Physiological aspects of UV-excitation of DNA

Solar ultraviolet (UV) radiation, mainly UV-B (280-315 nm), is one of the most potent genotoxic agents that adversely affects living organisms by altering their genomic stability. DNA through its nucleobases has absorption maxima in the UV region and is therefore the main target of the deleterious radiation. The main biological relevance of UV radiation lies in the formation of several cytotoxic and mutagenic DNA lesions such as cyclobutane pyrimidine dimers (CPDs), 6-4 photoproducts (6-4PPs), and their Dewar valence isomers (DEWs), as well as DNA strand breaks. However, to counteract these DNA lesions, organisms have developed a number of highly conserved repair mechanisms such as photoreactivation, excision repair, and mismatch repair (MMR). Photoreactivation involving the enzyme photolyase is the most frequently used repair mechanism in a number of organisms. Excision repair can be classified as base excision repair (BER) and nucleotide excision repair (NER) involving a number of glycosylases and polymerases, respectively. In addition to this, double-strand break repair, SOS response, cell-cycle checkpoints, and programmed cell death (apoptosis) are also operative in various organisms to ensure genomic stability. This review concentrates on the UV-induced DNA damage and the associated repair mechanisms as well as various damage detection methods.