Hairless mice were fed diets containing different levels of vitamin E or received topical applications of the vitamin for three weeks before a single exposure equivalent to one minimal erythematous dose of ultraviolet light provided by an artificial sunlight source. Lipid peroxidation and suppression of incorporation of thymidine into DNA were used to estimate the degree of damage caused by the radiation. Restriction of dietary vitamin E had little effect on degree of epidermal lipid peroxidation or on thymidine incorporation into DNA. High dietary levels of the vitamin did not alter the degree of lipid peroxidation; however, the incorporation of thymidine was restored to levels comparable to those of unirradiated animals. Topical administration of a 1% solution of the vitamin in ethanol 1 or 24 hours before irradiation also restored thymidine incorporation and reduced the degree of lipid peroxidation. The results suggest that both dietary and topical vitamin E are effective in protecting the epidermis against some of the early damage induced by ultraviolet radiation.