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.