Vitamin A metabolism: alpha-tocopherol modulates tissue retinol levels in vivo, and retinyl palmitate hydrolysis in vitro.

The steady-state concentrations of retinol in rat tissues varied as a function of dietary alpha-tocopherol. The liver, kidney, and intestinal retinol concentrations increased in animals fed an alpha-tocopherol-deficient diet despite a decrease (liver) or no change (kidney and intestine) in the concentrations of total vitamin A. In contrast, in lung the concentrations of both retinol and total vitamin A decreased. alpha-Tocopherol inhibited retinyl palmitate hydrolase in vitro in liver, kidney, and intestine; had minimal effect on the testes hydrolase; and stimulated the lung hydrolase. Fifty percent inhibition of the liver hydrolase was provided by an alpha-tocopherol concentration (100 microM), close to that reported in livers of rats fed a purified diet, constituted with moderately low amounts of alpha-tocopheryl acetate. Phylloquinone (vitamin K1) inhibited the retinyl palmitate hydrolase in vitro in all tissues tested, and was about fivefold more potent than alpha-tocopherol. The effects of phylloquinone and alpha-tocopherol on the liver hydrolase were additive, not synergistic. The antioxidant N,N'-diphenyl-p-phenylenediamine, the most effective synthetic vitamin E substitute known, had little effect on the hydrolase. These data show that alpha-tocopherol effects vitamin A metabolism in several tissues, and suggest that it may be a physiological effector of tissue retinol homeostasis.