DNA adducts and P450 induction in human, rat and avian liver cells after exposure to polychlorobiphenyls

Dubois, Michel; Pfohl‐Leszkowicz, Annie; Grosse, Yann; Kremers, Pierre

doi:10.1016/0165-1218(95)90053-5

Cited by 48 publications

(26 citation statements)

References 38 publications

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“…If not repaired, DSBs may result in loss of chromosomes and/or 74 cell death, mutations, chromosomal rearrangements (Thacker, 1986;Jackson, 1999) and 75 carcinogenesis (Jeggo, 1998;Kanaar et al, 1998;Pfeiffer, 1998). 76 Dubois et al (1995) have shown that, when exposed in vitro, PCBs caused genotoxic 77 effects on avian cells. Also, gel electrophoresis has been applied to study DSBs after 78 genotoxic exposure in glaucous gulls (Larus hyperboreus) (Krøkje et al, 2006) and in fish 79 blood cells (Theodorakis et al, 1994).…”

Section: Introduction 50mentioning

confidence: 99%

DNA double-strand breaks in relation to persistent organic pollutants in a fasting seabird

Fenstad

Jenssen

Moe

et al. 2014

Ecotoxicology and Environmental Safety

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Section: Introduction 50mentioning

confidence: 99%

DNA double-strand breaks in relation to persistent organic pollutants in a fasting seabird

Fenstad

Jenssen

Moe

et al. 2014

Ecotoxicology and Environmental Safety

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“…An increase in the frequency of DNA adducts (detected by 32 P-postlabelling) was observed in primary human hepatocytes from three different donors (Borlak et al, 2003), but not in cultured human hepatocarcinoma HepG2 cells or dexamethasone-treated primary rat fetal hepatocytes (Dubois et al, 1995). A dose-dependent increase in structural chromosomal aberration starting at concentrations of less than 1 µg/mL was seen in cultured human lymphocytes (Sargent et al, 1989).…”

mentioning

confidence: 80%

“…In human lymphocytes, PCB-77 induced structural chromosomal aberration, but no increase in the frequency of micronucleated cells and sister-chromatid exchange was observed (Sargent et al, 1989;Dubois et al, 1995;Belpaeme et al, 1996b).…”

Section: Pcb-28 Pcb-52 Pcb-77mentioning

confidence: 99%

Polychlorinated Biphenyls and Polybrominated Biphenyls

Agudo

Aronson²,

Bonefeld-Jörgensen³

et al. 2008

Organic Pollutants

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initiated a programme on the evaluation of the carcinogenic risk of chemicals to humans involving the production of critically evaluated monographs on individual chemicals. The programme was subsequently expanded to include evaluations of carcinogenic risks associated with exposures to complex mixtures, lifestyle factors and biological and physical agents, as well as those in specific occupations. The objective of the programme is to elaborate and publish in the form of monographs critical reviews of data on carcinogenicity for agents to which humans are known to be exposed and on specific exposure situations; to evaluate these data in terms of human risk with the help of international working groups of experts in carcinogenesis and related fields; and to indicate where additional research efforts are needed. The lists of IARC evaluations are regularly updated and are available on the Internet at http:// monographs.iarc.fr/.This programme has been supported since 1982 by Cooperative Agreement U01 CA33193 with the United States National Cancer Institute, Department of Health and Human Services. Additional support has been provided since 1986 by the European Commission Directorate-General for Employment, Social Affairs, and Inclusion, initially by the Unit of Health, Safety and Hygiene at Work, and since 2014 by the European Union Programme for Employment and Social Innovation "EaSI" (2014-2020) The International Agency for Research on Cancer welcomes requests for permission to reproduce or translate its publications, in part or in full. Requests for permission to reproduce or translate IARC publications -whether for sale or for non-commercial distribution -should be addressed to the IARC Communications Group at: publications@iarc.fr.The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the Secretariat of the World Health Organization concerning the legal status of any country, territory, city, or area or of its authorities, or concerning the delimitation of its frontiers or boundaries.The mention of specific companies or of certain manufacturers' products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.The IARC Monographs Working Group alone is responsible for the views expressed in this publication. IARC Library Cataloguing in Publication Data NOTE TO THE READERThe term 'carcinogenic risk' in the IARC Monographs series is taken to mean that an agent is capable of causing cancer. The Monographs evaluate cancer hazards, despite the historical presence of the word 'risks' in the title.Inclusion of an agent in the Monographs does not imply that it is a carcinogen, only that the published data have been examined. Equally, the fact that an agent has not yet been evaluated in a Monograph does not mean that...

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“…Indeed, a study examining retention of PCBs in rats after oral application found hydroxylated PCB metabolites in both, the lungs and livers (Bergman et al, 1994). Such activated biphenyls may result in the formation of DNA adducts and subsequently DNA damage (Dubois et al, 1995;Wong et al, 1979), a mechanism that could result in cancer initiation.…”

Section: Introductionmentioning

confidence: 99%

Mutagenicity of 3-methylcholanthrene, PCB3, and 4-OH-PCB3 in the lung of transgenic BigBlue® rats

Maddox

Wang

Kirby

et al. 2008

Environmental Toxicology and Pharmacology

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Recent findings of high levels of predominantly lower chlorinated biphenyls in indoor and outdoor air open the question of possible health consequences. Lower chlorinated biphenyls are more readily metabolized to reactive and potentially harmful intermediates, acting as mutagens and cancer initiators. The goal of this study was to assess the mutagenicity of PCB3 in the lungs of rats. Male BigBlue® 334 Fisher transgenic rats, which carry the bacterial lacI gene as a target of mutagenicity, were given intraperitoneal injections of corn oil, 3-methylcholanthrene (3-MC, positive control), 4-monochlorobiphenyl (PCB3) or its metabolite 4-hydroxy-PCB3 (4-OH-PCB3) weekly for 4 weeks. Lungs tissue was harvested to determine mutant frequencies, mutation spectra, and pathological changes. 3-MC caused a 15-fold increase in mutant frequency and an increase in transversion type mutations; a very early occurrence of this type of mutation in lung tissue was previously identified in Ki-ras oncogenes of lung tumors from 3-MC exposed mice. The 2-fold increase in the mutant frequency after treatment with PCB3 and 4-OH-PCB3 was not statistically significant, but a shift in the mutation spectra, especially with PCB3, and an increase in mutations outside of the hotspot region for spontaneous mutations (bp 1-400), suggest that PCB3 and possibly 4-OH-PCB3 are mutagenic in the rat lung.

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DNA adducts and P450 induction in human, rat and avian liver cells after exposure to polychlorobiphenyls

Cited by 48 publications

References 38 publications

DNA double-strand breaks in relation to persistent organic pollutants in a fasting seabird

DNA double-strand breaks in relation to persistent organic pollutants in a fasting seabird

Polychlorinated Biphenyls and Polybrominated Biphenyls

Mutagenicity of 3-methylcholanthrene, PCB3, and 4-OH-PCB3 in the lung of transgenic BigBlue® rats

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