ABSTRACT
UVR AND PHOTODAMAGE MECHANISMS UVR photodamage occurs through direct and indirect mechanisms. Direct absorption of UV energy drives biochemical reactions that result in molecular changes and production of reactive oxygen species (ROS). UVA wavelengths, which penetrate deeply into skin, induce formation of ROS, which act as mediators of indirect photodamage resulting in oxidative stress and adduct formation of biomolecules. DNA has absorption maxima in UV wavelength range and is therefore a direct target of UV damage, forming cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs). These DNA photoproducts are mainly induced by UVB, but with some contribution from UVA (1,2). They interfere with biological processes and induce signals that inform cellular decisions for entry into one of two main pathways: cell survival through initiation of cellular repair processes or cell death by apoptosis (3). ROS produced in the skin following UV irradiation are key mediators of oxidative damage to the skin. Cell damage from UV also occurs through peroxidation of membrane lipids via generation of lipid peroxides. UV irradiation results in the rapid depletion of several endogenous skin enzymes and antioxidants such as glutathione reductase and catalase. Exposure to UV radiation suppresses the immune response, and UV-induced immune suppression is a major risk factor for skin cancer induction (4). Multiple mechanisms are involved depending upon the doses and the type of irradiation (acute or chronicle): DNA damage, production of cytokines, and inammatory mediators (5). UV exposure affects antigen-presenting cell function and induces immune tolerance in part through the induction of regulatory T cells (6).
