Weber, S.U., Tavakkol*, A., Nabi*, Z., Jothi, S., Polefka*, T.G., Packer, L. Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, California, *Personal Care Products, Colgate-Palmolive Co., Piscataway, New Jersey.

Recent reports suggest that exposure to tropospheric ozone (O3) poses an oxidative stress to murine skin. So far, no data is available on human skin. Monolayers of human keratinocytes cannot serve as a model of human skin for O3 exposure, since O3 mainly reacts within the stratified stratum corneum (SC). We chose a organotypic model of human epidermis (Epiderm™) with a differentiated SC to study the effects of environmental O3 exposure. The tissue was exposed to 5 p.p.m. O3 for 2 h, which did not affect the tissue viability, as measured by LDH release. Mock exposure to air only for 2 h was used as control. Glutothione (GSH), Vitamin C, uric acid, and Vitamin E as anti-oxidants, and malondialdehyde (MDA) as an indicator of lipid peroxidation were analyzed by HPLC in whole tissue. Uric acid levels were not changed while GSH increased by 40% (p < 0.05). Vitamin E, the major lipophilic antioxidant, was not depleted by this dose of O3. Vitamin C was not detected in the tissue culture. No significant MDA production was observed. To study the effects of O3 on exogenous Vitamin E, 20 ul of a 0.5% preparation of a-tocopherol in PEG 400 was added to the wells 2 h prior to O3 exposure. This pretreatment increased Vitamin E levels by 2.5 fold. Ozone exposure depleted this added Vitamin E by 30% (p < 0.001). However, the Vitamin E remaining in the skin was still significantly higher than the endogenous portion (p < 0.001). These results indicate that specific cellular changes are induced by a single acute exposure to O3 in the organotypic skin model. Pathophysiological consequences remain to be investigated.


EpiDerm, Melanin, Ozone, Peptide agonist, SLIGRL

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