文献DOI： 10.1002/jbt.10058
文献PMID： 12616644
文献原文链接： http://doi.org.sci-hub.tw/10.1002/jbt.10058
《Diabetes, oxidative stress, and antioxidants: a review》
糖尿病、氧化应激和抗氧化剂：综述
【Abstract】
Increasing evidence in both experimental and clinical studies suggests that oxidative stress plays a major role in the pathogenesis of both types of diabetes mellitus. Free radicals are formed disproportionately in diabetes by glucose oxidation, nonenzymatic glycation of proteins, and the subsequent oxidative degradation of glycated proteins. Abnormally high levels of free radicals and the simultaneous decline of antioxidant defense mechanisms can lead to damage of cellular organelles and enzymes, increased lipid peroxidation, and development of insulin resistance. These consequences of oxidative stress can promote the development of complications of diabetes mellitus. Changes in oxidative stress biomarkers, including superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase, glutathione levels, vitamins, lipid peroxidation, nitrite concentration, nonenzymatic glycosylated proteins, and hyperglycemia in diabetes, and their consequences, are discussed in this review. In vivo studies of the effects of various conventional and alternative drugs on these biomarkers are surveyed. There is a need to continue to explore the relationship between free radicals, diabetes, and its complications, and to elucidate the mechanisms by which increased oxidative stress accelerates the development of diabetic complications, in an effort to expand treatment options.
摘要翻译：
越来越多的实验和临床研究证据表明，氧化应激在两种类型的糖尿病发病机制中起主要作用。在糖尿病中，自由基通过葡萄糖氧化、蛋白质的非酶糖化和随后糖化蛋白质氧化降解而不成比例地增加。异常高水平的自由基和同时抗氧化防御机制下降，可能导致细胞器和酶的损害、脂质过氧化增加和胰岛素抵抗进展。氧化应激的这些后果可促进糖尿病并发症发生发展。本文综述了糖尿病氧化应激生物标志物，包括超氧化物歧化酶、过氧化氢酶、谷胱甘肽还原酶、谷胱甘肽过氧化物酶、谷胱甘肽水平、维生素、脂质过氧化、亚硝酸盐浓度、非酶糖化蛋白和高血糖的变化及其后果。对各种常规和替代药物对这些生物标志物的影响进行了体内研究。有必要继续探讨自由基、糖尿病及其并发症之间的关系，并阐明氧化应激增加加速糖尿病并发症发展机制，努力扩大治疗的选择方案。
