers), and PSA (prostate cancer). Also called biomarker. [NIH] Tumor model: A type of animal model which can be used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Tumor suppressor gene: Genes in the body that can suppress or block the development of cancer. [NIH] Tumour: 1. Swelling, one of the cardinal signs of inflammations; morbid enlargement. 2. A new growth of tissue in which the multiplication of cells is uncontrolled and progressive; called also neoplasm. [EU] Tunicamycin: An N-acetylglycosamine containing antiviral antibiotic obtained from Streptomyces lysosuperificus. It is also active against some bacteria and fungi, because it inhibits the glucosylation of proteins. Tunicamycin is used as tool in the study of microbial

Dictionary 225

biosynthetic mechanisms. [NIH] Typhimurium: Microbial assay which measures his-his+ reversion by chemicals which cause base substitutions or frameshift mutations in the genome of this organism. [NIH] Ultraviolet radiation: Invisible rays that are part of the energy that comes from the sun. UV radiation can damage the skin and cause melanoma and other types of skin cancer. UV radiation that reaches the earth's surface is made up of two types of rays, called UVA and UVB rays. UVB rays are more likely than UVA rays to cause sunburn, but UVA rays pass deeper into the skin. Scientists have long thought that UVB radiation can cause melanoma and other types of skin cancer. They now think that UVA radiation also may add to skin damage that can lead to skin cancer and cause premature aging. For this reason, skin specialists recommend that people use sunscreens that reflect, absorb, or scatter both kinds of UV radiation. [NIH] Urea: A compound (CO(NH2)2), formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]

Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Vaccination: Administration of vaccines to stimulate the host's immune response. This includes any preparation intended for active immunological prophylaxis. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vaccinia: The cutaneous and occasional systemic reactions associated with vaccination using smallpox (variola) vaccine. [NIH] Vaccinia Virus: The type species of Orthopoxvirus, related to cowpox virus, but whose true origin is unknown. It has been used as a live vaccine against smallpox. It is also used as a vector for inserting foreign DNA into animals. Rabbitpox virus is a subspecies of vaccinia virus. [NIH] Vacuoles: Any spaces or cavities within a cell. They may function in digestion, storage, secretion, or excretion. [NIH] Variola: A generalized virus infection with a vesicular rash. [NIH] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasodilator: An agent that widens blood vessels. [NIH] Vector: Plasmid or other self-replicating DNA molecule that transfers DNA between cells in nature or in recombinant DNA technology. [NIH] Vegetative: 1. Concerned with growth and with nutrition. 2. Functioning involuntarily or unconsciously, as the vegetative nervous system. 3. Resting; denoting the portion of a cell cycle during which the cell is not involved in replication. 4. Of, pertaining to, or characteristic of plants. [EU] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venous: Of or pertaining to the veins. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary

226

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artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Vesicular: 1. Composed of or relating to small, saclike bodies. 2. Pertaining to or made up of vesicles on the skin. [EU] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Viral Load: The quantity of measurable virus in the blood. Change in viral load, measured in plasma, is used as a surrogate marker in HIV disease progression. [NIH] Viremia: The presence of viruses in the blood. [NIH] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] Vulgaris: An affection of the skin, especially of the face, the back and the chest, due to chronic inflammation of the sebaceous glands and the hair follicles. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]

Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Xenograft: The cells of one species transplanted to another species. [NIH] Xeroderma Pigmentosum: A rare, pigmentary, and atrophic autosomal recessive disease affecting all races. It is manifested as an extreme photosensitivity to ultraviolet light as the result of a deficiency in the enzyme that permits excisional repair of ultraviolet-damaged DNA. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] X-ray therapy: The use of high-energy radiation from x-rays to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external-beam radiation therapy) or from materials called radioisotopes. Radioisotopes produce radiation and can be placed in or near the tumor or in the area near cancer cells. This type of radiation treatment is called internal radiation therapy, implant radiation, interstitial radiation, or brachytherapy. Systemic radiation therapy uses a radioactive substance, such as a

Dictionary 227

radiolabeled monoclonal antibody, that circulates throughout the body. X-ray therapy is also called radiation therapy, radiotherapy, and irradiation. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Zearalenone: (S-(E))-3,4,5,6,8,10-Hexahydro-14,16-dihydroxy-3-methyl-1H-2benzoxacyclotetradecin-1,7(8H)-dione. One of a group of compounds known under the general designation of resorcylic acid lactones. Cis, trans, dextro and levo forms have been isolated from the fungus Gibberella zeae (formerly Fusarium graminearum). They have estrogenic activity, cause toxicity in livestock as feed contaminant, and have been used as anabolic or estrogen substitutes. [NIH] Zebrafish: A species of North American fishes of the family Cyprinidae. They are used in embryological studies and to study the effects of certain chemicals on development. [NIH] Zygote: The fertilized ovum. [NIH]

