title: Vitamin E alters hepatic antioxidant enzymes in rats treated with dehydroepiandrosterone (DHEA).
abstract: The effects of vitamin E on hepatic antioxidant enzymes and plasma indicators of tissue damage were studied in rats treated with dehydroepiandrosterone (DHEA). Thirty-two male Sprague-Dawley rats were randomly allotted to one of four groups of eight rats each. Rats were treated with DHEA [100 mg/(kg body wt.d), i.p.], vitamin E (1 g/kg diet), or DHEA+vitamin E, or were untreated (controls) for 5 wk. Treatment with DHEA reduced (P < 0.05) weight gain, fat pad weight and carcass lipid concentration and increased carcass protein and ash concentration compared with control rats. The DHEA-treated rats had significantly lower concentrations of serum triglycerides and total cholesterol, yet greater amounts of liver lipid, than did control rats. Supplementation of DHEA-treated rats with vitamin E had no significant effect on weight gain, carcass composition or plasma metabolites compared with rats treated with DHEA alone. The rate of hepatic peroxisomal fatty acid oxidation in DHEA-treated rats was approximately 240% of that in control or vitamin E-supplemented rats. The specific activities of enzymes that defend against oxidative stress (e.g., glutathione reductase, glutathione transferase, catalase) or are indicators of tissue damage (e.g., alanine and aspartate aminotransferases) were all significantly higher in DHEA-treated rats compared with control rats. Supplementation of DHEA-treated rats with vitamin E generally reduced these indices of oxidative stress compared with rats treated with DHEA alone, suggesting that vitamin E may have a protective effect against potential oxidative damage associated with DHEA treatment.
authors.affiliation: Department of Food, Nutrition and Food Service Management, University of North Carolina, Greensboro 27412.
authors.forename: M K
authors.initials: MK
authors.lastname: McIntosh
authors.forename: A H
authors.initials: AH
authors.lastname: Goldfarb
authors.forename: L N
authors.initials: LN
authors.lastname: Curtis
authors.forename: P S
authors.initials: PS
authors.lastname: Cote
mesh_terms: D000818:Animals; D000975:Antioxidants; D001823:Body Composition / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002374:Catalase / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D003687:Dehydroepiandrosterone / Q000494:pharmacology*; D005227:Fatty Acids / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D050356:Lipid Metabolism; D008099:Liver / Q000187:drug effects / Q000201:enzymology* / Q000648:ultrastructure; D008297:Male; D008830:Microbodies / Q000378:metabolism; D008854:Microscopy, Electron; D010084:Oxidation-Reduction; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000097:blood; D014810:Vitamin E / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D005227:Fatty Acids; D014280:Triglycerides; D014810:Vitamin E; D003687:Dehydroepiandrosterone; D002784:Cholesterol; D002374:Catalase; D005980:Glutathione Reductase; D005982:Glutathione Transferase