Abstract
Topical application of vitamin E has been shown to decrease the incidence of ultraviolet (UV)-induced skin cancer in mice. Vitamin E provides protection against UV-induced skin photodamage through a combination of antioxidant and UV absorptive properties. Topical application of α-tocopherol on mouse skin inhibits the formation of cyclobutane pyrimidine photoproducts. However, topically applied α-tocopherol is rapidly depleted by UVB radiation in a dose-dependent manner. The photooxidative fate of the α-tocopherol depends on the local environment of the vitamin E. α-Tocopherol quinone and α-tocopherol quinone epoxides are principal photoproducts of vitamin E that has penetrated into the epidermal layer of the skin, whereas tocopherol dimers and trimers are formed from α-tocopherol in a bulk phase at the skin surface. Dimer and trimer products may participate in prevention of UV-induced photodamage.
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