Abstract
Oxidative stress is a well-accepted etiological mechanism that contributes to neuronal dysfunction. Role of oxidative stress as a mechanism of retinopathy in controlled type 2 diabetic patients was evaluated. Participants were divided into three groups: Group 1 as 30 normal eyes of 15 subjects, Group 2 comprised 24 eyes of 12 diabetic patients without retinopathy and Group 3 comprised 23 eyes of 12 diabetic patients with different grades of retinopathy (8 eyes with maculopathy). A complete ophthalmological examination was performed. Oxidative stress markers were measured in blood. Macular thickness was different in all quadrants among all groups and showed a tendency to increase in Group 3 due to diabetic retinopathy with insignificant changes in parapapillary retinal nerve fiber layer thickness although thinning was noted also with retinopathy. Non-significant differences in GST and lipid peroxide levels were observed between the three studied groups, whereas vitamin C and GSH levels were higher in diabetic patients when compared to those in controls. As oxidative stress, hyperglycemia and local inflammation are involved in the pathogenesis of DR, the present study proved that the progressive damage can be retarded in controlled type 2 diabetic patients using different treatment modalities that abated oxidative stress.
Highlights
Oxidative stress is a well-accepted etiological mechanism that contributes to neuronal dysfunction
Based on the fact that several oxidative stress biomarkers have been identified to play a critical role in the pathogenesis of T2DM, and that many of these markers affect retinopathy as a curve status of cardiovascular disease (CVD), the objective of this study is to find the contribution of GSH, vitamin C, Glutathione S-Transferase (GST) together with lipid peroxides as markers of antioxidant/oxidative stress signaling in the development of retinopathy in medically controlled T2DM
Higher GSH and vitamin C as anti-oxidants concomitant with non-significantly lower lipid peroxides as marker of oxidative stress were observed in controlled diabetic patients with or without retinopathy compared to healthy non diabetic control
Summary
Oxidative stress is a well-accepted etiological mechanism that contributes to neuronal dysfunction. Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia due to defects in insulin production and/or insulin action together with impaired carbohydrates, lipids, and protein metabolism It has long term health complications due to the damage, dysfunction, and failure of different organs[1]. Complications can be delayed and reduced by maintaining tight glycemic control, avoiding oxidative stress, and local inflammation[2] It is still not clear why these complications develop in some patients with poor glycemic control and not in others. Previous studies suggested that hyperglycemia-induced cellular damage, oxidative stress and reactive oxygen species (ROS) are key players for mediating the development of diabetic complications, including retinopathy[5]. DNA and activate downstream pathways that lead to pancreatic β cell damage This mechanism influences microvascular and macrovascular c omplications[6,7]. The changed metabolic environment usually leads to a decrease in cellular NADPH thereby leading to a reduction in NADPH dependent synthesis of the protective antioxidant glutathione (GSH)[11,12]
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