The interaction of ultraviolet radiation with biological matter results in direct damage such as pyrimidine dimers in DNA. It also results in indirect damage provoked by the production of reactive oxygen species (ROS) catalyzed by photosensitizers. Photosensitizers can be endogenous (e.g., tryptophan) or exogenous (e.g., TiO2 and other photostable UVA sunscreens). Direct damage triggers an inflammatory response and the oxidative and proteolytic bursts that characterize its onset. The inflammatory reaction multiplies the effects of one single photon. Indirect damage, such as the peroxidative cascade in membrane lipids, can extend to thousands of molecular modifications per absorbed photon. Sunscreens should therefore be formulated in the presence of appropriate antioxidants. Superoxide and singlet oxygen are the main ROS that need to be tackled: this review describes some of the molecular, biochemical, cellular, and clinical consequences of exposure to UV radiation as well as some results associated with scavengers and quenchers of superoxide and singlet oxygen, as well as with inhibitors of singlet oxygen production.
Keywords: antioxidants; cell blebbing; peroxidative cascade; singlet oxygen; skin aging; superoxide; ultraviolet.