229

INDEX A Abdomen, 177, 184, 203, 205, 212, 221 Abdominal, 177, 211, 212 Absolute risk, 80, 177 Acceptor, 177, 205, 211, 224 Acetaldehyde, 177, 178 Acetaminophen, 11, 18, 177 Acetone, 137, 145, 177, 204 Acne, 177, 218 Acyl, 177, 212 Adaptability, 177, 186 Adaptation, 6, 177, 208 Adduction, 10, 12, 40, 42, 177 Adenine, 31, 177 Adenocarcinoma, 177, 199 Adenosine, 177, 201, 213 Adjustment, 177 Adverse Effect, 178, 220 Aerobic, 178, 196, 207 Affinity, 6, 25, 33, 84, 178, 220 Affinity Chromatography, 6, 25, 178 Agar, 26, 34, 42, 178, 190, 201 Age-Adjusted, 13, 178 Agonist, 119, 178, 182, 192, 209 Albumin, 7, 9, 13, 48, 49, 58, 60, 61, 71, 74, 79, 82, 83, 85, 89, 94, 103, 151, 178, 213 Alcohol Dehydrogenase, 43, 178 Aldehyde Reductase, 5, 26, 46, 52, 70, 79, 150, 179 Aldehydes, 5, 20, 179 Algorithms, 179, 184 Alimentary, 179, 211 Alkaline, 136, 179, 180, 185, 188, 211 Alkaloid, 179, 185, 187, 208, 209 Alkylating Agents, 10, 14, 179 Alkylation, 8, 62, 179 Alleles, 7, 179 Allo, 147, 179 Allylamine, 179 Alpha Particles, 179, 217 Alternative medicine, 179 Amine, 6, 179 Amino Acid Sequence, 147, 150, 179, 180, 195, 197 Amino Acids, 28, 31, 143, 147, 179, 188, 197, 212, 214, 216, 222, 225 Ammonia, 25, 36, 131, 133, 135, 179, 180, 225

Amphetamines, 180, 187 Amplification, 17, 180 Anabolic, 180, 192, 227 Anaesthesia, 180, 202 Anal, 79, 103, 106, 110, 116, 117, 120, 134, 180, 205 Analgesic, 11, 177, 180, 204 Analog, 134, 180 Anaphylatoxins, 180, 188 Anatomical, 180, 202, 213 Anginal, 180, 210 Animal model, 9, 19, 22, 93, 180, 224 Anions, 178, 180, 203, 219 Anomalies, 180, 223 Anthraquinones, 35, 180 Antibacterial, 147, 180, 197, 220 Antibiotic, 120, 143, 147, 180, 182, 220, 224 Antibodies, 61, 82, 134, 150, 180, 181, 199, 201, 208, 213 Antibody, 24, 29, 30, 31, 38, 39, 40, 57, 82, 84, 87, 134, 178, 180, 181, 188, 194, 199, 200, 201, 202, 204, 206, 208, 210, 217, 219, 220, 227 Antibody Affinity, 87, 180 Anticarcinogenic, 11, 181 Antidepressant, 8, 181 Antifungal, 131, 143, 146, 147, 181, 197, 223 Antigen, 49, 67, 85, 178, 180, 181, 182, 188, 194, 200, 201, 202, 206, 217, 219 Antigen-Antibody Complex, 181, 188 Anti-infective, 181, 196, 200, 222 Anti-Infective Agents, 181, 196 Anti-inflammatory, 177, 181, 191, 198 Antimicrobial, 26, 143, 146, 181, 222 Antimycotic, 117, 181 Antineoplastic, 179, 181 Antineoplastic Agents, 179, 181 Antioxidant, 5, 76, 93, 118, 119, 181, 182, 185, 195, 211, 220, 222 Antipyretic, 177, 181 Antiseptic, 177, 181 Antiserum, 39, 134, 181, 182 Antiviral, 181, 203, 224 Anus, 180, 181, 188 Apoptosis, 11, 14, 16, 22, 92, 181 Approximate, 141, 182

230

Aflatoxin

Aqueous, 128, 135, 136, 137, 182, 183, 190, 193, 200 Arachidonic Acid, 67, 182, 204, 215 Arginine, 143, 180, 182, 200, 211 Arterial, 179, 182, 201, 216 Arterioles, 182, 184, 185 Artery, 182, 216 Ascorbic Acid, 94, 111, 182 Aspergillosis, 85, 182 Assay, 13, 65, 120, 134, 151, 182, 188, 201, 217, 225 Astringents, 182, 206 Asymptomatic, 182, 199 Atmospheric Pressure, 136, 182 Atrophy, 182, 209 Attenuation, 182, 208 Avian, 75, 120, 182 Avidity, 181, 182 B Baclofen, 8, 182 Bacterial Physiology, 177, 183 Bactericidal, 183, 194 Bacterium, 143, 183, 189 Base, 7, 16, 27, 35, 145, 177, 183, 190, 191, 195, 196, 197, 204, 213, 225 Base Sequence, 183, 196, 197 Benign, 19, 183, 209, 217 Benzo(a)pyrene, 16, 93, 151, 183 Benzoic Acid, 36, 112, 183 Bile, 183, 197, 205, 221 Bilirubin, 178, 183 Binding agent, 145, 183 Bioassay, 25, 183 Bioavailability, 9, 10, 183 Biochemical, 10, 16, 27, 50, 56, 70, 86, 87, 94, 97, 117, 179, 183, 197, 219 Biogenesis, 39, 183 Biological response modifier, 183, 203 Bioluminescence, 183, 205 Biomarkers, 7, 9, 10, 12, 21, 45, 48, 49, 54, 58, 64, 72, 74, 79, 82, 85, 88, 89, 183 Biotechnology, 23, 44, 161, 183 Biotin, 184, 210 Biotransformation, 9, 19, 27, 50, 56, 60, 74, 83, 89, 98, 110, 115, 116, 184 Bladder, 58, 184, 215, 225 Blastocyst, 184, 213 Blood Coagulation, 184, 185 Blood Glucose, 184, 199, 203 Blood pressure, 184, 201, 208, 210, 220 Blood vessel, 184, 205, 220, 221, 223, 225 Blot, 184, 210

