Ozone-exposure depletes vitamin E and induces lipid peroxidation in murine stratum corneum

Abstract

The presence of ozone (O3) in photochemical smog is an important health concern. We hypothesized that the stratum corneum (SC), as the outermost skin layer and the permeability barrier of the skin, represents a sensitive target for O3-induced oxidative stress. To test this hypothesis, SKH-1 hairless mice were anesthetized and exposed for 2 h to O3 by using two strategies: (i) single exposures to 0 (n = 12), 1 (n = 4), 5 (n = 4), and 10 (n = 4) ppm; and (ii) repeated daily exposures to 0 ppm (controls; n = 4) and 1 ppm (n = 4) for six consecutive days. New techniques based on the removal of SC by tape stripping were used to analyze the biologic effects of O3 with respect to vitamin E depletion and lipid peroxidation. SC tissue was extracted from the tape and immediately analyzed by HPLC for vitamin E and malondialdehyde (MDA) concentrations. After in vivo exposure to increasing O3 doses, vitamin E was depleted and MDA formation was increased, both in a dose-dependent manner. Remarkably, repeated low-level O3 exposures resulted in cumulative oxidative effects in the SC: As compared with O3 exposures of 0 ppm (α-tocopherol, 8.95 ± 1.3 pmol per mg; γ-tocopherol, 3.00 ± 0.3 pmol per mg; MDA, 3.69 ± 0.3 pmol per mg), vitamin E was depleted (α-tocopherol, 2.90 ± 0.6 pmol per mg, p < 0.001; γ-tocopherol, 0.5 ± 0.1 pmol per mg, p < 0.001) and MDA levels were increased (4.5 ± 0.2; p < 0.01). This report demonstrates the unique susceptibility of the SC to oxidative damage upon exposure to O3.