Effect of UVB on Hydrolysis of α-Tocopherol Acetate to α-Tocopherol in Mouse Skin

We have assessed the hydrolysis of α-tocopherol acetate (α-TAc) to the active antioxidant α-tocopherol (α-TH) in mouse epidermis and in supernatant from epidermal homogenates. Topically administered α-TH prevents UVB photocarcinogenesis in C3H mice, whereas α-TAc does not. Hydrolysis in skin was monitored in mice treated topically with deuterium labeled α-TAc (d3-α-TAc). Epidermal samples were isolated from mice and analyzed for endogenous (d0-α-TAc) and d3-α-TH by gas chromatography-mass spectrometry. Within 24 h, the levels of d3-α-TH increased up to 10-fold over endogenous d0-α-TH levels; however, in mice irradiated with UVB prior to the application of d3-α-TAc, levels of d3-α-TH increased up to 30–40-fold over endogenous d0-α-TH. This enhancement of α-TAc hydrolysis increased with increasing UVB dose. Prior UVB exposure may increase hydrolysis of α-TAc by increasing epidermal esterase activity. Nonspecific esterase activity was measured in the 2000 ×g supernatant from epidermis of unirradiated and irradiated mice. α-Napthyl acetate, a nonspecific esterase substrate, was converted to α-napthol in supernatants from unirradiated mice. Hydrolysis to α-napthol increased ≈3-fold in supernatants from irradiated mice. Hydrolysis of α-TAc to α-TH also occurred in supernatant from unirradiated mice, and this hydrolysis increased ≈3-fold in supernatant from irradiated animals. These data indicate that nonspecific esterase activity was increased by UVB in the skin, that α-TAc is converted to α-TH in the homogenate fraction containing nonspecific esterase, and that UVB exposure modulates the metabolism of α-TAc to α-TH in vivo