Bisphenol A (BPA), which is an applied endocrine disrupting chemical in industry for producing epoxy resins and polycarbonate plastics and naringin, is an active flavanone glycoside of grapefruit and many citrus fruits. The present study evaluated the protective effect of naringin against cardiotoxicity induced by BPA. Male Wistar rats were divided into six groups. Control group received oral olive oil; and BPA group orally were administrated 50 mg/kg of BPA for 30 d consecutively to induce toxicity. 40, 80, and 160 mg/kg of naringin were orally administered for 30 consecutive, along with BPA. Naringin group orally received 160 mg/kg of naringin for 30 d consecutively. Animals were sacrificed and their biochemical, histological, and oxidative stress parameters were measured 24 h after the last treatment. Heart injury was induced by BPA as an evidence with a significant increase in levels of aspartate aminotransferase, lactate dehydrogenase, creatine kinase-MB, triglyceride, lipid peroxidation, and a significant decrease in levels of glutathione, superoxide dismutase, catalase, and glutathione peroxidase and triggered myocardial disorganization, myofibrillar loss, congestion of red blood cells, and the inflammation. However, there were not any changes in the total cholesterol, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, and alanine aminotransferase. Moreover, our results indicated that administering 80 and 160 mg/kg of naringin significantly altered all examined endpoints that were induced by BPA. Both concentrations of 80 and 160 mg/kg of naringin were more effective than 40 mg/kg. These findings indicated that naringin had a protective effect against cardiotoxicity induced by BPA through lipid-lowering properties, antioxidant activity, and suppressed lipid peroxidation.
Keywords: Bisphenol A; heart; naringin; oxidative stress; rat; toxicity.