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

Patricia L. Foster, Wells G. Wilkinson, Judith K. Miller, Amy D. Sullivan, Wane M. Barnes

Research output: Contribution to journalArticle

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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.

Original languageEnglish
Pages (from-to)171-181
Number of pages11
JournalMutation Research DNA Repair Reports
Volume194
Issue number3
DOIs
StatePublished - Nov 1988

Keywords

  • DNA repair
  • Dibromoethane
  • EDB
  • Escherichia coli
  • Miscoding lesions

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