Base Excision Repair in Physiology and Pathology of the Central Nervous System

被引：19

作者：

Bosshard, Matthias ^{[1
]}

Markkanen, Enni ^{[1
]}

van Loon, Barbara ^{[1
]}

机构：

[1] Univ Zurich Irchel, Inst Vet Biochem & Mol Biol, CH-8057 Zurich, Switzerland

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2012年 / 13卷 / 12期

基金：

瑞士国家科学基金会;

关键词：

brain; neurodegeneration; reactive oxygen species; DNA damage; base excision repair; DNA-POLYMERASE-BETA; STRAND BREAK REPAIR; DEOXYRIBONUCLEIC-ACID POLYMERASE; OXIDATIVELY DAMAGED DNA; AMYOTROPHIC-LATERAL-SCLEROSIS; HOGG1 SER326CYS POLYMORPHISM; HUMAN APURINIC ENDONUCLEASE; ADP-RIBOSE POLYMERASE; SPINAL MOTOR-NEURONS; INDUCED BRAIN TRAUMA;

D O I：

10.3390/ijms131216172

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Relatively low levels of antioxidant enzymes and high oxygen metabolism result in formation of numerous oxidized DNA lesions in the tissues of the central nervous system. Accumulation of damage in the DNA, due to continuous genotoxic stress, has been linked to both aging and the development of various neurodegenerative disorders. Different DNA repair pathways have evolved to successfully act on damaged DNA and prevent genomic instability. The predominant and essential DNA repair pathway for the removal of small DNA base lesions is base excision repair (BER). In this review we will discuss the current knowledge on the involvement of BER proteins in the maintenance of genetic stability in different brain regions and how changes in the levels of these proteins contribute to aging and the onset of neurodegenerative disorders.

引用

页码：16172 / 16222

页数：51

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