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Enhanced Metabolism and Mutagenesis of Nitrosopyrrolidine in Liver Fractions Isolated from Chronic Ethanol-consuming Hamsters¹

Naylor Dana Institute for Disease Prevention, American Health Foundation [G. D. M., C. B. C., S. S. H.], and Department of Microbiology, New York Medical College [E. C. M.], Valhalla, New York 10595

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 -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 -hydroxylation of NPY is probably the mechanism by which NPY is converted to a mutagen and that this pathway can be induced by ethanol.

¹ Supported by National Cancer Institute Grants CA-012376 and RR 05775.

² To whom requests for reprints should be addressed.

Received 6/30/78. Accepted 11/21/78.