Materials and Methods: Forty-eight female Wistar rats were randomly assigned to six groups (n = 8 each): Sham; TD (torsion/detorsion + normal saline); TDO30 (T/D + 30 mg/kg eugenol); TDO60 (T/D + 60 mg/kg eugenol); CO30 (healthy + 30 mg/kg eugenol); and CO60 (healthy + 60 mg/kg eugenol). Following a 10-day treatment period, ovarian tissues were harvested. Oxidative stress markers, including superoxide dismutase (SOD), glutathione peroxidase (GPx), and malondialdehyde (MDA), were measured. The expression of pro-apoptotic markers Bax and caspase-3 was evaluated at both gene and protein levels.

Results: The TD group exhibited significantly reduced SOD and GPx activities and increased MDA levels compared with the Sham group (P < 0.001). Eugenol treatment significantly restored antioxidant enzyme activities and reduced lipid peroxidation in TDO groups (P < 0.001). Moreover, TD markedly upregulated Bax and caspase-3 expression, whereas eugenol administration significantly attenuated these pro-apoptotic alterations.

Conclusions: Eugenol ameliorates oxidative stress and modulates apoptosis-related molecular markers in ovarian tissue following TD injury. These findings support its potential as a candidate for further investigation in the context of ovarian ischemia–reperfusion injury.