Body Fluids, 183, 184, 220, 224 Bone Marrow, 102, 105, 184, 201, 205, 206, 208, 221, 224 Bone Marrow Cells, 102, 105, 184, 206 Boron, 184, 190 Bowel, 46, 180, 184, 191, 203, 204, 212, 221 Brachytherapy, 184, 203, 204, 217, 226 Bronchi, 185 Bronchial, 71, 185 Buccal, 185, 200 Butylated Hydroxyanisole, 93, 105, 185 C Cadmium, 107, 185 Cadmium Poisoning, 185 Calcium, 56, 94, 106, 129, 185, 188, 210 Calcium Hydroxide, 94, 185 Callus, 185, 193 Capillary, 6, 185, 186, 219, 226 Capillary Fragility, 185, 186, 219 Capsaicin, 108, 185 Carbohydrate, 185, 198, 210, 214, 219 Carbon Dioxide, 185, 213, 218 Carcinogen, 4, 6, 9, 10, 11, 15, 19, 22, 46, 70, 128, 148, 150, 151, 177, 183, 185, 194, 195, 208 Carcinogenicity, 15, 50, 99, 137, 143, 150, 185 Carcinoma, 6, 9, 12, 13, 14, 15, 24, 43, 45, 47, 50, 51, 52, 59, 60, 62, 64, 65, 66, 67, 73, 75, 76, 81, 82, 84, 85, 88, 89, 104, 115, 118, 155, 185, 199 Cardiac, 179, 185, 221 Cardiopulmonary, 185, 208 Carotenoids, 12, 185 Carrier Proteins, 186, 213, 217 Case report, 186, 187 Case series, 186, 187 Catechin, 94, 186 Cathode, 186, 193 Cations, 119, 186, 203 Cause of Death, 12, 186, 191 Cell Cycle, 102, 186, 225 Cell Death, 14, 16, 181, 186, 209 Cell Division, 182, 186, 206, 207, 213, 219, 223 Cell membrane, 186, 213 Cell proliferation, 11, 186 Cell Respiration, 186, 207, 218 Central Nervous System, 180, 186, 187, 204, 219 Centrifugation, 186, 207 Chemical Warfare, 186, 191

231

Chemical Warfare Agents, 186, 191 Chemoprevention, 9, 10, 21, 57, 74, 105, 186 Chemopreventive, 9, 21, 89, 187 Chemoprotective, 9, 114, 187 Chemotactic Factors, 187, 188 Chemotherapy, 14, 155, 187 Chloroform, 145, 187 Chlorophyll, 9, 187, 197 Cholesterol, 98, 183, 187, 205, 206, 221 Cholinergic, 187, 209 Chromatin, 30, 181, 187, 205, 223 Chromosomal, 28, 61, 71, 180, 187, 197, 200, 207, 213 Chromosome, 52, 66, 105, 187, 189, 199, 204, 207, 214, 219 Chronic, 4, 9, 12, 13, 14, 52, 63, 67, 76, 95, 150, 155, 187, 192, 199, 202, 216, 222, 226 Cirrhosis, 52, 75, 155, 187 Clinical Medicine, 187, 214 Clinical study, 92, 187 Clinical trial, 3, 7, 161, 187, 217 Cloning, 28, 37, 51, 52, 53, 184, 187 Coca, 187 Cocaine, 15, 187 Codon, 4, 7, 11, 15, 24, 48, 53, 64, 65, 75, 76, 79, 83, 187, 197 Coenzyme, 182, 188 Cofactor, 188, 216 Collagen, 186, 188, 196 Colloidal, 178, 188, 193, 219 Colon, 11, 69, 188, 204 Colorectal, 12, 188 Colorectal Cancer, 12, 188 Comet Assay, 47, 188 Complement, 31, 180, 188, 189, 197, 213 Complementary and alternative medicine, 101, 123, 189 Complementary medicine, 101, 189 Complementation, 34, 189 Computational Biology, 161, 189 Conjugated, 20, 27, 183, 189, 190 Conjugation, 63, 66, 111, 184, 189 Connective Tissue, 182, 184, 188, 189, 196, 221 Consciousness, 180, 189, 192, 216 Contraindications, ii, 189 Cortisol, 178, 189 Cortisone, 189, 191 Cost-benefit, 21, 189 Coumarin, 5, 54, 189 Cowpox, 190, 225

Cowpox Virus, 190, 225 Crossing-over, 190, 217 Cryopreservation, 190, 192 Culture Media, 38, 178, 190 Cultured cells, 55, 190 Curative, 155, 190, 209, 223 Curcumin, 118, 190 Cutaneous, 190, 213, 225 Cyclic, 146, 147, 190, 215 Cysteine, 122, 190, 222 Cytokine, 18, 190 Cytoplasm, 181, 186, 190, 205, 208, 223 Cytosine, 4, 190 Cytotoxicity, 16, 53, 55, 58, 62, 116, 179, 190 D Dairy Products, 47, 84, 190 Data Collection, 7, 191 Deamination, 11, 191, 225 Death Certificates, 12, 191 Decidua, 191, 213 Decontamination, 94, 154, 191 Degenerative, 191, 199 Deletion, 7, 181, 191 Deoxyguanosine, 9, 191 Deoxyribonucleic, 36, 191, 218 Deoxyribonucleic acid, 36, 191, 218 Deoxyribonucleotides, 191, 210 Dermatitis, 191, 193 Detoxification, 5, 19, 20, 23, 29, 43, 56, 57, 66, 84, 129, 133, 145, 191 Deuterium, 191, 200 Developed Countries, 191, 196 Developing Countries, 87, 191 Dexamethasone, 113, 191 Diabetes Mellitus, 191, 199 Diagnostic procedure, 127, 191 Diarrhoea, 191, 200 Digestion, 179, 183, 184, 191, 203, 205, 221, 225 Digestive system, 191, 197 Dihydrotestosterone, 192, 218 Dihydroxy, 192, 218, 227 Dimethyl, 11, 94, 137, 192 Dimethyl Sulfoxide, 94, 192 Dimethylnitrosamine, 135, 192 Diploid, 55, 189, 192, 213 Direct, iii, 4, 5, 6, 12, 17, 30, 68, 187, 192, 218 Discrete, 8, 192 Disease Progression, 192, 226 Disease Vectors, 192, 202

