Sinha Rajeshwar P, Häder Donat-P
Laboratory of Photobiology and Molecular Microbiology, Centre of Advanced Study in Botany, Banaras Hindu University, Varanasi, 221005, India.
Top Curr Chem. 2015;356:203-48. doi: 10.1007/128_2014_531.
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.
太阳紫外线（UV）辐射，主要是UV-B（280 - 315纳米），是最具潜在遗传毒性的因子之一，它通过改变生物体的基因组稳定性对其产生不利影响。DNA通过其核碱基在紫外线区域有吸收最大值，因此是这种有害辐射的主要靶标。紫外线辐射的主要生物学关联在于形成多种具有细胞毒性和致突变性的DNA损伤，如环丁烷嘧啶二聚体（CPD）、6-4光产物（6-4PP）及其杜瓦价键异构体（DEW），以及DNA链断裂。然而，为了对抗这些DNA损伤，生物体已经发展出许多高度保守的修复机制，如光复活、切除修复和错配修复（MMR）。涉及光解酶的光复活是许多生物体中最常用的修复机制。切除修复可分为碱基切除修复（BER）和核苷酸切除修复（NER），分别涉及多种糖基化酶和聚合酶。除此之外，双链断裂修复、SOS反应、细胞周期检查点和程序性细胞死亡（凋亡）在各种生物体中也发挥作用，以确保基因组稳定性。本综述集中讨论紫外线诱导的DNA损伤、相关的修复机制以及各种损伤检测方法。
