Bisphenol A (BPA) is a widely used endocrine-disrupting chemical that has been linked to oxidative stress and inflammation. This study investigated whether carvacrol (CAR), a natural monoterpene with antioxidant potential, mitigates BPA-induced hepatorenal toxicity in rats. Forty-two male Wistar albino rats were allocated into six groups (n = 7/group): control, vehicle (corn oil), BPA (25 mg/kg/day), and BPA co-administered with CAR (12.5, 25, or 50 mg/kg/day) by oral gavage for 30 days. Oxidative status was assessed in liver and kidney homogenates by measuring malondialdehyde (MDA), reduced glutathione (GSH), and the activities of superoxide dismutase (SOD) and catalase (CAT). In addition, histopathological evaluations were performed, and pro-inflammatory gene expression (NF-κB, TNF-α, and IFN-γ) was quantified by RT-qPCR. BPA induced a consistent pro-oxidant pattern, including increased hepatic MDA with depleted antioxidant defenses, and upregulated inflammatory transcripts. Carvacrol attenuated these alterations in a dose-dependent manner, and the CAR50 group was associated with statistically supported improvements across the oxidative stress panel, pro-inflammatory transcript expression, and histopathology scores. Overall, these findings identify carvacrol as a candidate for further preclinical evaluation against BPA-triggered oxidative and inflammatory disturbances in vivo; however, human-relevant extrapolation will require careful attention to dose scaling, bioavailability, and metabolism.
Küçükbüğrü et al. (2026) studied this question.