232

Aflatoxin

Disinfectant, 192, 194 Dissection, 5, 192 Dissociation, 4, 178, 192, 203 Dissociative Disorders, 192 Dopamine, 187, 192, 209 Dosimetry, 72, 192 Drug Interactions, 18, 193 Drug Resistance, 21, 193 Drug Tolerance, 193, 223 Duodenum, 183, 193, 221 E Eczema, 142, 193 Effector, 188, 193 Efficacy, 9, 10, 19, 21, 89, 155, 193 Elastic, 193, 222 Electrolysis, 180, 186, 193 Electrolyte, 193, 220 Electrons, 181, 183, 186, 193, 203, 211, 217 Electrophoresis, 24, 188, 193, 201 Embryo, 55, 184, 193, 202, 214, 223 Embryogenesis, 22, 193 Emesis, 193, 224 Emulsions, 178, 193 Endemic, 51, 193 Endocrine Glands, 193 Endogenous, 3, 12, 14, 20, 22, 192, 193, 194, 224 Endotoxic, 194, 205 Endotoxin, 17, 194 Enhancer, 194, 218 Enterocytes, 46, 194 Environmental Exposure, 7, 14, 22, 194, 211 Environmental Health, 6, 59, 61, 65, 69, 71, 72, 78, 88, 89, 160, 162, 194 Enzymatic, 32, 43, 53, 84, 185, 188, 194, 206 Enzyme, 18, 20, 22, 25, 26, 32, 33, 38, 40, 65, 70, 77, 78, 79, 83, 89, 96, 111, 114, 138, 178, 179, 188, 193, 194, 195, 198, 200, 204, 207, 213, 214, 216, 218, 222, 224, 226 Enzyme-Linked Immunosorbent Assay, 70, 79, 194 Epichlorohydrin, 147, 148, 194 Epidemiological, 6, 11, 19, 194 Epithelial, 71, 177, 191, 194, 198, 211 Epithelial Cells, 71, 194 Epithelium, 194 Epitope, 61, 194 Erythrocytes, 184, 194, 218 Esophagus, 192, 194, 197, 221 Estrogen, 194, 227

Ethanol, 36, 94, 137, 178, 194, 195 Ether, 137, 195 Ethoxyquin, 5, 20, 26, 60, 195 Ethylene Dibromide, 131, 195 Eukaryotic Cells, 195, 211 Excipients, 195, 196, 212 Excisional, 195, 226 Excitation, 141, 149, 150, 180, 195, 209 Excitatory, 182, 195 Exogenous, 3, 20, 22, 184, 193, 194, 195 Exon, 76, 195 External-beam radiation, 195, 203, 217, 226 Extracellular, 189, 195, 196, 220 Extracellular Matrix, 189, 195, 196 Extraction, 131, 134, 137, 144, 146, 195 F Family Planning, 161, 195 Fasciculation, 195, 209 Fat, 48, 96, 109, 131, 182, 184, 195, 204, 205, 210, 220, 222 Fatty acids, 22, 108, 178, 195, 198, 215, 223 Fatty Liver, 109, 195 Fermentation, 36, 38, 143, 178, 195, 196 Fetus, 196, 213, 214 Fibroblasts, 12, 46, 55, 62, 80, 88, 196 Fibrosis, 78, 97, 179, 196 Filtration, 128, 196 Flatus, 196, 197 Flavobacterium, 24, 36, 101, 119, 120, 196 Flavoring Agents, 196, 212 Fluorescence, 26, 27, 42, 128, 135, 141, 149, 150, 196 Fold, 13, 21, 196, 207 Food Chain, 99, 129, 196 Food Coloring Agents, 196 Food Preservatives, 103, 196 Frameshift, 4, 196, 225 Frameshift Mutation, 4, 196, 225 Free Radicals, 181, 192, 196 Fumigation, 129, 197 Fungistatic, 183, 197, 220 Fungus, 29, 33, 128, 138, 141, 144, 197, 227 G Gallbladder, 177, 192, 197 Gamma Rays, 197, 208, 217 Gas, 135, 180, 185, 196, 197, 200, 208, 210, 222 Gasoline, 195, 197 Gastric, 12, 197 Gastroenterology, 45, 46, 77, 155, 197

233

Gastrointestinal, 27, 92, 150, 185, 194, 197, 198, 204, 219, 222, 224 Gastrointestinal tract, 92, 194, 197, 198, 204, 219, 224 Gene Expression, 16, 28, 43, 84, 197 Genetic Code, 197, 210 Genetic Engineering, 138, 184, 187, 197 Genetic Techniques, 17, 197 Genetics, 22, 52, 142, 189, 197 Genomics, 20, 197 Genotype, 7, 89, 197, 212 Gentian Violet, 142, 197 Gestation, 198, 213 Ginger, 120, 123, 198 Glucocorticoid, 191, 198 Glucose, 41, 71, 115, 182, 184, 191, 198, 199, 203, 219 Glucosinolates, 19, 198 Glutathione Peroxidase, 198, 219 Glutathione Transferase, 111, 198 Glycerol, 198, 213 Glycerophospholipids, 198, 213 Glycine, 101, 183, 198, 209 Glycoside, 198, 219 Goats, 29, 190, 198 Goblet Cells, 194, 198 Gonadal, 198, 221 Gossypol, 131, 198 Governing Board, 198, 214 Graft, 198, 202 Graft Rejection, 198, 202 Gram-negative, 17, 194, 196, 199 Grasses, 199, 200 Guanine, 21, 23, 67, 72, 78, 79, 94, 191, 199 H Haematological, 111, 199 Haematology, 199 Hair follicles, 199, 226 Haploid, 199, 213 Haptens, 178, 199, 217 Helminths, 199, 202 Hemoglobin, 6, 194, 199 Hemoglobin A, 6, 199 Hemorrhage, 199, 221, 224 Hepatic, 10, 17, 33, 37, 50, 56, 62, 65, 66, 72, 78, 93, 108, 111, 115, 150, 178, 199 Hepatitis, 6, 9, 12, 13, 14, 20, 22, 26, 47, 49, 52, 63, 64, 66, 67, 73, 75, 76, 77, 84, 85, 87, 89, 93, 102, 155, 199 Hepatitis C, 75, 199 Hepatocyte, 13, 199 Hepatoma, 51, 150, 199

