The Association between Mn-SOD Gene Polymorphism and Peripheral Neuropathy in Type2 Diabetic Patients of Babylon Province-Iraq

Background: Oxidative stress has been known to be implicated in the onset and development of impaired insulin secretion and insulin resistance and both are involved in diabetes. The mechanisms involved in oxidative stress-induced diabetic peripheral neuropathy include the generation of reactive oxygen species ROS, excesses reactive nitrogen species RNS, lipid peroxidation, DNA damage, and reduction in cellular antioxidants. Polymorphisms in genes responsible for encoding these antioxidant enzymes causes the development of diabetic peripheral neuropathy (DPN). Aim: this study was aimed to indicated the role of genes encoding manganese (Mn-SOD) superoxide dismutase in the pathogenesis of DPN in a type2 diabetic patients of Babylon province. Ala(-9)Val polymorphism of Mn-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 Mn-SOD polymorphisms. This technique included the use of PCR primers (Forward and Reverse) to produce a restriction site in the amplified Mn-SOD gene product just with the polymorphic base. Then, the product of (PCR) was digested with Bsh TI restriction enzyme to detect Ala(-9) polymorphic position. The results of Ala(-9)Val polymorphism showed that the frequency of Ala/Ala, Ala/Val, and Val/Val were 63.3%, 20%, and 13.3% in healthy control subject and 36.6%, 33.3%, and 30% in diabetic without neuropathy countered by 23.3%, 20%, and 56.6% in diabetic with neuropathy. This proposed that the Ala(-9)Val polymorphism in the Mn-SOD gene is significantly associated with a risk for progression of diabetic peripheral neuropathy. Conclusions: Homozygote pattern Ala/Ala were more frequent in control groups compared with homozygote pattern Val/Val were significantly more frequent in diabetic peripheral neuropathy patients.