Prevention of photocarcinogenesis by dietary vitamin E

Abstract

Ultraviolet B (UV‐B) irradiation of C3H/HeN mice induces skin cancer. In this study, the ability of dietary d‐a‐tocopheryl acetate to reduce photocarcinogenesis was tested in this murine model. Skin cancers developed in 67.5% of UV‐B∼irradiated mice by 31 weeks after the first UV exposure. Supplementation with 100 or 200 IU of d‐α‐tocopheryl acetate per kilogram of diet led to a reduction of the incidence to 46% and 19%, respectively. The latter value was significantly different from that found in mice fed the basal diet (p = 0.039, one‐sided P value by log‐rank test). Skin levels of α‐tocopherol varied with the dietary dose of d‐a‐tocopheryl acetate. No toxicity was evident in unirradiated mice fed the vitamin E‐supplemented diet, but 40% of the UV‐B‐irradiated mice fed 200 IU of vitamin E per kilogram of diet died by 31 weeks after the first UV‐B treatment. Decreased relative spleen weight was observed in the UV‐B‐irradiated mice fed the vitamin E‐supplemented diet. In summary, oral d‐a‐tocopheryl acetate prevented photocarcinogenesis, but at doses that were toxic to inbred C3H/HeN mice after exposure to 8.6 × 10⁵ J/m² of UV‐B irradiation.