In Vivo Exposure to Ozone Depletes Vitamins C and E and Induces Lipid Peroxidation in Epidermal Layers of Murine Skin

Abstract

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 ( α-tocopherol and ascorbic acid) and the lipid peroxidation product malondialdehyde (MDA) measured. In the upper epidermis, O 3 significantly depleted α-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 α-tocopherol and strongly induces lipid peroxidation in skin. High MDA 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.