Biochemical analysis of damage induced in yeast by formaldehyde I. Induction of single-strand breaks in DNA and their repair

Magaña‐Schwencke, Nieve; Ekert, B.; Moustacchi, E.

doi:10.1016/0027-5107(78)90023-4

Cited by 47 publications

(10 citation statements)

References 18 publications

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“…The formaldehyde-induced SSBs appear to be NER-dependent as the breaks do not accumulate post-formaldehyde exposure in rad4Δ or rad1Δ strains, suggesting that these SSBs are intermediates generated during the repair process. These results are consistent with a previous report showing a Rad3-dependent accumulation of SSBs following formaldehyde exposure [20]. PFGE analyses also suggest that some SSBs may be dependent on the presence of Mre11 (Supplementary Fig.…”

Section: Discussionsupporting

confidence: 93%

Cellular pathways for DNA repair and damage tolerance of formaldehyde-induced DNA-protein crosslinks

2009

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Although it is well established that DNA-protein crosslinks are formed as a consequence of cellular exposure to agents such as formaldehyde, transplatin, ionizing and ultraviolet radiation, the biochemical pathways that promote cellular survival via repair or tolerance of these lesions are poorly understood. To investigate the mechanisms that function to limit DNA-protein crosslink-induced cytotoxicity, the Saccharomyces cerevisiae non-essential gene deletion library was screened for increased sensitivity to formaldehyde exposure. Following low-dose, chronic exposure, strains containing deletions in genes mediating homologous recombination showed the greatest sensitivity, while under the same exposure conditions, deletions in genes associated with nucleotide excision repair conferred only low to moderate sensitivities. However, when the exposure regime was changed to a high-dose acute (short-term) formaldehyde treatment, the genes that conferred maximal survival switched to the nucleotide excision repair pathway, with little contribution of the homologous recombination genes. Data are presented which suggest that following acute formaldehyde exposure, repair and/or tolerance of DNA-protein crosslinks proceeds via formation of nucleotide excision repair-dependent single-strand break intermediates and without a detectable accumulation of doublestrand breaks. These data clearly demonstrate a differential pathway response to chronic versus acute formaldehyde exposures and may have significance and implications for risk extrapolation in human exposure studies.

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Section: Discussionsupporting

confidence: 93%

Cellular pathways for DNA repair and damage tolerance of formaldehyde-induced DNA-protein crosslinks

2009

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“…The same is true for excision-repair deficient mutants of Saccharomyces cerevisiae (74). In addition, more pronounced genetic effects of formaldehyde were found with cell lines of Xeroderma pigmentosum as compared with normal human fibroblasts in culture (75 ments, dose-response relationships could only be demonstrated with difficulty or not at all, and all data are consistent with the classification of formaldehyde as a weak mutagen. Formaldehyde has been shown to interact with other mutagens such as x-rays, ultraviolet radiation and hydrogen peroxide, and to at least double the frequencies of mutants expected from treatment with these agents.…”

Section: Formaldehydesolutions Early Experiments Insupporting

confidence: 68%

Report of the Federal Panel on Formaldehyde

1982

Environmental Health Perspectives

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The Federal Panel on Formaldehyde concluded that definitive experiments exist which demonstrate the mutagenicity and carcinogenicity of formaldehyde under laboratory conditions. Formaldehyde induces both gene mutations and chromosomal aberrations in a variety of test systems. Inhalation of formaldehyde causes cancer of the nose in rats. The concentrations of formaldehyde in inhaled air that caused nasal cancer in Fisher 344 rats are within the same order of magnitude as those to which humans may be exposed. The data presently available do not permit a direct assessment of the carcinogenicity of formaldehyde to man. Epidemiologic studies on exposed human populations are in progress and may further clarify the situation. Other experimental and human studies on toxic effects such as teratogenicity and reproductive disorders are as yet inadequate for a health risk assessment.The CIIT 24 month study on animal carcinogenicity has not yet been completely evaluated. Additional data are expected on the effects of prolonged exposure to lower doses of formaldehyde and on the possible carcinogenicity of formaldehyde in the mouse. The panel recommends that, for a comprehensive health risk assessment, further experiments be conducted on the effects of other modes of exposure (ingestion and skin penetration), the effects in humans, and on the pharmacokinetics of formaldehyde in man and animals and the possible role for formaldehyde in reproductive and chronic respiratory disorders.It is the conclusion of the panel that formaldehyde should be presumed to pose a carcinogenic risk to humans.

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“…furmaldehyde has been Shown to induce 0355-3140/81/020095-6 single-strand breaks in DNA (deoxyribonuCleic acid) of both prokaryotic a!Ild eucaryotic cells (11,16 (18). Tumors were suggested to be due to the formation of bis(chloromethyl)ether, a known agent causing nasal cancer (9).…”

Section: Carcinogenicity Of Formaldehydementioning

confidence: 99%

Formaldehyde exposure in work and the general environment. Occurrence and possibilities for prevention.

Niemelä¹,

Vainio²

1981

Scand J Work Environ Health

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Biochemical analysis of damage induced in yeast by formaldehyde I. Induction of single-strand breaks in DNA and their repair

Cited by 47 publications

References 18 publications

Cellular pathways for DNA repair and damage tolerance of formaldehyde-induced DNA-protein crosslinks

Cellular pathways for DNA repair and damage tolerance of formaldehyde-induced DNA-protein crosslinks

Report of the Federal Panel on Formaldehyde

Formaldehyde exposure in work and the general environment. Occurrence and possibilities for prevention.

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