Dietary vitamin E, hepatic aryl hydrocarbon hydroxylase and the metabolic activation of procarcinogens to mutagens

Abstract

Vitamin E deficiency for 12 weeks significantly reduced the hepatic aryl hydrocarbon hydroxylase (AHH) activity in rats. This resulted in a reduced ability to mutagenically activate benzo (a) pyrene (BP) and 2‐aminofluorene (2‐AF) as compared with equivalent preparations from vitamin E‐supplemented rats. PCB treatment of vitamin E‐deficient and supplemented rats increased AHH activity, and the ability of rats in both dietary groups to activate BP to mutagens. In contrast, PCB treatment caused a reduction in the mutagenic activation of aryl amines.