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PMID: 3054522 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

An analysis of the mutagenicity of 1,2-dibromoethane to Escherichia coli: influence of DNA repair activities and metabolic pathways.

Mutation research ·Vol. 194 ·No. 3 ·1988-11-00 ·Pages 171-81

Foster PL, Wilkinson WG, Miller JK, Sullivan AD, Barnes WM

Abstract

The mutagenicity of 1,2-dibromoethane (EDB) to Escherichia coli was reduced by the UV light-induced excision repair system but unaffected by the loss of a major apurinic/apyrimidinic site repair function. At high doses, 70-90% of the EDB-induced mutations were independent of SOS-mutagenic processing and approximately 50% were independent of glutathione conjugation. The SOS-independent mutations induced by EDB were unaffected by the enzymes that repair alkylation-induced DNA lesions. EDB-induced base substitutions were dominated by GC to AT and AT to GC transitions. These results suggest that EDB-induced premutagenic lesions have some, but not all, of the characteristics of simple alkyl lesions.

MeSH Terms
Biotransformation DNA Repair Escherichia coli/drug effects,genetics Ethylene Dibromide/toxicity Hydrocarbons, Brominated/toxicity In Vitro Techniques Microsomes, Liver/metabolism Mutagenicity Tests Mutation/drug effects SOS Response, Genetics
Chemicals
Hydrocarbons, Brominated Ethylene Dibromide
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Foster P L
Division of Environmental Health, Boston University School of Public Health, Boston University School of Medicine, MA 02118.
Wilkinson W G
Miller J K
Sullivan A D
Barnes W M
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Article Info
Journal
Mutation research
Abbr.
Mutat Res
ISSN
0027-5107
Published
1988-11-00
Pages
171-81
Language
English
Region
Netherlands
NLM ID
0400763
PMCID
PMC2988426
Subset
IM
Grants
NCI NIH HHS · R01 CA037880 · United States
NCI NIH HHS · R01 CA037880-08 · United States
NIGMS NIH HHS · GM24956 · United States
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