机构:
Univ Oxford, John Radcliffe Hosp, Inst Mol Med, Imperial Canc Res Fund Labs, Oxford OX3 9DS, EnglandUniv Oxford, John Radcliffe Hosp, Inst Mol Med, Imperial Canc Res Fund Labs, Oxford OX3 9DS, England
Norbury, CJ
[1
]
Hickson, ID
论文数: 0引用数: 0
h-index: 0
机构:
Univ Oxford, John Radcliffe Hosp, Inst Mol Med, Imperial Canc Res Fund Labs, Oxford OX3 9DS, EnglandUniv Oxford, John Radcliffe Hosp, Inst Mol Med, Imperial Canc Res Fund Labs, Oxford OX3 9DS, England
Hickson, ID
[1
]
机构:
[1] Univ Oxford, John Radcliffe Hosp, Inst Mol Med, Imperial Canc Res Fund Labs, Oxford OX3 9DS, England
DNA damaging agents;
DNA repair;
genome instability;
cell cycle checkpoints;
apoptosis;
D O I:
10.1146/annurev.pharmtox.41.1.367
中图分类号:
R9 [药学];
学科分类号:
1007 ;
摘要:
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 (1-6), we restrict our coverage of the DNA repair field to base excision repair and DNA double-strand break repair.