Age-associated neurodegeneration and oxidative damage to lipids, proteins and DNA

被引:165
|
作者
Radak, Zsolt [1 ]
Zhao, Zhongfu
Goto, Sataro [2 ]
Koltai, Erika
机构
[1] Semmelweis Univ, Fac Phys Educ & Sport Sci, Res Inst Sport Sci, TF, Budapest, Hungary
[2] Juntendo Univ, Grad Sch, Inst Hlth & Sports Sci & Med, Chiba, Japan
关键词
Oxidative stress; Hormesis; Oxidative damage repair; Aging; AMYLOID-BETA-PEPTIDE; METHIONINE SULFOXIDE REDUCTASE; ALZHEIMERS-DISEASE BRAIN; MITOCHONDRIAL-DNA; 8-OXOGUANINE-DNA GLYCOSYLASE; SYNAPTIC PLASTICITY; ENZYME-ACTIVITY; FREE-RADICALS; LON PROTEASE; MOUSE-BRAIN;
D O I
10.1016/j.mam.2011.10.010
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
Lipids, proteins and DNA in the central nervous system have a high sensitivity to oxidative stress. Reactive oxygen species (ROS)-induced damage increases with aging, especially in the last quarter of the life span. The so called base level of oxidative modification of lipids could be important to cell signaling, and membrane remodeling, but the ROS-mediated post translation modifications of proteins could be important to the homeostasis of protein turnover. Low levels of 8-oxo-7,8-dihydroguanine (8-oxoG) might be necessary for transcription. A high level of accumulation of lipid peroxidation, oxidative protein damage or 8-oxoG, on the other hand, accelerates the progress of aging and neurodegenerative diseases. Therefore, agents that induce the activity of repair enzymes, such as Ca(2(+))-independent phospholipase A(2) (iPLA(2)beta), methionine sulfoxide reductase, and 8-oxoguanine DNA glycosylase, or the activity of enzymes that could prevent the accumulation of oxidized, toxic proteins, such as proteasome, Lon protease, neprilysin or insulin degrading enzyme, may act as potential therapeutic tools to slow the aging process and the progress of neurodegenerative diseases. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码:305 / 315
页数:11
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