Skin cancer, the most common cancer in the United States, is diagnosed in more than 1.5 million people yearly and more than 90% of the cases are believed to be related to sun exposure. Prolonged solar UV radiation in the form of UVA (320–400 nm) and UVB (290–320 nm) may cause premature wrinkling, elastosis and skin cancer. Sunscreens are widely used to protect skin from acute and chronic consequences of sun exposure. This article discusses current knowledge on the biological process of UV-induced skin damage. Of particular interest is the role of antioxidants in the prevention of carcinogenesis.
DNA absorption of solar UVB may lead to photo-adduct formation of two adjacent pyrimidine bases, which can result in C to T or CC to TT point mutations. Although this damage is constantly being repaired by specific repair enzymes, accumulations of these mutations may occur, inducing the buildup of p53 tumor suppressing genes. The induction and accumulation of p53 protein by UVR exposure induces a cell-cycle arrest at the G1 phase and allows for the repair of DNA damage before replication. When excessive DNA damage accumulates, p53 directly up-regulates the expression of pro-apoptotic genes. These DNA mutations accumulate and ultimately increase activity of the p53 tumor suppressor gene, an early genetic event in the development of UV-induced skin cancers.
Excerpt Only This is a shortened version or summary of the article that appeared in the January 2007 issue of Cosmetics & Toiletries magazine. The full content is not currently available online.