Role of Oxidative Stress in Polycystic Ovary Syndrome

Polycystic ovary syndrome (PCOS) is a multifactorial disorder affecting many women of reproductive age, typically due to hyperandrogenemia, hyperinsulinemia, and enigmatic genetic factors. The complex nature of PCOS is reflected in the broad spectrum of the disorder's clinical presentation, including metabolic and reproductive disorders. As a result, while the European Society for Human Reproduction and Embryology and the American Society for Reproductive Medicine (ESHRE/ASRM) have agreed on a consensus definition of PCOS to help clinical investigators, the condition is recognized to have multiple clinical phenotypes. Oxidative stress (OS) occurs when destructive reactive oxygen species (ROS) outbalance antioxidants, causing DNA damage and/or cell apoptosis. Moreover, reactive nitrogen species (RNS), such as nitrogen oxide (NO) with an unpaired electron also are highly reactive and toxic. In a quest to delineate the role of OS in the pathogenesis of PCOS, investigators have examined patients with the disorder for a wide array of OS biomarkers, including malondialdehyde (MDA), protein carbonyl, total antioxidant capacity (TAC), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione (GSH).