Five variants of the superoxide dismutase genes in Turkish women with polycystic ovary syndrome

Introduction: Polycystic ovary syndrome (PCOS) is one of the most common endocrine–reproductive–metabolic disorders of women at reproductive age. Many investigations have revealed that reactive oxygen species (ROS) level is significantly increased in patients with PCOS compared to healthy women. Object: The goal of the current study is to investigate the association between superoxide dismutase (SOD) variants and the risk of PCOS among Turkish women. Method and subjects: Three hundred twelve voluntary premenopausal women (148 healthy controls and 164 patients with PCOS) 18–45 years of age were include the study. All volunteers underwent physical examination and biochemical hormones evaluation. Five selected variants in SOD1 (+35 A/C (rs2234694) and SOD2 (–102 C ' T, 3′UTRT ' A (rs2842980), 3′UTRA ' G (rs5746136), and Ala16ValC ' T (rs4880) were analysed by using polymerase chain reaction and restriction fragment length polymorphism (PCR–RFLP) method. Result: 3′UTRA ' G and Ala16ValC ' T variants showed significant differences between study groups. In the additive model of rs5746136 variant having AG and GG genotype increased the PCOS risk 2-fold (OR: 1.7, 95% CI: 1.08–2.77, p = 0.003) and 5-fold (OR: 5, 95% CI: 1.7–14.2,p = 0.003) compared to AA genotype, respectively. To have a GG + AG genotype increased the PCOS risk 2-fold (OR: 2.95% Cl: 1.2–3.1, p = 0.003) compared to AA genotype in “G” dominant model. In case of the “G” recessive model, having a GG genotype increased the PCOS risk 4-fold (OR: 3.8, 95% CI: 1.3–10.4, p = 0.01) compared to AA + AG genotype. The TT genotype of rs4880 showed almost 2-fold (OR: 1.8, 95% CI: 1.12–3.0) increased PCOS risk in the “T” recessive model. Conclusion: It is quite likely that the variants which result in decreased function in the antioxidant defence mechanism related genes contribute to PCOS aetiology with inhibiting/reducing of ROS elimination. © 2020 Informa UK Limited, trading as Taylor & Francis Group.