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Effects of Dietary Selenium and Vitamin E on Hepatic Mixed-Function Oxidase Activities and In Vivo Covalent Binding of Aflatoxin B₁ in Rats¹

Institute of Health, Chinese Academy of Medical Sciences, Beijing, The People's Republic of China in cooperation with Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853 and Department of Poultry and Avian Sciences, Cornell University, Ithaca, NY 14853

Male weanling Fischer-344 rats were fed a selenium (Se)-vitamin E (VE) deficient Torula ycast basal dict or that dict supplemented with graded levels of Se (0.2–6.0 ppm as Na₂SeO₃) or VE (100 IU/kg as all-rac-2-tocopheryl acetate), or both, for 4 or 6 weeks. Se deficiency and excess (6.0 ppm) markedly depressed in vivo covalent binding of aflatoxin (AFB₁) to macromolecules in livers of rats killed 2 hours after an i.p. dose of 1 mg/kg tritiated AFB₁. VE supplementation had no effect. Prior phenobarbital (PB) treatment generally decreased adducts without changing diet-related trends. Some hepatic enzyme capabilities were also measured. Cytochrome b₃ content and cytochrome c reductase activity were unaffected by diet. VE increased cytochrome P-450 content, ethylmorphine N-demethylase and benz()pyrene hydroxylase activities; all these were unaffected by Se levels. Se deficiency and excess (but not VE deficiency) increased glucuronyl transferase. PB induction affected all diet groups and was more in agreement with MFO activity than transferase. Adduct formation was more consistently related to transferase activity than to MFO activities. The contrasting effects of SE and VE on AFB₁ adducts in rats and chicks are discussed.

KEY WORDS: • selenium • vitamin E • aflatoxin adducts • metabolism

¹ Supported by USPHS Grants PO1 CA26755 and RO1 ES01354, Hatch Project NYC-399412, and a grant from the Herman Frasch Foundation.

² Reprint requests should be addressed to T. Colin Campbell, Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853.

Manuscript received 7 July 1981.