The skin is continuously exposed to a variety of hazardous environmental insults, such as ultraviolet light, ozone, and ionizing radiation. These exposures result in the production of free radicals and reactive oxygen species, which may play a role in the development of inflammatory skin disorders, skin cancer, cutaneous autoimmune disorders, phototoxicity, and premature ageing. A variety of antioxidant defense mechanisms are present to prevent oxidative stress; however, UV irradiation has been shown to overwhelm these mechanisms. We hypothesized that UV-light exposure results in the formation of free radicals, which causes antioxidant depletion, lipid peroxidation and DNA damage. To experimentally evaluate the effects of simulated solar light (SSL) on SKH-1 hairless mice, animals were exposed to SSL (13.7 mJ (CIE)/cm2 ) for 1 hour, 5 days a week for 3 weeks. Twenty-four hours following the last exposure, mice were sacrificed. The skin was evaluated for changes in several parameters of oxidative stress. A significant amount of GSH oxidation as well as decreases in the levels of protein thiols, total antioxidant reserves, and vitamin E were seen as a result of exposure to SSL. A significant increase in lipid peroxidation and myeloperoxidase activity (MPO), indicating infiltration of neutrophils into the skin, was observed following SSL irradiation. The production of pyrimidine dimmers seen after exposure is indicative of DNA damage occurring as a result of the direct action of SSL on DNA. Histological evaluation of the skin following exposure to SSL irradiation showed increased skin thickness and inflammatory cell infiltration. These data indicate that SSL exposure induces the production of pyrimidine dimmers and free radicals in the skin, which result in the development of oxidative stress and inflammatory cell infiltration.
The Toxicologist. Society of Toxicology 43nd Annual Meeting and ToxExpo, March 21-25, 2004, Baltimore, Maryland