Deciphering the interplay between oxidative stress and inflammation in polycystic ovary syndrome: outcome of a case-control study.

CONTEXT: Low-grade inflammation (LGI) and oxidative stress (OS) are key features in women with polycystic ovary syndrome (PCOS), but the interplay between these factors and genetic makeup in PCOS pathogenesis remains unclear. OBJECTIVE: This study investigated OS indicators, sub-inflammation, and their correlations in women with hyperandrogenic and insulin-resistant PCOS, examining the relationship with WNT3 gene expression. METHODOLOGY: A case-control study included 270 age-matched women (135 with PCOS and 135 healthy controls). Participants underwent detailed medical and clinical examinations, followed by biochemical, hormonal, inflammation, and OS and WNT3 gene expression assessments. RESULTS: Serum levels of inflammatory markers TNFα (24.98 ± 3.07vs.20.07 ± 6.83), IL6 (4.08 ± 0.90vs.3.09 ± 0.90), and IL1β (12.03 ± 2.81vs.8.61 ± 4.02) were significantly higher in women with PCOS compared to controls (p < 0.001). Total oxidant stress (TOS) was significantly elevated in PCOS cases (6.16 ± 0.46vs.1.82 ± 0.71), whereas antioxidant enzymes Superoxide Dismutase (SOD) and catalase were higher in controls (p < 0.001). Waist circumference positively correlated with IL1β, LDL, and triglycerides, and negatively with HOMA, QUICKI, HDL, and TNFα (p < 0.05). TNFα positively correlated with IL1β (r = 0.26, p < 0.0001). TOS correlated positively with HOMA, TNFα, IL1β, and LDL, and negatively with SOD, catalase, and testosterone (p < 0.0001). Catalase positively correlated with QUICKI and SOD, and negatively with HOMA and TOS (p < 0.0001). WNT3 gene mRNA expression was undetectable in peripheral blood samples from both PCOS cases and controls. CONCLUSION: The study underscores the significant role of OS and sub-inflammation in PCOS pathophysiology. However, WNT3 gene expression in peripheral blood was undetectable; suggesting further research with different tissues or more sensitive methods is needed.