Norbury C J, Hickson I D
Imperial Cancer Research Fund Laboratories, Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford, OX3 9DS, United Kingdom.
Annu Rev Pharmacol Toxicol. 2001;41:367-401. doi: 10.1146/annurev.pharmtox.41.1.367.
Cells are constantly under threat from the cytotoxic and mutagenic effects of DNA damaging agents. These agents can either be exogenous or formed within cells. Environmental DNA-damaging agents include UV light and ionizing radiation, as well as a variety of chemicals encountered in foodstuffs, or as air- and water-borne agents. Endogenous damaging agents include methylating species and the reactive oxygen species that arise during respiration. Although diverse responses are elicited in cells following DNA damage, this review focuses on three aspects: DNA repair mechanisms, cell cycle checkpoints, and apoptosis. Because the areas of nucleotide excision repair and mismatch repair have been covered extensively in recent reviews, we restrict our coverage of the DNA repair field to base excision repair and DNA double-strand break repair.
细胞不断受到DNA损伤剂的细胞毒性和诱变作用的威胁。这些损伤剂既可以是外源性的,也可以在细胞内形成。环境DNA损伤剂包括紫外线和电离辐射,以及食品中遇到的各种化学物质,或作为空气传播和水传播的物质。内源性损伤剂包括甲基化物质和呼吸过程中产生的活性氧。尽管DNA损伤后细胞会引发多种反应,但本综述聚焦于三个方面:DNA修复机制、细胞周期检查点和细胞凋亡。由于核苷酸切除修复和错配修复领域在最近的综述中已有广泛涵盖,我们将DNA修复领域的讨论限制在碱基切除修复和DNA双链断裂修复。