Hesperidin protects against spermatological damages and testicular apoptosis induced by Bisphenol-A in adult male Wistar rats

Abstract

Bisphenol-A (BPA) is a prevalent environmental toxin affecting male fertility. Hesperidin (HSD) is a natural compound widely used as an antioxidant to combat damage induced by various environmental toxins. Hesperidin has remarkable pharmacological potential, which includes antioxidant, anti-inflammatory, anti-carcinogenic, and anti-apoptotic qualities. This study evaluated the protective effects of hesperidin on Bisphenol A-induced spermatological damage and testicular apoptosis in male rats. Thirty-five male Wistar rats were randomly divided into five equal-number groups. The control group orally received saline (1 mL); group B received Bisphenol A at 50 mg/kg/body weight orally, group C was administered with 200 mg/kg of Hesperidin only. Groups D and E orally received hesperidin at 100 and 200 mg/kg for 28 days, respectively, followed by treatment with 50 mg/kg Bisphenol-A for 28 days. The parameters, including sperm characteristics (sperm morphology, motility, and count), were measured, and the immunohistochemical testicular expression of Bcl-2-associated X protein (BAX) and B-cell lymphoma-2 (Bcl2) was determined. BPA significantly (P < 0.05) reduced normal morphology, progressive motility, and sperm count. High immunopositive cell expression of BAX immunoprotein and low immunopositive cell expression of Bcl2 immunoprotein were also observed in the BPA-exposed group. Hesperidin pretreatment before exposure to Bisphenol-A increased progressive motility, sperm count, and normal morphology and reduced Bisphenol A-mediated apoptosis by downregulating BAX expression, whereas testicular Bcl-2 immunopositive cell expression levels increased. Our findings suggest that hesperidin may protect against spermatological damages and apoptosis induced by Bisphenol-A in adult male Wistar rats.