SUPPRESSION OF HEPATIC PROSTAGLANDIN-F2-ALPHA IN RATS BY DIETARY ALPHA-TOCOPHEROL ACETATE IS INDEPENDENT OF TOTAL HEPATIC ALPHA-TOCOPHEROL

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>0.73, p<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<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.