Ameliorative effects of Abelmoschus esculentus and selected antioxidant interventions against Bisphenol A-induced oxidative stress and testosterone alterations in male Wistar rats

Bisphenol A (BPA), a widely prevalent environmental endocrine disruptor, has been implicated in the induction of testicular oxidative stress and subsequent impairment of male reproductive function. This study investigated the ameliorative effects of N -acetylcysteine (NAC), α-tocopherol, and A. esculentus on BPA-induced oxidative stress and testosterone alterations in male Wistar rats. Thirty-six adult male Wistar rats were randomly assigned into six groups ( n = 6): control, BPA only, BPA + A. esculentus , BPA + N -acetylcysteine (NAC), BPA + A. esculentus + NAC, and BPA + A. esculentus + α-tocopherol. Following exposure and intervention, testicular oxidative stress biomarkers; including malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), and nitric oxide (NO) as well as serum testosterone levels were evaluated. BPA exposure resulted in significant oxidative perturbations, evidenced by elevated lipid peroxidation (MDA) and nitric oxide levels, accompanied by disruptions in endogenous antioxidant defenses (SOD, CAT, and GSH) and a marked reduction in serum testosterone. Co-administration of NAC, α-tocopherol, and A. esculentus elicited variable yet generally favorable responses, including attenuation of lipid peroxidation and partial restoration of antioxidant enzyme activity and testosterone levels. However, some oxidative stress markers remained significantly altered compared to controls, indicating incomplete recovery. In conclusion, BPA induces pronounced oxidative stress and hormonal disruption in male Wistar rats. Antioxidant interventions involving NAC, A. esculentus , and α-tocopherol-containing combinations demonstrated partial modulatory effects against BPA-induced oxidative stress and testosterone disruption. These findings highlight the potential of antioxidant-based interventions as supportive strategies against environmental toxicant-induced reproductive dysfunction.