Dicarbonyl stress in cell and tissue dysfunction contributing to ageing and disease

被引：289
作者：
Rabbani, Naila [1 ]
Thornalley, Paul J. [1 ]
机构：
[1] Univ Warwick, Univ Hosp, Warwick Med Sch, Clin Sci Res Labs, Coventry CV2 2DX, W Midlands, England
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2015年 / 458卷 / 02期
基金：
英国生物技术与生命科学研究理事会;
关键词：
Glycation; Oxidative stress; Hypoxia; Inflammation; Diabetes; Cardiovascular disease; GLYOXALASE; 1; OXIDATIVE STRESS; COPY NUMBER; METHYLGLYOXAL; GLYCATION; PRODUCTS; ACCUMULATION; NITRATION; ARGININE; SYSTEM;
D O I：
10.1016/j.bbrc.2015.01.140
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：
Dicarbonyl stress is the abnormal accumulation of dicarbonyl metabolites leading to increased protein and DNA modification contributing to cell and tissue dysfunction in ageing and disease. Enzymes metabolising dicarbonyls, glyoxalase 1 and aldoketo reductases, provide an efficient and stress-response enzyme defence against dicarbonyl stress. Dicarbonyl stress is produced by increased formation and/or decreased metabolism of dicarbonyl metabolites, and by exposure to exogenous dicarbonyls. It contributes to ageing, disease and activity of cytototoxic chemotherapeutic agents. (C) 2015 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license
引用
收藏
页码：221 / 226
页数：6
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