Hepatotoxic, 17, 139, 140, 178, 199 Hepatotoxicity, 17, 107, 109, 114, 151, 199 Herbicides, 31, 200 Heredity, 197, 200 Heterogeneity, 178, 200 Histones, 187, 200 Homologous, 179, 190, 200, 219, 222 Hormonal, 155, 182, 200 Hormone, 179, 183, 189, 200, 202, 215, 223 Horseradish Peroxidase, 194, 200 Hybrid, 200, 210 Hybridization, 14, 200, 210 Hybridoma, 134, 200 Hydrogen, 34, 60, 95, 177, 178, 179, 183, 185, 191, 198, 200, 205, 208, 209, 210, 211, 216 Hydrogen Peroxide, 34, 95, 198, 200, 205 Hydrolysis, 40, 46, 69, 184, 200, 212, 214, 216 Hydrophilic, 132, 147, 200 Hydrophobic, 181, 198, 200, 205 Hyperkeratosis, 142, 200 Hypersensitivity, 94, 201, 204 Hypertension, 201, 208 Hypertrophy, 200, 201, 208 Hypoxanthine, 67, 201 I Imidazole, 4, 184, 201 Immersion, 135, 201 Immune response, 13, 95, 105, 181, 189, 198, 199, 201, 222, 225, 226 Immune system, 59, 201, 202, 204, 225, 226 Immunization, 201, 202, 214 Immunoassay, 38, 61, 78, 194, 201 Immunocompromised, 95, 201 Immunodiffusion, 178, 201 Immunoelectrophoresis, 178, 201 Immunogenic, 201, 205, 217 Immunologic, 9, 187, 201, 217 Immunology, 93, 178, 200, 201 Immunosuppressant, 179, 201 Immunosuppression, 178, 201 Immunosuppressive, 198, 201, 202 Immunosuppressive therapy, 201, 202 Immunotherapy, 155, 202 Impairment, 66, 202, 206 Implant radiation, 202, 203, 204, 217, 226 In vitro, 6, 15, 18, 20, 34, 35, 49, 67, 83, 86, 87, 88, 110, 115, 116, 202, 219 In vivo, 9, 11, 15, 16, 17, 34, 96, 105, 110, 111, 118, 119, 202, 223 Incubated, 101, 202

234

Aflatoxin

Induction, 5, 11, 16, 19, 24, 25, 29, 35, 41, 62, 66, 111, 114, 135, 202 Infertility, 58, 202 Infestation, 33, 142, 202 Inflammation, 177, 178, 181, 191, 192, 196, 199, 202, 204, 213, 226 Ingestion, 4, 12, 128, 150, 185, 200, 202, 207, 208, 213 Inhalation, 195, 202, 213 Initiation, 11, 112, 202, 215, 224 Initiator, 10, 202 Inoculum, 35, 202 Inorganic, 202, 205 Insecticides, 36, 202, 212 Insight, 11, 202 Insulin, 45, 202, 203, 204 Insulin-dependent diabetes mellitus, 203 Insulin-like, 45, 203 Interferon, 25, 203 Interferon-alpha, 203 Interleukin-2, 84, 203 Internal Medicine, 69, 197, 203 Internal radiation, 203, 204, 217, 226 Interstitial, 78, 184, 203, 204, 226 Intestinal, 194, 203, 211 Intestine, 34, 184, 188, 193, 200, 203, 204 Intoxication, 17, 140, 203, 226 Intracellular, 11, 68, 197, 202, 203, 206, 215, 219 Intramuscular, 203, 211 Intravenous, 203, 211 Intrinsic, 178, 203 Invertebrates, 192, 203, 205 Ionization, 21, 104, 116, 203 Ionizing, 41, 179, 194, 203, 217 Ions, 120, 183, 192, 193, 200, 203 Irradiation, 96, 110, 203, 216, 227 Irrigation, 33, 35, 140, 204 Isocyanates, 19, 204 Isoenzyme, 15, 204 K Kb, 160, 204 Keto, 5, 20, 26, 51, 70, 79, 204 Ketoacidosis, 177, 204 Ketone Bodies, 177, 204 Kinetic, 24, 39, 40, 203, 204 L Labile, 188, 204 Large Intestine, 188, 192, 203, 204, 217 Laxative, 178, 204 Lesion, 11, 16, 87, 204, 205 Lethal, 13, 142, 183, 204, 208

