Seher Polat1, Yasin Şimşek2. 1. Medical Faculty, Department of Medical Genetics, Erzincan University, Erzincan, Turkey. 2. Endocrinology Department, Kayseri Training and Research Hospital, Kayseri, Turkey.
Abstract
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.
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.
Entities:
Keywords:
Antioxidant enzymes; SOD1; SOD2; gene polymorphism; polycystic over syndrome