Quercetin modulates the interplay between DNMT gene expression, oxidative stress, and trace elements in DHEA-induced polycystic ovary syndrome rat model.

Emerging evidence links epigenetic modifications, oxidative stress, and trace element imbalances to the pathogenesis of Polycystic ovary syndrome (PCOS). This study investigates the interplay between these mechanisms in a rat model of PCOS and evaluates the ameliorative effects of quercetin, a flavonoid with phytoestrogenic properties. PCOS was induced in female rats using dehydroepiandrosterone (DHEA, 6 mg/100 g body weight). After confirmation of PCOS induction, Quercetin (15 mg/kg/day) was administered via oral gavage for 30 days post-induction. Expression of DNA methyltransferase (DNMT) genes was assessed in ovarian tissue, while serum levels of trace elements (Zn, Cu, Mg, Fe) and oxidative stress markers in the liver were analyzed. PCOS induction significantly reduced hepatic Gpx, CAT, SOD, and GR activities, decreased GSH levels, and lowered serum concentrations of Zn, Cu, and Mg. Conversely, DNMT1 and DNMT3a expression, serum Fe levels, and hepatic MDA were elevated. Quercetin reversed these alterations, restoring antioxidant enzyme activities, GSH levels, and Zn concentrations while reducing MDA levels and DNMT3a expression. DNMT3b expression remained unchanged across groups. This study highlights the coordinated role of epigenetic dysregulation, oxidative stress, and trace element imbalances in the pathogenesis of PCOS. Quercetin appears to offer potential as an adjunctive treatment option for PCOS treatment when paired with trace element supplementation.