Vitamin E inhibits the UVAI induction of "light" and "dark" cyclobutane pyrimidine dimers, and oxidatively generated DNA damage, in keratinocytes.

Solar ultraviolet radiation (UVR)-induced DNA damage has acute, and long-term adverse effects in the skin. This damage arises directly by absorption of UVR, and indirectly via photosensitization reactions. The aim of the present study was to assess the effects of vitamin E on UVAI-induced DNA damage in keratinocytes in vitro. Incubation with vitamin E before UVAI exposure decreased the formation of oxidized purines (with a decrease in intracellular oxidizing species), and cyclobutane pyrimidine dimers (CPD). A possible sunscreening effect was excluded when similar results were obtained following vitamin E addition after UVAI exposure. Our data showed that DNA damage by UVA-induced photosensitization reactions can be inhibited by the introduction of vitamin E either pre- or post-irradiation, for both oxidized purines and CPD (including so-called "dark" CPDs). These data validate the evidence that some CPD are induced by UVAI initially via photosensitization, and some via chemoexcitation, and support the evidence that vitamin E can intervene in this pathway to prevent CPD formation in keratinocytes. We propose the inclusion of similar agents into topical sunscreens and aftersun preparations which, for the latter in particular, represents a means to mitigate on-going DNA damage formation, even after sun exposure has ended.