DNA Damage, Repair, and Mutation Induction by (+)-
 Syn
 and (−)-
 Anti
 -Dibenzo[
 a,l
 ]Pyrene-11,12-Diol-13,14-Epoxides in Mouse Cells

Yoon, Jung Hoon; Besaratinia, Ahmad; Feng, Zhaohui; Tang, Moon Shong; Amin, Shantu; Luch, Andreas; Pfeifer, Gerd P.

doi:10.1158/0008-5472.can-04-1094

Cited by 38 publications

(36 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been shown that methylation of cytosines at CpG dinucleotides enhances the extent of acrolein binding to guanines in synthetically generated human p53 DNA fragments (17) (48). Briefly, the pSP189 plasmid was methylated in vitro using the SssI methylase (New England Biolabs) according to the manufacturer's instructions.…”

Section: Cancer Researchmentioning

confidence: 99%

Lack of Mutagenicity of Acrolein-Induced DNA Adducts in Mouse and Human Cells

2007

Self Cite

View full text Add to dashboard Cite

Acrolein is an endogenous metabolite and a ubiquitous environmental pollutant. Recently, it has been suggested that acrolein is a major etiologic agent for tobacco smokingrelated lung cancer. Despite the known DNA-damaging effects of acrolein, its mutagenicity to mammalian cells remains uncertain. We have investigated acrolein-induced DNA damage in relation to mutagenesis, with special focus on DNA repair, in mouse and human cells. We mapped the formation of acrolein-induced DNA adducts and the kinetics of repair of the induced lesions in the cII transgene, the mutational target, in acrolein-treated transgenic mouse fibroblasts. Acrolein-DNA adducts were formed preferentially at specific nucleotide positions, mainly at G:C base pairs, along the cII transgene. The induced acrolein-DNA adducts were moderately resistant to DNA repair. Quantification of cII mutant frequency in acrolein-treated cells, however, revealed that acrolein was not mutagenic to these cells at doses sufficient to produce DNA adducts. Determination of supF mutant frequency in DNA repair-proficient and DNA repair-deficient human fibroblasts transfected with acrolein-treated plasmids confirmed a lack of acrolein mutagenicity. Because CpG methylation may intensify acrolein-DNA adduction, we examined whether the extent of CpG methylation in the supF gene can determine acroleininduced mutagenesis in human cells. Enhancement of acrolein-DNA adduction by methylating CpGs in the supF sequence did not elicit a mutagenic response in human fibroblasts, however. We conclude that acrolein is not mutagenic to mouse and human fibroblasts, regardless of DNA repair capacity or methylation status of CpGs, possibly because of a highly accurate replication bypass of the induced lesions. [Cancer Res 2007;67(24):11640-7]

show abstract

Section: Cancer Researchmentioning

confidence: 99%

Lack of Mutagenicity of Acrolein-Induced DNA Adducts in Mouse and Human Cells

2007

Self Cite

View full text Add to dashboard Cite

show abstract

“…Dibenzo[a,l]pyrene, one of the fjord region compounds, has been demonstrated to be the most carcinogenic PAH [19]. Also benzo[c]chrysene possesses both a bay region and a fjord region in the same molecule.…”

Section: Polycyclic Aromatic Hydrocarbonsmentioning

confidence: 99%

Impact of Environmental Contaminants on Breast Cancer / Wpływ Zanieczyszczenia Środowiska Na Raka Piersi

Kráľová

Jampílek

2015

Ecological Chemistry and Engineering S

View full text Add to dashboard Cite

Breast cancer is the most frequent cancer in women. It is believed that among the causes of breast cancer, hereditary factors account for only 5-10% of risk and the environmental exposures to environmental contaminants account for an additional 30-50% of risk. This paper summarizes findings related to the risk of breast cancer due to exposure to following environmental contaminants: polycyclic aromatic hydrocarbons, polychlorinated biphenyls and dioxins, organochlorine pesticides, organophosphorous pesticides, bisphenol A, phthalates, parabens, organic solvents, atmospheric pollutants, alkylphenols, metals, ionizing radiation, electromagnetic field and light pollution. Results obtained in in vitro experiments with breast cancer cell lines and in vivo with model rodents as well as in population based case-control studies are presented and the mode of action of individual environmental contaminants on mammary gland is discussed. Attention is also devoted to the effects of the timing of exposure to environmental contaminants (mainly exposition during development of the mammary gland) on breast cancer risk. Outcomes of professional exposure to some environmental contaminants on breast cancer risk are analysed as well.

show abstract

“…Dibenzo [a,l]pyrene induced morphological cell transformation in mouse embryo fibroblast C3H10T½Cl8 cells and was more active than benzo [a]pyrene . Dibenzo [a,l]pyrene induced mutations in the cII locus of Big-Blue mouse embryonic fibroblasts (Yoon et al, 2004).…”

Section: Cyp1b1mentioning

confidence: 99%

Integrating Field Analyses with Laboratory Exposures to Assess Ecosystems Health

Hellou¹,

Beach²,

Leonard³

et al. 2012

Polycyclic Aromatic Compounds

View full text Add to dashboard Cite

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, life-style 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 chemical carcinogenesis Publications of the World Health Organization enjoy copyright protection in accordance with the provisions of Protocol 2 of the Universal Copyright Convention. All rights reserved.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 noncommercial distribution -should be addressed to WHO Press, at the above address (fax: +41 22 791 4806; email: permissions@who.int).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 under some circumstances. 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 it is not carcinogenic.The evaluations of carcinogenic risk are made by international working groups of independent scientists and are qualitative in nature. No recommendation is given for regulation or legislation.Anyone who is aware of published data that may alter the evaluation of the carcinogenic risk of an agent to humans is encouraged to make this information available to the Section of IARC Monographs, International Agency for...

show abstract

DNA Damage, Repair, and Mutation Induction by (+)- Syn and (−)- Anti -Dibenzo[ a,l ]Pyrene-11,12-Diol-13,14-Epoxides in Mouse Cells

Abstract: ABSTRACT

Cited by 38 publications

References 45 publications

Lack of Mutagenicity of Acrolein-Induced DNA Adducts in Mouse and Human Cells

Lack of Mutagenicity of Acrolein-Induced DNA Adducts in Mouse and Human Cells

Impact of Environmental Contaminants on Breast Cancer / Wpływ Zanieczyszczenia Środowiska Na Raka Piersi

Integrating Field Analyses with Laboratory Exposures to Assess Ecosystems Health

Contact Info

Product

Resources

About