Polycystic Ovary Syndrome and Oxidative Stress—From Bench to Bedside

Abstract

Oxidative stress (OS) is a condition that occurs as a result of an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify and neutralize them. It can play a role in a variety of reproductive system conditions, including polycystic ovary syndrome (PCOS), endometriosis, preeclampsia, and infertility. In this review, we briefly discuss the links between oxidative stress and PCOS. Mitochondrial mutations may lead to impaired oxidative phosphorylation (OXPHOS), decreased adenosine triphosphate (ATP) production, and an increased production of ROS. These functional consequences may contribute to the metabolic and hormonal dysregulation observed in PCOS. Studies have shown that OS negatively affects ovarian follicles and disrupts normal follicular development and maturation. Excessive ROS may damage oocytes and granulosa cells within the follicles, impairing their quality and compromising fertility. Impaired OXPHOS and mitochondrial dysfunction may contribute to insulin resistance (IR) by disrupting insulin signaling pathways and impairing glucose metabolism. Due to dysfunctional OXPHOS, reduced ATP production, may hinder insulin-stimulated glucose uptake, leading to IR. Hyperandrogenism promotes inflammation and IR, both of which can increase the production of ROS and lead to OS. A detrimental feedback loop ensues as IR escalates, causing elevated insulin levels that exacerbate OS. Exploring the relations between OS and PCOS is crucial to fully understand the role of OS in the pathophysiology of PCOS and to develop effective treatment strategies to improve the quality of life of women affected by this condition. The role of antioxidants as potential therapies is also discussed.

Mechanisms and Target Parameters in Relation to Polycystic Ovary Syndrome and Physical Exercise: Focus on the Master Triad of Hormonal Changes, Oxidative Stress, and Inflammation

“…In a previous study, Zeber-Lubecka et al summarized that any defects at the level of mtDNA replication affect the formation of numerous mutations; thus, mtDNA damage can be a contributor in the pathogenesis of PCOS. They demonstrated that mitochondrial mutations can lead to impaired oxidative phosphorylation, disruption to insulin signaling pathways, and result in an increased ROS production and a consequent oocyte impairment [ 67 ]. Sang-Hea Lee et al have demonstrated that the number of mtDNA copies were found to be lower in women with PCOS than in the control groups [ 68 ], with a negative correlation with the severity of the syndrome.…”

Exploring Therapeutic Potential of Catalase: Strategies in Disease Prevention and Management

“…Antioxidants, notably catalase, can alleviate oxidative stress and inflammation in these conditions, potentially improving fertility and pregnancy outcomes [ 153 ]. While research on catalase in reproductive health is still evolving, its role in combating oxidative stress suggests potential benefits in maintaining fertility and supporting healthy pregnancies.…”

Cellular senescence of granulosa cells in the pathogenesis of polycystic ovary syndrome

“…The characteristic morphological features of polycystic ovaries are the accumulation of antral follicles of 5–8 mm and follicular growth failure ( Franks et al , 2000 , 2008 ). Its pathophysiology has not been well characterized, but various mechanisms, including endoplasmic reticulum (ER) stress ( Harada, 2022 ; Koike et al , 2023 ), oxidative stress ( Zeber-Lubecka et al , 2023 ), and abnormal inflammation and immunity ( Lima et al , 2018 ) have been implicated. Women with PCOS have high serum concentrations of pro-inflammatory molecules, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, and IL-18 ( Kaya et al , 2010 ; Alissa et al , 2021 ; Mazloomi et al , 2023 ).…”