Suppression of hepatic prostaglandin F2α in rats by dietary α-tocopherol acetate is independent of total hepatic α-tocopherol

• Published in: Prostaglandins, leukotrienes and essential fatty acids Vol. 47; no. 1; pp. 63 - 68
• Main Authors: DUITSMAN, P. K, CHEN, H. W, COOK, L. R, HENDRICH, S
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier 01.09.1992
• Subjects: alpha-Tocopherol - analogs & derivatives; Animals; Biological and medical sciences; Diet; Dinoprost - biosynthesis; Female; Fundamental and applied biological sciences. Psychology; Liver - drug effects; Liver - metabolism; Phenobarbital - toxicity; Prostaglandins. Arachidonic acid metabolites; Rats; Rats, Inbred F344; Tocopherols; Vertebrates: endocrinology; Vitamin E - administration & dosage; Vitamin E - analogs & derivatives; Vitamin E - metabolism; Vitamin E - pharmacology; Vertebrata; Mammalia; Rat; Diet; Arachidonic acid derivatives; Liver; Rodentia; Vitamin; α-Tocopherol; Prostaglandin F2α
• ISSN: 0952-3278; 1532-2823
• DOI: 10.1016/0952-3278(92)90187-N

Groups of eight weanling female F344/N rats were fed semipurified diets that supplied 0, 50, 500, 5000, or 15,000 mg alpha-tocopherol acetate/kg diet, with and without 0.05% phenobarbital (PB) for 9 weeks. Both plasma and hepatic alpha-tocopherol levels, measured by HPLC, strongly correlated with alpha-tocopherol intake (r greater than 0.73, p less than 0.0001). Phenobarbital both depleted hepatic alpha-tocopherol and increased plasma alpha-tocopherol significantly. Although treatment with PB for 9 weeks significantly increased GST activity, PB did not affect hepatic prostaglandin (PG)F2 alpha status, as determined by radioimmunoassay. PGF2 alpha was significantly greater (by 52%) in rats fed no alpha-tocopherol than in rats fed 15,000 mg alpha-tocopherol acetate/kg diet. Hepatic PGF2 alpha status was correlated inversely but weakly with dietary alpha-tocopherol (r = -0.24, p less than 0.05). Hepatic PGF2 alpha status was not correlated with hepatic or plasma alpha-tocopherol status. This finding suggests either that there is a small depletion-resistant subcellular alpha-tocopherol pool which regulates PGF2 alpha production or that alpha-tocopherol alters PGF2 alpha production in vivo by an indirect mechanism.