期刊
BIOCHIMIE
卷 94, 期 9, 页码 1837-1848出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biochi.2012.01.020
关键词
Type 2 diabetes; Superoxide anion; Reactive oxygen species; Atherosclerosis; Renal dysfunction; Retina dysfunction; Nerve dysfunction
Most known pathways of diabetic complications involve oxidative stress. The mitochondria electron transport chain is a significant source of reactive oxygen species (ROS) in insulin secretory cells, insulin peripheral sensitive cells and endothelial cells. Elevated intracellular glucose level induces tricarboxylic acid cycle electron donor overproduction and mitochondrial proton gradient increase leading to an increase in electron transporter lifetime. Subsequently, the electrons leaked combine with respiratory oxygen (O-2) resulting in superoxide anion (O-center dot(2)-) production. Advanced glycation end products derive ROS via interaction with their receptors. Elevated diacylglycerol and ROS activate the protein kinase C pathway which, in turn, activates NADPH oxidases. A vicious circle of pathway derived ROS installs. Pathologic pathways induced ROS are activated and persistent though glycemia returns to normal due to hyperglycemia memory. Endothelial nitric oxide synthase may produce both superoxide anion (O-center dot(2)-) and nitric oxide (NO) leading to peroxynitrite ((ONOO-)-O-center dot) generation. Homocysteine is also implicated in oxidative stress pathogenesis. In this paper we have highlighted the pathologic mechanisms of ROS on atherosclerosis, renal dysfunction, retina dysfunction and nerve dysfunction in type 2 diabetes. Cell oxidant stress delivery have pivotal role in cell dysfunction onset and progression of angiopathies but an early introduction of good glycemic control may protect cells more efficiently than antioxidants. (C) 2012 Elsevier Masson SAS. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据