On the relationship between vitamin A and vitamin E in the rat.

I . The effect of vitamin E on the metabolism, utilization and storage of vitamin A has been studied in the rat. 2. Male weanling rats were given a vitamin A-deficient, vitamin E-deficient diet until growth had ceased for 3 days, and each rat was then given 50 i.u. vitamin A palmitate. The rats were divided into four groups and given the diet with the addition of 10 % methyl oleate or 10 yo cod-liver oil methyl esters, or either of these diets supplemented with IOO ppm D-Utocopheryl acetate. There was no increase in maximum weight-gain response in the two groups given vitamin E. There was a significantly lower weight-gain response in the groups given cod-liver oil methyl esters. This effect was not influenced by the presence of vitamin E in the diet. 3. Weanling rats of both sexes were made deficient in vitamins A and E and then divided into two groups. One group received, every other day, 1-75 i.u. vitamin A palmitate and 0.6 mg D-a-tocopherol given together; the second group received the two vitamins, in the same amounts, on alternate days. After zS days there was no difference in the growth of the two groups of rats, irrespective of sex. 4. Vitamin A-depleted, vitamin E-deficient rats were given 17.5 I ,ug [14C-carbinol]retiny1 acetate and then a vitamin A-deficient, vitamin E-deficient diet or that diet supplemented with IOO ppm D-a-tocopheryl acetate. After 6 days, the total remaining [‘*C]retinol and its lipidsoluble metabolites were measured in the carcasses of the rats. Vitamin E administration did not affect the metabolism of the vitamin A dose or its effect on growth. 5. Vitamin E-deficient rats were givenvitaminA until their liver reserves exceeded 30000 i.u. and were then divided into two groups. One group received a diet deficient in vitamins A and E and the other received, in addition to this diet, a weekly oral supplement of I mg D-cc-tocopheryl acetate. The vitamin E supplement significantly decreased the rate of vitamin A depletion from the liver during the next 6 weeks. This effect, which was not found to occur when the initial liver reserves were only 3000 i.u., suggests a role for vitamin E in connexion with the capacity of the liver to bind vitamin A. 6. The relationship between vitamin A and vitamin E in vivo cannot, in the light of these results, be regarded as that between an antioxidant and a peroxidizable substrate.