Oxidative genome damage and its repair: Implications in aging and neurodegenerative diseases

被引：110
作者：
Hegde, Muralidhar L. [1 ]
Mantha, Anil K. [1 ]
Hazra, Tapas K. [1 ,2 ]
Bhakat, Kishor K. [1 ]
Mitra, Sankar [1 ]
Szczesny, Bartosz [1 ]
机构：
[1] Univ Texas Med Branch, Dept Biochem & Mol Biol, Galveston, TX 77555 USA
[2] Univ Texas Med Branch, Dept Internal Med, Galveston, TX 77555 USA
来源：
MECHANISMS OF AGEING AND DEVELOPMENT | 2012年 / 133卷 / 04期
关键词：
DNA base excision repair; DNA glycosylases; Single-strand break repair; Protein-protein and protein-DNA interactions; Aging; Neurodegenerative disorders; Reactive oxygen species; BASE EXCISION-REPAIR; HUMAN DNA GLYCOSYLASE; AMYOTROPHIC-LATERAL-SCLEROSIS; STRAND BREAK REPAIR; MAMMALIAN MITOCHONDRIAL GENOMES; HOGG1 SER326CYS POLYMORPHISM; AP-ENDONUCLEASE APE1/REF-1; ALZHEIMERS-DISEASE; POLYMERASE-BETA; LIGASE-III;
D O I：
10.1016/j.mad.2012.01.005
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Reactive oxygen species (ROS), generated endogenously during respiration or exogenously by genotoxic agents, induce oxidized bases and single-strand breaks (SSBs) in DNA that are repaired via the base excision/SSB repair (BER/SSBR) pathway in both the nucleus and mitochondria. Tightly regulated BER/SSBR with multiple sub-pathways is highly complex, and is linked to the replication and transcription. The repair-initiating DNA glycosylases (DGs) or AP-endonuclease (APE1) control the sub-pathway by stably interacting with downstream proteins usually via their common interacting domain (CID). A nonconserved CID with disordered structure usually located at one of the termini includes the sequences for covalent modifications and/or organelle targeting. While the DGs are individually dispensable, the SSBR-initiating APE1 and polynucleotide kinase 3' phosphatase (PNKP) are essential. BER/SSBR of mammalian nuclear and mitochondrial genomes share the same early enzymes. Accumulation of oxidative damage in nuclear and mitochondrial genomes has been implicated in aging and various neurological disorders. While defects in BER/SSBR proteins have been linked to hereditary neurodegenerative diseases, our recent studies implicated transition metal-induced inhibition of NEIL family DGs in sporadic diseases. This review focuses on the recent advances in repair of oxidatively damages in mammalian genomes and their linkage to aging and neurological disorders. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
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页码：157 / 168
页数：12
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