In vivo exposure to ozone depletes vitamins C and E and induces lipid peroxidation in epidermal layers of murine skin

To evaluate skin susceptibility to ozone (O-3) and to localize possible oxidative damage within the skin layers, hairless mice were exposed to 10 ppm O-3 or air (0 ppm O-3(-)) for 2 h. The mice were euthanized, the skin removed and frozen. Three skin layers (upper epidermis, lower epidermis/papillary dermis, and dermis) were separated, antioxidant concentrations (alpha-tocopherol and ascorbic acid) and the lipid peroxidation product malondialdehyde (MDA) measured. In the upper epidermis, O-3 significantly depleted alpha-tocopherol (22%; p < .05) and ascorbic acid (55%; p < .01). These antioxidants were unchanged by O-3 in the lower skin layers. More remarkably, MDA increased ten-fold in the upper epidermis (p < .001) and two-fold in the lower epidermis/papillary epidermis (p < .05); it was unchanged in the dermis. Thus, exposure to O-3 in vivo depletes ascorbic acid and a-tocopherol and strongly induces lipid peroxidation in skin. High MI)A concentrations measured in the upper epidermis suggest that O-3 reacts directly with fatty acids on the skin surface layers. These results further suggest that chronic exposure to lower O-3 concentrations found in urban smog could potentially have implications for skin health. (C) 1997 Elsevier Science Inc.