UV-B-Induced photooxidation of vitamin E in mouse skin.

Topically applied alpha-tocopherol (alpha-TH, vitamin E) inhibits UV-B (290-320 nm) photocarcinogenesis, yet alpha-TH undergoes rapid photooxidation by UV-B in vitro. To examine the effect of UV-B on alpha-TH in vivo, we studied the fate of alpha-TH in UV-B-irradiated mouse skin. [14C]-alpha-TH was applied to mouse skin at various times prior to UV-B irradiation. UV-B irradiation for 1 h at a dose rate of 2.6-2.9 J m-2 s-1 resulted in consumption of 40-60% of the applied dose and formation of oxidation products. The major product fraction formed in UV-B-irradiated mice treated topically with alpha-TH contained an alpha-TH dihydroxy dimer and its two-electron oxidation product, a spirodimer. Products previously identified as being derived from photochemical or peroxyl radical scavenging reactions of alpha-TH were also observed, including alpha-tocopherolquinone (alpha-TQ), alpha-tocopherolquinone 2, 3-epoxide (alpha-TQE 1), alpha-tocopherolquinone 5,6-epoxide (alpha-TQE 2), and 8a-(hydroperoxy)epoxytocopherones. These results indicate that topically applied alpha-TH is extensively oxidized in skin and suggest that alpha-TH photoproducts may be involved in the observed effects of topically applied vitamin E in UV-B-irradiated skin.