The effect of chronic alcohol intake upon the hepatic microsomal carcinogen-activation system

Ethanol was administered to mice either by repeated intraperitoneal injection, or orally in the drinking water over an extended period of time. Following intraperitoneal ethanol pre-treatment further groups of mice received an injection of benzo(a)pyrene. Alcohol intake decreased the level of microsomal aryl hydrocarbon hydroxylase which corresponded to the observed decrease in DNA binding of benzo(a)pyrene. In contrast, the number of tumors which developed in the alcohol pre-treated mice exceeded those of the control animals.