Department of Medicine, University of Florida-College of Medicine, Jacksonville, 32209, USA.
Am J Ther. 2011 May;18(3):266-78. doi: 10.1097/MJT.0b013e3181b7badf.
There is ample empiric evidence to indicate that oxidative stress contributes to the pathogenesis of coronary artery disease and has a key role in the onset and progression of diabetes and its complications. Diabetes leads to depletion of the cellular antioxidant defense system and is associated with an increase in the production of free radicals. Oxidative stress can be the result of multiple pathways. Some of these are related to substrate-driven overproduction of mitochondrial reactive oxygen species, advanced glycation end product formation, glucose autoxidation, and depletion of micronutrients and cellular elements with antioxidative properties. There are numerous observational studies in the literature showing a beneficial outcome of the consumption of antioxidant vitamins. However, the interventional trials portray a different picture. The divide between the robust experimental evidence of the pathogenetic role of increased oxidative load in diabetes and the overwhelming failure of antioxidants to show any health benefits in clinical trials may well be characterized as the "antioxidant paradox."
有大量的经验证据表明，氧化应激是导致冠状动脉疾病发病机制的一个重要因素，在糖尿病及其并发症的发生和发展中也起着关键作用。糖尿病可导致细胞抗氧化防御系统耗竭，并与自由基产生增加有关。氧化应激可能是多种途径的结果。其中一些与线粒体活性氧物质的底物驱动过度产生、糖基化终产物形成、葡萄糖自动氧化以及具有抗氧化特性的微量营养素和细胞成分的耗竭有关。文献中有许多观察性研究表明，抗氧化维生素的摄入有有益的结果。然而，干预试验却描绘了一幅不同的画面。在糖尿病中，增加氧化负荷的发病机制作用的强有力的实验证据与抗氧化剂在临床试验中未能显示出任何健康益处之间存在明显的分歧，这种分歧很可能被描述为“抗氧化剂悖论”。