Leukotrienes, 182, 204 Levo, 204, 227 Linkage, 7, 22, 204 Lipid, 20, 42, 96, 98, 111, 114, 116, 147, 193, 198, 203, 204, 205, 211 Lipid A, 147, 205 Lipid Peroxidation, 96, 111, 114, 116, 205, 211 Lipopolysaccharide, 17, 199, 205 Lipoprotein, 199, 205 Liver cancer, 9, 11, 20, 28, 45, 52, 54, 60, 69, 73, 76, 77, 80, 81, 87, 89, 102, 151, 155, 205 Liver Transplantation, 155, 205 Localization, 14, 25, 68, 205 Localized, 17, 155, 202, 205, 213 Locomotion, 205, 213 Locoregional, 155, 205 Longitudinal study, 13, 205 Luminescence, 141, 205 Lymphatic, 202, 205, 221 Lymphatic system, 205, 221 Lymphocytes, 61, 181, 201, 203, 205, 206, 221, 226 Lymphocytic, 59, 65, 206 Lymphoid, 98, 180, 205, 206 Lysine, 30, 57, 76, 86, 132, 143, 200, 206 M Malignancy, 9, 77, 206 Malignant, 177, 181, 205, 206, 209, 217 Malnutrition, 178, 182, 206 Malondialdehyde, 4, 206 Mammary, 10, 206 Mannans, 197, 206 Meat, 80, 110, 145, 206 Mediator, 203, 206, 219 MEDLINE, 161, 206 Megakaryocytes, 184, 206 Meiosis, 206, 207, 222 Melanoma, 206, 225 Membrane, 61, 101, 186, 188, 195, 199, 206, 208, 211, 213, 214, 220, 224 Membrane Lipids, 206, 213 Mental, iv, 3, 160, 162, 192, 206, 214, 216, 219 Mental Disorders, 206, 214 Mental Health, iv, 3, 160, 162, 206, 214, 216 Mental Processes, 192, 206, 216 Mercury, 149, 206 Mesenteric, 207, 214 Meta-Analysis, 64, 207

235

Metabolite, 4, 18, 29, 65, 67, 86, 113, 130, 131, 184, 192, 207 Methanol, 128, 207 Methyltransferase, 28, 40, 207 Microbe, 137, 207, 223 Microbiological, 130, 207 Micronuclei, 71, 102, 207 Microorganism, 188, 207, 212, 226 Microsomal, 18, 70, 78, 82, 83, 87, 95, 96, 108, 111, 116, 151, 178, 207 Microsome, 94, 97, 207 Milk Thistle, 207, 220 Mineralization, 185, 207 Miscible, 131, 207 Mitochondria, 16, 207, 211 Mitochondrial Swelling, 207, 209 Mitosis, 182, 207, 208 Mitosporic Fungi, 182, 207 Mitotic, 70, 208 Modeling, 80, 81, 208 Modification, 197, 208 Molecular, 7, 9, 10, 16, 17, 18, 21, 22, 37, 49, 50, 51, 55, 59, 61, 65, 68, 69, 70, 71, 72, 82, 83, 85, 93, 110, 112, 132, 147, 161, 163, 184, 189, 208, 224 Monitor, 7, 208, 210 Monoclonal, 30, 33, 38, 39, 57, 84, 87, 93, 134, 204, 208, 217, 227 Monoclonal antibodies, 33, 39, 93, 134, 208 Monocrotaline, 17, 208 Monocytes, 66, 208 Mononuclear, 49, 67, 208 Morphological, 38, 193, 197, 208 Morphology, 199, 208 Mucins, 194, 198, 208 Mucosa, 194, 208, 221 Multidrug resistance, 49, 208 Muscle Hypertonia, 208, 209 Mustard Gas, 208 Mutagen, 53, 148, 183, 208 Mutagenesis, 9, 10, 11, 14, 47, 83, 102, 105, 107, 116, 209 Mutagenic, 10, 11, 66, 72, 73, 96, 142, 178, 179, 192, 209 Mutagenicity, 31, 54, 55, 68, 87, 93, 106, 113, 115, 117, 120, 209 Mutate, 11, 209 Mycological, 73, 142, 209 Myeloma, 200, 209 N Natural selection, 183, 209 Necrosis, 18, 181, 195, 198, 209, 221

Nematocide, 195, 209 Neonatal, 15, 209 Neoplasm, 209, 224 Neuromuscular, 17, 209, 218 Neuromuscular Diseases, 17, 209 Neurons, 187, 195, 209, 222 Neurotoxic, 209, 219 Neurotransmitter, 177, 192, 198, 209, 222 Neutralization, 145, 209 Neutrons, 179, 203, 209, 217 Neutrophil, 17, 209 Niacin, 209, 224 Nicotine, 20, 209 Nifedipine, 33, 210 Nitrogen, 71, 73, 179, 210, 224 Nuclear, 16, 189, 193, 195, 197, 209, 210, 221 Nuclei, 179, 189, 193, 197, 200, 207, 209, 210, 216, 223 Nucleic acid, 6, 25, 30, 62, 75, 150, 183, 190, 197, 200, 201, 210, 218 Nucleic Acid Hybridization, 200, 210 Nucleus, 181, 187, 190, 191, 195, 197, 205, 206, 207, 208, 209, 210, 216, 221 Nutritive Value, 19, 132, 196, 210 O Occupational Exposure, 48, 210 Odds Ratio, 210, 218 Oligodeoxyribonucleotides, 42, 210 Oligonucleotide Probes, 23, 210 Oltipraz, 20, 21, 60, 68, 74, 79, 210 Oncogene, 23, 24, 34, 45, 46, 59, 66, 83, 210 Oncogenic, 16, 211 Organelles, 101, 186, 190, 208, 211, 213 Ornithine, 147, 211 Osmotic, 178, 207, 211, 219 Oxidation, 5, 19, 45, 53, 67, 75, 109, 110, 151, 177, 179, 181, 184, 190, 198, 205, 211 Oxidation-Reduction, 184, 211 Oxidative Stress, 7, 108, 211 Oxides, 198, 211 P P53 gene, 4, 61, 73, 76, 79, 211 Palliative, 211, 223 Pancreas, 177, 183, 184, 192, 197, 202, 211, 221, 224 Paneth Cells, 194, 211 Papillary, 200, 211 Parasite, 196, 211 Parasitic, 199, 202, 211 Parenteral, 77, 211 Pathogen, 30, 202, 212

