Bisphenol A (BPA), an endocrine-disrupting chemical, is widely used in industrial production. However, it is considered a ubiquitous environmental contaminant worldwide. Bisphenol-A acts like estrogen by interacting with the l estrogen receptors and is known to cause ovarian toxicity. The current investigation aimed to examine the effects of quercetin and melatonin on bisphenol-A–induced oxidative stress in ovarian and uterine tissues. Thirty-two female rats weighing (200±10 g) were divided into four groups. Group 1: intake standard diet; Group 2: bisphenol-A (120 mg/kg body weight) via oral gavage; Group 3: bisphenol-A (120 mg/kg body weight) + quercetin (50 mg/kg body weight via oral administration); and Group 4: bisphenol-A (120 mg/kg body weight) + melatonin (50 mg/kg body weight through oral). After a six-week experimental period, serum, ovaries, and uteruses were collected for hormonal analysis, ovarian and uterine analysis of oxidative stress biomarkers, and histopathological examination. The findings revealed that BPA decreased serum estradiol (E2) significantly. In addition, malondialdehyde (MDA) showed a significant increase. Whereas ovarian and uterine antioxidant enzyme levels, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), were significantly diminished histological abnormalities in the ovaries and uterus were observed in the BPA group. However, the administration of melatonin and quercitrin significantly inhibited the debilitating effects of BPA on the reproduction of female rats. Moreover, melatonin and quercetin exerted protective effects against oxidative stress caused by BPA. In a conclusion, both quercetin and melatonin had protective effects against BPA-induced ovarian and uterine oxidative stress.