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* Graduate Center for Nutritional Sciences,
Graduate Center for Toxicology,
** Department of Nutrition and Food Science,
Department of Pathology and Laboratory Medicine, and

Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, KY 40506
3To whom correspondence should be addressed. E-mail: hglauert{at}uky.edu.
In this study, the effect of dietary vitamin E on the hepatic tumor-promoting activity of PCB-77 and PCB-153 in female Sprague-Dawley rats (175200 g) was investigated. One week after diethylnitrosamine injection, rats were fed purified diets containing 10, 50, or 250 mg/kg vitamin E in the form of
-tocopheryl acetate. Starting 1 wk later, we injected rats i.p. with vehicle (corn oil) or PCB-77 or PCB-153 (300 µmol/kg) every 14 d for 4 injections. All rats were killed 10 d after the last PCB injection. The number and volume of placental glutathione S-transferase (PGST)positive foci were increased by PCB-77 but not by PCB-153. Vitamin E did not affect the induction of PGST-positive foci. PCB-77, but not PCB-153, increased hepatic NF-
B activity. In conclusion, dietary vitamin E supplementation does not protect against the induction of altered hepatic focal lesions by PCBs.
KEY WORDS: polychlorinated biphenyls vitamin E altered hepatic foci NF-
B
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