236

Aflatoxin

Pathologic, 182, 201, 212, 216 Pathologic Processes, 182, 212 Peptide, 147, 212, 214, 216, 217, 224 Perennial, 212, 224 Peripheral blood, 52, 58, 203, 212 Peripheral Nervous System, 209, 212, 222 Peripheral Nervous System Diseases, 209, 212 Peritoneal, 30, 69, 212 Peritoneum, 212 Peroxide, 137, 212 Pesticides, 63, 104, 111, 145, 200, 202, 212 Phagocytosis, 30, 212 Pharmaceutic Aids, 196, 212 Pharmacokinetic, 212 Pharmacologic, 212, 223 Phenotype, 14, 15, 189, 212 Phospholipases, 18, 212 Phospholipases A, 18, 212 Phospholipids, 132, 195, 205, 206, 213 Phosphorus, 185, 213 Photosensitivity, 213, 226 Physiologic, 178, 183, 213, 215, 217 Physiology, 85, 88, 96, 98, 197, 213 Pigment, 131, 183, 198, 206, 213 Placenta, 75, 213, 215 Plant Components, 62, 213 Plasma, 7, 17, 49, 76, 178, 180, 186, 199, 209, 213, 219, 226 Plasma cells, 180, 209, 213 Plasma protein, 178, 213, 219 Plasmid, 82, 213, 225 Plastids, 211, 213 Pneumonia, 189, 213 Point Mutation, 17, 213 Poisoning, 67, 75, 185, 203, 207, 213, 219 Pollen, 214, 217 Polymerase, 4, 17, 30, 214, 215 Polymorphic, 14, 214 Polymorphism, 63, 82, 214 Polypeptide, 134, 179, 188, 200, 214, 216 Polyploid, 15, 214 Polyposis, 188, 214 Polysaccharide, 181, 214 Portal Vein, 17, 214 Post-translational, 18, 214 Potentiation, 17, 214 Practice Guidelines, 162, 214 Precancerous, 187, 214 Precursor, 26, 34, 39, 114, 182, 192, 193, 194, 214, 224 Prenatal, 89, 193, 214

Prevalence, 13, 77, 210, 214 Primary Prevention, 21, 214 Probe, 16, 210, 214 Progeny, 10, 31, 189, 215 Progesterone, 215, 221 Progression, 5, 22, 180, 215, 224 Progressive, 187, 193, 209, 215, 224 Promoter, 5, 65, 143, 215 Promotor, 215, 218 Prone, 4, 215 Prophylaxis, 11, 215, 218, 225 Prospective study, 205, 215 Prostaglandin, 110, 215, 223 Prostaglandins A, 215 Prostate, 183, 215, 224 Protein C, 178, 179, 187, 205, 215, 216, 225 Protein Conformation, 179, 216 Protein S, 18, 30, 107, 184, 197, 216 Proteolytic, 188, 216 Protons, 179, 200, 203, 216, 217 Protozoa, 37, 183, 189, 207, 216, 221 Pruritic, 193, 216 Psoriasis, 208, 216, 218 Psychoactive, 216, 223, 226 Psychology, 192, 216 Public Health, 19, 57, 76, 94, 99, 106, 148, 162, 183, 216 Public Policy, 161, 216 Publishing, 23, 216 Pulmonary, 78, 85, 115, 184, 204, 208, 216, 222, 225 Pulmonary Artery, 184, 208, 216, 226 Pulse, 24, 39, 208, 216 Pyrimidine Dimers, 17, 216 Q Quercetin, 105, 217 Quinoxaline, 6, 217 R Radiation, 34, 41, 55, 96, 141, 150, 189, 194, 195, 196, 197, 201, 203, 217, 225, 226 Radiation therapy, 195, 203, 204, 217, 226 Radioactive, 191, 200, 202, 203, 204, 208, 210, 211, 217, 226 Radioimmunoassay, 56, 151, 217 Radioisotope, 210, 217 Radiolabeled, 204, 217, 227 Radiotherapy, 184, 204, 217, 227 Randomized, 9, 193, 217 Ras gene, 61, 217 Reagent, 8, 217 Receptor, 119, 177, 181, 192, 217, 219 Recombinant, 5, 10, 75, 82, 217, 225

237

Recombination, 29, 63, 70, 189, 217 Rectum, 181, 188, 192, 196, 197, 204, 215, 217 Recurrence, 187, 217 Red blood cells, 194, 217, 219 Reductase, 5, 51, 52, 70, 218 Refer, 1, 137, 185, 188, 205, 209, 218, 224 Refraction, 218, 220 Regimen, 193, 218 Relative risk, 81, 177, 218 Respiration, 185, 208, 218 Respiratory Paralysis, 177, 218, 219 Response Elements, 5, 218 Retinoids, 22, 218 Reversion, 218, 225 Ribonucleic acid, 30, 218 Rigidity, 213, 218 Risk factor, 6, 9, 12, 13, 14, 151, 155, 215, 218 Rod, 183, 196, 218 Rodenticides, 212, 218 Ruminants, 131, 198, 218 Rutin, 217, 218 S Saponins, 117, 219, 221 Saxitoxin, 53, 219 Scatter, 219, 225 Schizoid, 219, 226 Schizophrenia, 219, 226 Schizotypal Personality Disorder, 219, 226 Screening, 34, 37, 42, 79, 82, 104, 118, 134, 187, 219 Sebaceous, 219, 226 Segregation, 217, 219 Selenium, 49, 96, 105, 219 Sequence Analysis, 61, 219 Serologic, 201, 219 Serology, 12, 219 Serotonin, 209, 219, 224 Serum Albumin, 51, 57, 66, 86, 217, 219 Side effect, 133, 178, 219, 223 Silymarin, 109, 114, 207, 220 Skeletal, 5, 208, 220 Skeleton, 215, 220 Smallpox, 220, 225 Smooth muscle, 179, 180, 208, 220, 222 Sodium, 29, 42, 56, 106, 220 Soft tissue, 184, 220 Solvent, 19, 131, 137, 146, 148, 177, 187, 192, 194, 198, 207, 211, 220 Somatic, 193, 206, 207, 212, 220 Sorbic Acid, 43, 220

