5-Nitroacenaphthene: a newly recognized role for the nitro function in mutagenicity.
The direct-acting mutagenicity of 5-nitroacenaphthene for Salmonella typhimurium is dependent upon the reduction of the nitro function as evidenced by the significant decrease in mutagenicity seen with nitroreductase-deficient Salmonella strains. Addition of microsomal preparations results in a significant increase in mutagenicity and a by-passing of the block in nitroreductase-deficient and arylhydroxylamine esterifying-deficient enzyme strains. The results are taken to indicate that the microsome-induced mutagenicity is due primarily to oxidation of the acenaphthene moiety. The results are consistent with recent studies which indicate that the nitro function exercises a directing effect on ring oxidation.
D000073:Acenaphthenes / Q000494:pharmacology*; D000217:Acyltransferases / Q000502:physiology; D000818:Animals; D008862:Microsomes, Liver / Q000201:enzymology; D009152:Mutagenicity Tests; D009153:Mutagens / Q000494:pharmacology*; D009574:Nitro Compounds / Q000494:pharmacology*; D009601:Nitroreductases; D010084:Oxidation-Reduction; D010088:Oxidoreductases / Q000502:physiology; D051381:Rats; D012486:Salmonella typhimurium / Q000187:drug effects / Q000201:enzymology
D000073:Acenaphthenes; D009153:Mutagens; D009574:Nitro Compounds; D010088:Oxidoreductases; D009601:Nitroreductases; D000217:Acyltransferases; C036672:arylhydroxylamine esterifying enzyme; C033999:5-nitroacenaphthene