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紫外线辐射诱导DNA损伤与修复的分子机制

Molecular mechanisms of ultraviolet radiation-induced DNA damage and repair.

作者信息

Rastogi Rajesh P, Kumar Ashok, Tyagi Madhu B, Sinha Rajeshwar P

机构信息

Laboratory of Photobiology and Molecular Microbiology, Centre of Advanced Study in Botany, Banaras Hindu University, Varanasi 221005, India.

出版信息

J Nucleic Acids. 2010 Dec 16;2010:592980. doi: 10.4061/2010/592980.

DOI:10.4061/2010/592980
PMID:21209706
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3010660/
Abstract

DNA is one of the prime molecules, and its stability is of utmost importance for proper functioning and existence of all living systems. Genotoxic chemicals and radiations exert adverse effects on genome stability. Ultraviolet radiation (UVR) (mainly UV-B: 280-315 nm) is one of the powerful agents that can alter the normal state of life by inducing a variety of mutagenic and cytotoxic DNA lesions such as cyclobutane-pyrimidine dimers (CPDs), 6-4 photoproducts (6-4PPs), and their Dewar valence isomers as well as DNA strand breaks by interfering the genome integrity. To counteract these lesions, organisms have developed a number of highly conserved repair mechanisms such as photoreactivation, base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR). Additionally, double-strand break repair (by homologous recombination and nonhomologous end joining), SOS response, cell-cycle checkpoints, and programmed cell death (apoptosis) are also operative in various organisms with the expense of specific gene products. This review deals with UV-induced alterations in DNA and its maintenance by various repair mechanisms.

摘要

DNA是主要分子之一，其稳定性对于所有生命系统的正常运作和生存至关重要。具有基因毒性的化学物质和辐射会对基因组稳定性产生不利影响。紫外线辐射（UVR）（主要是UV-B：280-315纳米）是一种强大的因素，它可以通过诱导多种诱变和细胞毒性DNA损伤，如环丁烷嘧啶二聚体（CPD）、6-4光产物（6-4PP）及其杜瓦价异构体，以及通过干扰基因组完整性导致DNA链断裂，从而改变生命的正常状态。为了对抗这些损伤，生物体已经发展出许多高度保守的修复机制，如光复活、碱基切除修复（BER）、核苷酸切除修复（NER）和错配修复（MMR）。此外，双链断裂修复（通过同源重组和非同源末端连接）、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，但需要消耗特定的基因产物。本综述探讨了紫外线诱导的DNA改变及其通过各种修复机制的维持。

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