These experiments were carried out to evaluate oxidative damage to skin in response to ozone. The vitamin E contents of murine skin were measured following topical application of a 5% locotrienol-rich (TRF) solution in polyethylene glycol (PEG, vehicle), or vehicle alone, to 2 sites on the backs of hairless mice. After 2 h. the sites were washed, half of the sites covered and the mice exposed 10 ppm ozone for 2 h. Ozone-exposure to vehicle-treated sites increased epidermal malondialdehyde (MDA), but had no effect on inherent skin vitamin E. Ozone significantly depleted all forms of applied vitamin E in TRF-sites, suggesting oxidative damage to skin surface layers. To localize oxidative damage, skin from ozone-exposed hairless mice was separated into upper epidermis, lower epidermis, and dermis, then concentrations of vitamins E and C and MDA in the layers measured. Ozone depleted alpha-tocopherol (22%; p<0.05) and ascorbic acid (55%; p<0.01) only in the upper epidermis. More remarkably, MDA increased 10-fold in the upper epidermis (p<0.001) and 2-fold in the lower epidermis (plt;0.05), but was unchanged in the dermis. Thus, ozone exposure induces lipid peroxidation in the skin surface layers, and this occurs before depletion of antioxidants, such as vitamins K and C. Because ozone reacts with skin surface fatty acids, topical application of vitamin E may prove beneficial in preventing oxidative damage as a result of environmental ozone exposure.
|Original language||English (US)|
|State||Published - 1997|
ASJC Scopus subject areas
- Agricultural and Biological Sciences (miscellaneous)
- Biochemistry, Genetics and Molecular Biology(all)
- Cell Biology