Origin and pathophysiology of protein carbonylation, nitration and chlorination in age-related brain diseases and aging

被引:79
作者
Gonos, Efstathios S. [1 ]
Kapetanou, Marianna [1 ,2 ]
Sereikaite, Jolanta [3 ]
Bartosz, Grzegorz [4 ]
Naparlo, Katarzyna [5 ]
Grzesik, Michalina [5 ]
Sadowska-Bartosz, Izabela [5 ]
机构
[1] Natl Hellen Res Fdn, Inst Biol Med Chem & Biotechnol, Athens 11635, Greece
[2] Univ Athens, Dept Biochem & Mol Biol, Fac Biol, Athens 15701, Greece
[3] Vilnius Gediminas Tech Univ, Fac Fundamental Sci, Dept Chem & Bioengn, LT-2040 Vilnius, Lithuania
[4] Univ Lodz, Fac Biol & Environm Protect, Dept Mol Biophys, PL-90236 Lodz, Poland
[5] Univ Rzeszow, Fac Biol & Agr, Dept Analyt Biochem, PL-35601 Rzeszow, Poland
来源
AGING-US | 2018年 / 10卷 / 05期
关键词
oxidative stress; carbonylation; nitration; chlorination; proteasome; AMYLOID-BETA-PEPTIDE; MILD COGNITIVE IMPAIRMENT; MYELOPEROXIDASE-DERIVED OXIDANTS; REDOX PROTEOMICS IDENTIFICATION; CHAPERONE-MEDIATED AUTOPHAGY; HUMAN EMBRYONIC FIBROBLASTS; METAL-CATALYZED OXIDATION; BLOOD-SERUM PROTEINS; LIFE-SPAN EXTENSION; ALZHEIMERS-DISEASE;
D O I
10.18632/aging.101450
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Non-enzymatic protein modifications occur inevitably in all living systems. Products of such modifications accumulate during aging of cells and organisms and may contribute to their age-related functional deterioration. This review presents the formation of irreversible protein modifications such as carbonylation, nitration and chlorination, modifications by 4-hydroxynonenal, removal of modified proteins and accumulation of these protein modifications during aging of humans and model organisms, and their enhanced accumulation in age-related brain diseases.
引用
收藏
页码:868 / 901
页数:34
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