Pop-Busui Rodica, Sima Anders, Stevens Martin
Department of Internal Medicine, Division of Metabolism, Endocrinology and Diabetes, University of Michigan, Ann Arbor, MI, USA.
Diabetes Metab Res Rev. 2006 Jul-Aug;22(4):257-73. doi: 10.1002/dmrr.625.
This review will focus on the impact of hyperglycemia-induced oxidative stress in the development of diabetes-related neural dysfunction. Oxidative stress occurs when the balance between the production of reactive oxygen species (ROS) and the ability of cells or tissues to detoxify the free radicals produced during metabolic activity is tilted in the favor of the former. Although hyperglycemia plays a key role in inducing oxidative stress in the diabetic nerve, the contribution of other factors, such as endoneurial hypoxia, transition metal imbalances, and hyperlipidemia have been also suggested. The possible sources for the overproduction of ROS in diabetes are widespread and include enzymatic pathways, auto-oxidation of glucose, and mitochondrial superoxide production. Increase in oxidative stress has clearly been shown to contribute to the pathology of neural and vascular dysfunction in diabetes. Potential therapies for preventing increased oxidative stress in diabetic nerve dysfunction will be discussed.
本综述将聚焦于高血糖诱导的氧化应激在糖尿病相关神经功能障碍发展过程中的影响。当活性氧（ROS）的产生与细胞或组织清除代谢活动中产生的自由基的能力之间的平衡向ROS产生倾斜时，就会发生氧化应激。尽管高血糖在糖尿病神经中诱导氧化应激方面起关键作用，但也有人提出其他因素的作用，如神经内膜缺氧、过渡金属失衡和高脂血症。糖尿病中ROS过量产生的可能来源广泛，包括酶促途径、葡萄糖的自动氧化和线粒体超氧化物的产生。氧化应激的增加已被明确证明会导致糖尿病中神经和血管功能障碍的病理过程。本文将讨论预防糖尿病神经功能障碍中氧化应激增加的潜在治疗方法。
