الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Retinopathy, a severely disbling complication of diabetes mellitus, is leading cause of acquired blindness among young adults in developed counteries. Good diabetic control can attenuate the development of diabetic retinopathy. But such metabolic control is often difficult to achieve and additional therapies need to be identified by which retinopathy can be prevented or arrested. Hyperglycaemia plays a critical role in the development and progression of retinopathy, but the mechanism by which hyperglycaemia results in the development of retinopathy is not clear. Oxidative stress is increased in the retina in diabetic patients. The possible sources of increased oxidative stress might include increasing the generation of free radicals or impaired of antioxidants defense system. In this study, enzymatic antioxidants including superoxide dismutase (SOD), catalase, glutathione peroxidase (GSHPX) glutathione reductase (GSHR) enzyme were studied. Also reduced glutathione (GSH), as a nonenzymatic antioxidant, and malondialdehyde (MDA), as an end product of lipid peroxidation, were studied in addition to serum blood glucose and glycosylated haemoglobin HbA1C in diabetic retinopathy group only. The most important results of the present study are summarized and disscussed as follows: Glycosylated HbA1C was elevated in red blood cells of patients with diabetic retinopathy. MDA levels were elevated in red blood cells of patients with diabetic retinopathy. Mean levels of GSH were decreased in diabetic retinopathy patients. Patients with diabetic retinopathy showed a lowering of the levels of both GSHPX and GSHR enzymes. A marked reduction of SOD levels were observed in serum as well as a small reduction in its activity in red blood cells. The reduction of SOD in both serum and red blood cells of patients with diabetic retinopathy.