Department of Laboratory Medicine, China-Japan Friendship Hospital, Ministry of Health, Beijing, PR China.
Clin Chem Lab Med. 2011 Nov;49(11):1773-82. doi: 10.1515/CCLM.2011.250. Epub 2011 Aug 3.
Increasing evidences have suggested that oxidative stress plays a major role in the pathogenesis of diabetes mellitus (DM). Oxidative stress also appears to be the pathogenic factor in underlying diabetic complications. Reactive oxygen species (ROS) are generated by environmental factors, such as ionizing radiation and chemical carcinogens, and also by endogenous processes, including energy metabolism in mitochondria. ROS produced either endogenously or exogenously can attack lipids, proteins and nucleic acids simultaneously in living cells. There are many potential mechanisms whereby excess glucose metabolites traveling along these pathways might promote the development of DM complication and cause pancreatic β cell damage. However, all these pathways have in common the formation of ROS, that, in excess and over time, causes chronic oxidative stress, which in turn causes defective insulin gene expression and insulin secretion as well as increased apoptosis. Various methods for determining biomarkers of cellular oxidative stress have been developed, and some have been proposed for sensitive assessment of antioxidant defense and oxidative damage in diabetes and its complications. However, their clinical utility is limited by less than optimal standardization techniques and the lack of sufficient large-sized, multi-marker prospective trials.
越来越多的证据表明，氧化应激在糖尿病（DM）发病机制中起主要作用。氧化应激似乎也是潜在糖尿病并发症的致病因素。活性氧（ROS）由环境因素产生，如电离辐射和化学致癌物，也由内源性过程产生，包括线粒体中的能量代谢。无论是内源性还是外源性产生的 ROS，都可以同时攻击活细胞中的脂质、蛋白质和核酸。过量的葡萄糖代谢物沿着这些途径可能促进 DM 并发症的发展并导致胰腺β细胞损伤，其机制有很多种。然而，所有这些途径都有一个共同之处，即 ROS 的形成，ROS 过多且持续时间过长，会导致慢性氧化应激，进而导致胰岛素基因表达和胰岛素分泌缺陷以及细胞凋亡增加。已经开发出了许多用于确定细胞氧化应激生物标志物的方法，并且已经提出了一些方法用于敏感评估糖尿病及其并发症中的抗氧化防御和氧化损伤。然而，由于标准化技术不够理想以及缺乏足够的大型多标志物前瞻性试验，其临床应用受到限制。
