Abstract
Endothelial cell dysfunction has been implicated in a number of microvascular complications of diabetes. Microvascular changes in diabetic retinopathy present initially as leaky vessels in the neural retina which lead to deterioration of vision. Oxidative injury as a result of free radical production has been suggested as a mechanism of endothelial cell dysfunction caused by hyperglycemia.The NADPH oxidase complex catalyzes the formation of superoxide (O2·−); hydrogen peroxide (H2O2) is formed by dismutaion of O2·−. Cytochemical localization of the free radical derived oxidant, H2O2, was done by the cerium NADPH/NADH oxidase method in eyes of obese, noninsulin dependent diabetic BBZ/Wor rats with diabetes of five and ten months duration. Age matched, nondiabetic controls were eyes from BB/WorDRrats. Endothelial cell dysfunction, indicated by leaky vessels, was documented by colloidal gold immunocytochemical localization of extravasated endogenous serum albumin on sections of retina in which H2O2had been localized.
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