Metabolic activation of 2-acetylaminofluorene by isolated rat liver cells. Involvement of different metabolites causing DNA-repair and bacterial mutagenesis.
Isolated rat liver cells are able to metabolize 2-acetylaminofluorene (2-AAF) to reactive species, capable of producing mutagenic effects in Salmonella typhimurium TA 1518 and evoking unscheduled DNA synthesis within the hepatocytes. Indications are presented, that these genotoxic effects are caused by different reactive metabolites. Mutagenesis could be blocked almost completely by paraoxon, an inhibitor of the de-acetylation reaction, whereas induction of DNA excision repair was prevented by antagonizing the sulfation reaction by means of salicylamide.
D015073:2-Acetylaminofluorene / Q000378:metabolism* / Q000633:toxicity; D000818:Animals; D001419:Bacteria / Q000235:genetics*; D001711:Biotransformation; D004260:DNA Repair / Q000187:drug effects*; D008099:Liver / Q000378:metabolism*; D008297:Male; D009153:Mutagens; D010261:Paraoxon / Q000494:pharmacology; D051381:Rats; D012457:Salicylamides / Q000378:metabolism; D012486:Salmonella typhimurium / Q000235:genetics; D013936:Thymidine / Q000378:metabolism
D009153:Mutagens; D012457:Salicylamides; D015073:2-Acetylaminofluorene; D010261:Paraoxon; D013936:Thymidine