An analysis of the mutagenicity of 1,2-dibromoethane to Escherichia coli: influence of DNA repair activities and metabolic pathways.
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.
Foster
P L
PL
Division of Environmental Health, Boston University School of Public Health, Boston University School of Medicine, MA 02118.
Wilkinson
W G
WG
Miller
J K
JK
Sullivan
A D
AD
Barnes
W M
WM
D001711:Biotransformation; D004260:DNA Repair; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics; D015946:Ethylene Dibromide / Q000633:toxicity*; D006842:Hydrocarbons, Brominated / Q000633:toxicity*; D066298:In Vitro Techniques; D008862:Microsomes, Liver / Q000378:metabolism; D009152:Mutagenicity Tests; D009154:Mutation / Q000187:drug effects*; D013014:SOS Response, Genetics
D006842:Hydrocarbons, Brominated; D015946:Ethylene Dibromide