ABSTRACT
UV radiation (UVR) with a wavelength in the range of 280 to 320 nm (UVB) and 320 to 400 nm (UVA) negatively in—uences the skin [1]. UVB affects keratinocytes and melanocytes of the epider mis; UVA affects the basal layer of keratinocytes and £broblasts of the dermis [2-4]. Both types of UVR in—uence the cell DNA. UVB is absorbed by DNA and induces formation of cyclobutane pyrimidine dimers and pyrimidine [6-4] pyrimidone photoproducts. UVA generates large amounts of free radicals in cells, which, in effect, leads to oxidation of DNA bases and formation of 8-oxodeoxyguanosine [5]. Mutations in genes regulating proliferation, cell growth cycle, or apoptosis can lead to tumor transformation of skin cells [6,7]. Keratinocytes are more resistant to UVR compared to £broblasts, since they have a more ef£cient genome repair system [8]. Damaged keratinocytes are eliminated through apoptosis (sunburn cells) or give rise to nonmelanoma cancer cells: basal cancer cells and squamous cancer cells [9,10]. To a lesser extent, abnormal melanocytes undergo apoptosis, accumulate mutations, and transform into melanoma cells [11]. UVA-induced oxidative stress leads to cell membrane lipid peroxidation, as well as reduction of endogenous antioxidant enzyme activity: superoxide dismutase (SOD), catalase (CAT), peroxidise (GSH-Px), and glutathione reductase (GSH-R) [12]. UVB activates apoptotic proteins and proin—ammatory cytokines in the epidermis, destroys extracellular matrix proteins in the dermis, and is responsible for its photoaging [13-15].
