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甲基乙二醛在组织中产生自由基。

Free radical generation by methylglyoxal in tissues.

作者信息

Desai Kaushik M, Wu Lingyun

机构信息

Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada.

出版信息

Drug Metabol Drug Interact. 2008;23(1-2):151-73. doi: 10.1515/dmdi.2008.23.1-2.151.

DOI:10.1515/dmdi.2008.23.1-2.151
PMID:18533368
Abstract

Methylglyoxal (MG) is a reactive dicarbonyl intermediate of the glycolytic pathway. Increased oxidative stress is associated with conditions of increased MG, such as diabetes mellitus. Increased oxidative stress is due to an increase in highly reactive by-products of metabolic pathways, the so-called reactive oxygen species, such as superoxide anion, hydroxyl radical, hydrogen peroxide, nitric oxide and peroxynitrite. These reactive species react with a variety of proteins, enzymes, lipids, DNA and other molecules and disrupt their normal function. Oxidative stress causes many pathological changes that lead to vascular complications of diabetes mellitus, hypertension, neurodegenerative diseases and aging. In this review we summarize the correlation of elevated MG and various reactive oxygen species, and the enzymes that produce them or take part in their disposal, such as antioxidant enzymes and cofactors. The findings reported in various studies reviewed have started filling in gaps in our knowledge that will ultimately provide us with a clear picture of how the whole process that causes cellular dysfunction is initiated.

摘要

甲基乙二醛(MG)是糖酵解途径中的一种活性二羰基中间体。氧化应激增加与MG增加的情况有关,如糖尿病。氧化应激增加是由于代谢途径中高反应性副产物(即所谓的活性氧物种,如超氧阴离子、羟基自由基、过氧化氢、一氧化氮和过氧亚硝酸盐)的增加。这些活性物质与多种蛋白质、酶、脂质、DNA和其他分子发生反应,破坏它们的正常功能。氧化应激会导致许多病理变化,进而引发糖尿病的血管并发症、高血压、神经退行性疾病和衰老。在本综述中,我们总结了MG升高与各种活性氧物种以及产生它们或参与其清除的酶(如抗氧化酶和辅助因子)之间的相关性。在综述的各种研究中报告的发现开始填补我们知识上的空白,最终将为我们提供一幅关于导致细胞功能障碍的整个过程是如何启动的清晰图景。

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