Abstract

Background: Extracellular superoxide dismutase (EC-SOD) gene polymorphism play an essential role in the progression of diabetic complications. Reactive oxygen species (ROS) were known to damage neurons by enhancing nerve lipid peroxidation, the damaging mitochondrial DNA, break-down the respiratory chain, and the cross-linking of neuron proteins. Aim: the aim of this study was to investigate the relationship between (Ec-SOD) gene polymorphism and the pathogenesis of diabetic peripheral neuropathy in type2 diabetic patients. Arg(213)Gly polymorphism of Ec-SOD gene polymorphism were studied in type2 diabetic patients with (n=30) and without DPN (n=30). Results: Polymerase chain reaction (PCR) technique were used for detection Ec-SOD polymorphisms. This technique included the use of PCR primers (Forward and Reverse) to produce a restriction site in the amplified EC-SOD gene product just with the polymorphic base. Then, the product of (PCR) was digested with Eco52I restriction enzyme to detect Arg(-213)Gly polymorphic position. The results of Arg(-213)Gly polymorphism showed that the frequency of Arg/Arg, Arg/Gly, and Gly/Gly were 70%, 13.3%, and 16.6% in healthy control subject and 53.3%, 16.6%, and 30% in diabetic without neuropathy countered by 23.3%, 26.6%, and 50% in diabetic with neuropathy. This proposed that the Arg (-213)Gly polymorphism in the EcSOD gene is significantly associated with a risk for progression of diabetic peripheral neuropathy. Conclusions: Arg(-213)Gly polymorphism of Ec-SOD gene was associated with diabetic peripheral neuropathy in type2 diabetic patients of Babylon Province

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