Diabetic retinopathy, a severe sight-threatening complication of diabetes mellitus, accounts for a large number of cases of acquired, yet potentially avoidable, blindness. The principal mechanism of its pathogenesis appears to be alterations in the microvasculature of retina as the result of hyperglycemia. The elevated concentration of blood glucose is a harbinger of numerous molecular changes. These lead to various responses that result in microangiopathy. Oxidative stress, one such response, is attributed to disruption in the homeostasis of free radical production during the various vital processes such as the electron transport chain reaction and the scavenging mechanisms designed to neutralize these damaging molecules. This imbalance has been linked to the pathophysiology of diabetic retinopathy. Excessive formation of free radicals influences almost all pathways involved in normal human physiology. Thus, hyperglycemia-induced oxidative stress is one of the factors associated with biochemical changes. These changes are further responsible for the various structural and functional abnormalities seen in diabetic retinopathy.
Keywords: AGEs (advanced glycation end-products); ROS (reactive oxygen species); polyol pathway; protein kinase C; superoxide radical.
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