The combined action of chemical carcinogens on DNA repair in human cells.
Excision repair was studied in normal human and ataxia telangiectasia (AT) cells proficient in repair of UV and its mimetic chemicals, and in xeroderma pigmentosum group C (XP C) cells (deficient in repair of UV and its mimetics), after treatment with several combinations of chemical carcinogens, by the photolysis of bromodeoxyuridine incorporated into parental DNA during repair. Results indicate that repair was additive in AT, and XP C cells treated with N-acetoxy-2-acetylaminofluorene (AAAF) plus ethyl methanesulfonate (EMS) or methyl methanesulfonate (MMS) indicating that there are different rate limiting steps for removal of both types of damage. Data on the combinations of 4-nitroquinoline 1-oxide (4NQO) plus MMS or EMS are difficult to interpret, but they do not indicate inhibition of DNA repair.
D015073:2-Acetylaminofluorene / Q000494:pharmacology; D015112:4-Nitroquinoline-1-oxide / Q000494:pharmacology; D001973:Bromodeoxyuridine / Q000378:metabolism; D002273:Carcinogens / Q000494:pharmacology*; D002478:Cells, Cultured; D004260:DNA Repair / Q000187:drug effects* / Q000528:radiation effects; D005020:Ethyl Methanesulfonate / Q000494:pharmacology; D005347:Fibroblasts / Q000187:drug effects; D006801:Humans; D008741:Methyl Methanesulfonate / Q000494:pharmacology; D010777:Photochemistry; D014466:Ultraviolet Rays
D002273:Carcinogens; D015112:4-Nitroquinoline-1-oxide; D005020:Ethyl Methanesulfonate; D015073:2-Acetylaminofluorene; D008741:Methyl Methanesulfonate; D001973:Bromodeoxyuridine