DNA damage mediated by UV radiation and relative repair mechanisms in mammals

Ultraviolet (UV) radiation is one of the major environmental pathogenic factors for mammals and has been identified as a carcinogen for initiating and promoting human skin cancers. As the main chromophore for UV energy, DNA is the direct target and generates abundant photolesions, cyclobutene pyrimidine dimers (CPDs) and pyrimidine–pyrimidone (6–4) photoproducts (6–4PPs). The formation of CPDs and 6–4PPs is sequence specific and di-pyrimidine site is identified as the hotspots. Besides, some epigenetic regulations are involved in this process to influence the yield of photolesions. Upon UV radiation, the photolesions contribute to cell death and are the primary source of mutagenicity. To defend these detrimental effects to cells, DNA repair mechanisms and several signaling transduction pathways are collaborated to remove those photolesions. Nucleotide excision repair (NER) is the prominent way to recognize the damaged sites, excising the photolesions and repairing the DNA strand. Other cell responses have been along with NER system to complete the repair genetically. This review is focused on UV-induced DNA damage and summarizes current advances about the formation of CPDs and 6–4PPs as well as NER system and collaborated cell responses.