Enhanced metabolism and mutagenesis of nitrosopyrrolidine in liver fractions isolated from chronic ethanol-consuming hamsters.
The effect of chronic ethanol consumption on the ability of isolated liver fractions to metabolize the carcinogen N-nitrosopyrrolidine (NPY) was examined. Microsomal fractions of treated animals exhibited increased rates of alpha-hydroxylation of NPY. Similar increases in the specific activities of aniline hydroxylase, reduced nicotinamide adenine dinucleotide phosphate cytochrome c reductase, and the specific content of cytochrome P-450 were also observed. In contrast, no differences in the specific activities of benzo(a)pyrene hydroxylase or glucose-6-phosphatase were observed. Liver postmitochondrial supernatants from ethanol-consuming animals were able to produce 5 times more mutants than did control preparations. It is concluded that alpha-hydroxylation of NPY is probably the mechanism by which NPY is converted to a mutagen and that this pathway can be induced by ethanol.
D000437:Alcoholism / Q000150:complications / Q000378:metabolism*; D000818:Animals; D001711:Biotransformation; D006224:Cricetinae; D006801:Humans; D006900:Hydroxylation; D066298:In Vitro Techniques; D008297:Male; D008647:Mesocricetus; D008862:Microsomes, Liver / Q000378:metabolism*; D009153:Mutagens / Q000378:metabolism*; D009242:N-Nitrosopyrrolidine / Q000378:metabolism* / Q000494:pharmacology; D009369:Neoplasms / Q000209:etiology; D009602:Nitrosamines / Q000378:metabolism*
D009153:Mutagens; D009602:Nitrosamines; D009242:N-Nitrosopyrrolidine