Wilson David M, Bohr Vilhelm A
Laboratory of Molecular Gerontology, National Institute on Aging/NIH, Baltimore, MD 21224, USA.
DNA Repair (Amst). 2007 Apr 1;6(4):544-59. doi: 10.1016/j.dnarep.2006.10.017. Epub 2006 Nov 16.
Base excision repair (BER) is the major pathway responsible for averting the mutagenic and cytotoxic effects of spontaneous hydrolytic, oxidative, and non-enzymatic alkylation DNA damage. In particular, this pathway recognizes and repairs base modifications, such as uracil and 8-hydroxyguanine, as well as abasic sites and DNA single-strand breaks. In this review, we outline the basic mechanics of the BER process, and describe the potential association of this pathway with aging and age-related disease, namely cancer and neurodegeneration.
碱基切除修复（BER）是避免自发水解、氧化和非酶促烷基化DNA损伤所产生的诱变和细胞毒性作用的主要途径。特别是，该途径可识别并修复碱基修饰，如尿嘧啶和8-羟基鸟嘌呤，以及无碱基位点和DNA单链断裂。在本综述中，我们概述了BER过程的基本机制，并描述了该途径与衰老及衰老相关疾病（即癌症和神经退行性变）之间的潜在关联。
