The molecular determinants of sunburn cell formation

Sunburn cell (SBC) formation in the epidermis is a characteristic consequen ce of ultraviolet radiation (UVR) exposure at doses around or above the min imum erythema dose. SEC have been identified morphologically and biological ly as keratinocytes undergoing apoptosis. There is evidence that SEC format ion is a protective mechanism to eliminate cells at risk of malignant trans formation. The level of DNA photodamage is a major determinant of SEC induc tion by a process controlled by the tumor suppressor gene p53. However, ext ra-nuclear events also contribute to SEC formation, such as the activation of death receptors including CD95/Fas. UVR triggers death receptors either by direct activation of these surface molecules or by inducing the release of their ligands such as CD95 ligand or tumor necrosis factor. Oxidative st ress also appears to be involved, probably via mitochondrial pathways, resu lting in the release of cytochrome C. Pathways which modify SEC formation a re now extensively studied given the importance of apoptosis in eliminating irreparably damaged cells. A greater understanding of the mechanisms that induce and prevent UVR-induced apoptosis will contribute to our understandi ng of mechanisms relevant in genomic integrity.