Spasm, 209, 220 Spasticity, 182, 220 Specialist, 167, 220 Specificity, 10, 24, 41, 56, 82, 83, 125, 178, 179, 220 Spectroscopic, 51, 220 Spectrum, 10, 26, 67, 83, 93, 141, 150, 190, 220, 222 Sperm, 187, 214, 221 Spheroplasts, 118, 221 Spinal cord, 182, 186, 187, 212, 218, 221 Spleen, 134, 200, 205, 221 Splenic Vein, 214, 221 Spores, 30, 35, 146, 202, 221 Stabilization, 4, 221 Staging, 155, 221 Steatosis, 195, 221 Sterigmatocystin, 24, 26, 28, 29, 32, 36, 40, 51, 53, 75, 114, 126, 138, 221 Sterility, 202, 221 Steroid, 20, 58, 189, 219, 221 Stimulus, 195, 221 Stomach, 10, 12, 177, 192, 194, 197, 200, 218, 221 Stool, 188, 204, 221 Strand, 4, 11, 188, 214, 221 Streptomyces, 143, 221, 224 Stress, 5, 140, 185, 189, 211, 221 Stroke, 12, 160, 221 Stromal, 184, 221 Stromal Cells, 184, 221 Subacute, 135, 202, 222 Subclinical, 202, 222 Subcutaneous, 211, 222 Subspecies, 220, 222, 225 Substance P, 137, 207, 222 Substrate, 8, 39, 121, 142, 194, 222 Suction, 196, 222 Sulfamethazine, 61, 222 Sulfur, 131, 145, 198, 222 Sulfur Dioxide, 131, 145, 222 Supplementation, 94, 105, 106, 107, 109, 111, 222 Suppression, 10, 65, 84, 105, 129, 131, 222 Supraspinal, 182, 222 Surfactant, 147, 222 Synaptic, 209, 210, 222 Synaptic Transmission, 210, 222 Synergistic, 7, 10, 34, 85, 222 Systemic, 10, 85, 155, 184, 202, 204, 217, 222, 225, 226 Systemic therapy, 155, 222

238

Aflatoxin

T Telophase, 207, 223 Teratogenic, 142, 178, 179, 223 Teratogens, 134, 223 Terminator, 188, 223 Testosterone, 218, 223 Tetrahydrocannabinol, 88, 223 Therapeutics, 8, 51, 54, 87, 223 Thermal, 192, 209, 223 Threonine, 147, 223 Thrombosis, 216, 221, 223 Thromboxanes, 182, 223 Thyroxine, 178, 223 Ticks, 202, 223 Tolerance, 54, 177, 223 Tolnaftate, 35, 223 Tooth Preparation, 177, 223 Topical, 182, 192, 194, 200, 223 Toxic, iv, 5, 14, 17, 19, 20, 24, 45, 70, 87, 120, 128, 129, 131, 132, 133, 134, 135, 136, 138, 142, 148, 151, 178, 179, 187, 189, 190, 194, 198, 199, 207, 208, 209, 219, 222, 223, 224 Toxicity, 15, 18, 44, 57, 69, 88, 92, 98, 99, 106, 120, 129, 131, 135, 138, 142, 193, 207, 223, 227 Toxicokinetics, 223 Toxin, 4, 16, 19, 43, 119, 129, 131, 135, 137, 139, 140, 142, 148, 178, 194, 223, 224 Transcription Factors, 84, 218, 224 Transfection, 184, 224 Transferases, 20, 54, 56, 63, 78, 79, 224 Transfusion, 199, 224 Translational, 224 Trauma, 209, 224 Trees, 145, 224 Trichothecenes, 37, 154, 224 Trifluoroacetic Acid, 128, 224 Tryptophan, 55, 188, 219, 224 Tumor marker, 183, 224 Tumor model, 10, 224 Tumor suppressor gene, 4, 14, 15, 22, 23, 48, 53, 211, 224 Tumour, 46, 104, 224 Tunicamycin, 5, 224 Typhimurium, 4, 66, 70, 87, 225

U Ultraviolet radiation, 145, 225 Urea, 211, 225 Urethra, 215, 225 Urinary, 6, 7, 21, 45, 54, 67, 72, 76, 78, 82, 88, 89, 125, 225 Urine, 6, 9, 12, 21, 22, 25, 54, 57, 64, 72, 79, 82, 84, 94, 99, 184, 204, 225 V Vaccination, 225 Vaccine, 225 Vaccinia, 33, 62, 225 Vaccinia Virus, 33, 62, 225 Vacuoles, 211, 225 Variola, 225 Vascular, 93, 179, 202, 213, 225 Vasodilator, 192, 210, 225 Vector, 12, 69, 83, 225 Vegetative, 214, 225 Vein, 203, 210, 214, 221, 225 Venous, 216, 225 Ventricle, 216, 225, 226 Ventricular, 208, 226 Venules, 184, 185, 226 Vesicular, 207, 220, 225, 226 Veterinary Medicine, 92, 93, 98, 161, 226 Viral, 13, 23, 25, 54, 75, 149, 211, 226 Viral Load, 13, 226 Viremia, 13, 226 Virulence, 223, 226 Vitro, 32, 226 Vivo, 10, 18, 110, 226 Vulgaris, 123, 226 W White blood cell, 180, 202, 205, 206, 209, 213, 226 Withdrawal, 95, 226 X Xenograft, 180, 224, 226 Xeroderma Pigmentosum, 55, 82, 226 X-ray, 186, 196, 197, 203, 208, 210, 217, 226 X-ray therapy, 204, 226 Y Yeasts, 197, 212, 227 Z Zearalenone, 37, 42, 88, 227 Zebrafish, 22, 227 Zygote, 189, 227

239

240

Aflatoxin

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