Sinclair A J, Lunec J, Girling A J, Barnett A H
University Department of Geriatric Medicine, University of Wales College of Medicine, Cardiff, UK.
EXS. 1992;62:342-52. doi: 10.1007/978-3-0348-7460-1_34.
Free radical mechanisms are increasingly being implicated in the pathogenesis of tissue damage in diabetes. Various sources of free radicals may modulate oxidative stress in diabetes, including non-enzymatic glycosylation of proteins and monosaccharide autooxidation, polyol pathway activity, indirect production of free radicals through cell damage from other causes, and reduced antioxidant reserve. Ascorbic acid, which may be a principal modulator of free radical activity in diabetes, is shown to be consumed, presumably through free radical scavenging, thus preserving levels of other antioxidants such as glutathione.
自由基机制越来越多地被认为与糖尿病患者的组织损伤发病机制有关。自由基的各种来源可能会调节糖尿病中的氧化应激,包括蛋白质的非酶糖基化和单糖自氧化、多元醇途径活性、通过其他原因导致的细胞损伤间接产生自由基以及抗氧化储备减少。抗坏血酸可能是糖尿病中自由基活性的主要调节剂,据推测它通过清除自由基而被消耗,从而维持谷胱甘肽等其他抗氧化剂的水平。