Effect of UVB on hydrolysis of α-tocopherol acetate to α-tocopherol in mouse skin

We have assessed the hydrolysis of alpha-tocopherol acetate (alpha-TAc) to the active antioxidant alpha-tocopherol (alpha-TH) in mouse epidermis and in supernatant from epidermal homogenates. Topically administered alpha-TH prevents UVB photocarcinogenesis in C3H mice, whereas alpha-TAc does not. Hydrolysis in skin was monitored in mice treated topically with deuterium labeled alpha-TAc (d(3)-alpha-TAc). Epidermal samples were isolated from mice and analyzed for endogenous (d(0)-alpha-TAc) and d(3)-alpha-TH by gas chromatography-mass spectrometry, Within 24 h, the levels of d(3)-alpha-TH increased up to 10-fold over endogenous d(0)-alpha-TH levels; however, in mice irradiated with UVB prior to the application of d(3)-alpha-TAc, levels of d(3)-alpha-TH increased up to 30-40-fold over endogenous d(0)-alpha-TH. This enhancement of alpha-TAc hydrolysis increased with increasing UVB dose. Prior UVB exposure may increase hydrolysis of alpha-TAc by increasing epidermal esterase activity. Nonspecific esterase activity was measured in the 2000 X g supernatant from epidermis of unirradiated and irradiated mice. alpha-Napthyl acetate, a nonspecific esterase substrate, was converted to alpha-napthol in supernatants from unirradiated mice. Hydrolysis to alpha-napthol increased approximate to 3-fold in supernatants from irradiated mice. Hydrolysis of alpha-TAc to alpha-TH also occurred in supernatant from unirradiated mice, and this hydrolysis increased approximate to 3-fold in supernatant from irradiated animals. These data indicate that nonspecific esterase activity was increased by UVB in the skin, that alpha-TAc is converted to alpha-TH in the homogenate fraction containing nonspecific esterase, and that UVB exposure modulates the metabolism of alpha-TAc to alpha-TH in vivo.