2 Redox biology and endocrine dysregulation in PCOS 2.1 OS pathways in PCOS: sources of ROS and antioxidant defense impairment Emerging evidence identifies PCOS as a disorder of redox dyshomeostasis, contributing to its complex reproductive, endocrine, and metabolic manifestations ( Among endogenous sources, mitochondrial electron transport chain (ETC) inefficiency stands out as a dominant ROS generator in PCOS ( Androgen excess emerges not only as a hormonal hallmark of PCOS but also as a direct ROS instigator ( While ROS sources increase, antioxidant defenses in PCOS are often found depleted ( 2.2 Mitochondrial dysfunction, lipid peroxidation, and redox imbalance in oocytes and granulosa cells The competence of oocytes and their surrounding granulosa cells is fundamentally governed by mitochondrial health, balanced redox homeostasis, and membrane integrity ( LPO is an evident indicator of oxidative injury in ovarian cells
Clinicians should document the drug name, dose, route, indication, frequency, date of last dose, duration of therapy, recent dose changes, and gastrointestinal symptoms
All animals were accommodated in laboratory conditions for 1 week before treatment and maintained under the same conditions throughout the experiment
The identification of additional members involved in the AITC-induced responses is a key step to fully understand the complexity of this physiological process
Transparency is the foundation of trust in the supplement industry
Representative drugs like the highly selective HIF-2 antagonist Belzutifan (MK-6482) [488] inhibit the expression of pro-angiogenic and pro-survival genes, alleviating abnormal metabolic burden and vascular disruption in tumor tissues
