Evaluation of Relationship Between SOD1 50-bp Deletion Gene Polymorphism, Cu, Zn Level, and Viscosity in Postmenopausal Osteoporosis Patients with Vertebral Fractures.

Oxidative stress plays a role in the pathogenesis of bone loss, causing low bone mineral density (BMD) and associated osteoporotic fractures. In our study, we aimed to investigate the relationship of SOD1 50-bp insertion(Ins)/deletion(Del) polymorphism that is involved in oxidative stress metabolism, Cu and Zn element concentrations, and plasma viscosity level, with postmenopausal osteoporosis and related vertebral fractures. The study included 167 voluntary individuals. The 50-bp Ins/Del polymorphism of SOD1 was determined by allele-specific PCR. Plasma Cu and Zn levels were measured by atomic absorption spectrophotometry (AAS). The plasma viscosity was determined using the Harkness Capillary Viscometer device. In our study, the distribution of SOD1 promoter 50-bp Ins/Del polymorphism did not indicate a significant difference between the groups and in postmenopausal osteoporosis patients with and without fractures (p > 0.05). The Ins/Ins genotype was found to be common in individuals in both groups. The Cu and Zn levels of the study group were found to be between the normal reference values (p > 0.05). It was determined that plasma viscosity increased significantly in the group of osteoporotic patients and in patients with postmenopausal osteoporosis with fractures (p < 0.01). In addition, plasma viscosity was found to significantly increase in patients with Ins/Ins genotype and fractures (p < 0.01). Postmenopausal osteoporosis and associated vertebral fracture were found not to be directly related to SOD1 50-bp polymorphism and Cu and Zn element levels. Plasma viscosity levels were found to increase due to the increase in oxidative stress products. Further studies are needed to clarify the roles and relationships of SOD genes and trace elements in the development of postmenopausal osteoporosis and vertebral fracture.