The photoprotective effects of vitamin E

The photoprotective effects of vitamin E (α-tocopherol) have been studied extensively. Whereas most studies have been performed in animals, several studies exist investigating the photoprotective effects of topically applied vitamin E also in humans. When vitamin E is applied before UVR exposure, significantly reduced acute skin responses are observed, including erythema and edema, sunburn cell formation, lipid peroxidation, DNA adduct formation, and immunosuppression, as well as UVA-induced binding of photosensitizers. As shown in animals, skin wrinkling and skin tumor incidence due to chronic UVR exposure are also diminished by topical vitamin E. A human study proved that an alcohol-based lotion of Cosmeceuticals and Active Cosmetics 2% α-tocopherol significantly diminished the erythemal responses of skin redness and dermal blood flow when applied 30 minutes before UVR exposure.

Due to the fact that the lotion had no sunscreen properties, the observed photoprotective effects were attributed to the antioxidant properties of α-tocopherol. However, the photoprotective mechanism of action of α-tocopherol continues to be debated, since some studies have indicated that α-tocopherol may also act as a weak sunscreen. Vitamin E esters, and in particular vitamin E acetate, have also been shown to reduce solar UVR induced skin damage. Their photoprotective effects seem less pronounced compared to vitamin E; moreover, some studies have failed to show photoprotection by vitamin E esters. 

Vitamin E esters need to be hydrolyzed after skin absorption to act as antioxidants. Bioconversion of vitamin E acetate into the active form is slow and occurs only to a limited extent in skin. For instance, vitamin E acetate is not efficiently hydrolyzed in the stratum corneum and is converted to α-tocopherol only in the nucleated epidermis after penetration beyond the stratum corneum. The controversial observations of photoprotective effects of topically applied vitamin E acetate may consequently be explained by a limited bioavailability of the active, ester-cleaved form at the site of oxidative stress. Intriguingly, the bioconversion of vitamin E acetate is enhanced when skin is exposed to sun, possibly by a UVB-dependent increase in esterase activity, as has been demonstrated in murine epidermis.