The effects of Mn-SOD (SOD-2) level and SOD2 ala9val polymorphism on the development of alzheimer disease

Objective: In this study, we aimed to measure MnSOD levels and SOD-2 Ala9Val polymorphisms on Alzhemier patients.Materials and Method: The study was designed in Celal Bayar University, School of Medicine, Department of Clinical Biochemistry, Department of Neurology and Manisa Mental Hospital Neurology Clinic and was approved by the local ethical committee of the university hospital. We selected 53 Alzheimer?s patients (group 1), and 60 control samples (group 2) from age and sex matched healthy volunteersThe principle of the total SOD (EC 1.15.1.1) activity method is based, briefly, on the inhibition of nitroblue tetrazolium (NBT) reduction by O2? generated by xanthine/xanthine oxidase system. Mn-SOD genotypes were determined by means of real time PCR on a LightCycler analyzer (Roche DiagnosticsResults: There was no difference in Ala homozygosity (12.5%, 10.3% respectively), Ala/Val heterozygosity (50%, 50% respectively) and Val homozygosity (37.5%, 39.7% respectively) between group 1 and group 2. However, Ala/Val (OR: 0.82, %CI: 0.236-2.901) and Val/Val (OR: 0.78, %CI: 0.216-2.840) mutations were less prevalent in Alzheimer patients. MnSOD levels were significantly higher in group 1 (144 ± 67 U/gHb, 76 ± 51 U/gHb respectively, p=0.001), but higher total SOD levels did not reach a significant difference (224 ± 74 U/gHb, 198 ± 93 U/gHb respectively, p=0.108Conclusion: We consider that higher total SOD and MnSOD may be secondary to mitochondrial dysfunction which may play a role in the pathophysiology of Alzheimer disease.Key Words: Alzheimer Disease, MnSOD, Ala9Val, Total SOD