Bisphenol F induces testicular toxicity via upregulation of xanthine oxidase/uric acid signalling and downregulation of testicular steroidogenic enzymes in male Wistar rats

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Abstract OBJECTIVE: This study investigated the effect of bisphenol F (BPF) on testicular integrity and function. The roles of xanthine oxidase/uric acid signalling and steroidogenic enzymes were also probed. METHODOLOGY: Male Wistar rats were randomized into vehicle-treated control, BPF-treated (10, 30, and 50mg/kg), and BPF-treated recovery (animals treated with varying BPF doses and allowed a 28-day exposure free period for recovery) (n= 6 rats per group). The administration was via gavage and lasted for 28 days. Animals in the recovery groups were allowed a 28-day exposure-free period after the initial 28 days of BPF exposure.RESULTS: BPF resulted in the distortion of the testicular histoarchitecture, accompanied by a significant rise in testicular GGT and LDH activities but a decline in SDH activity. Also, BPF caused a significant reduction in plasma GnRH, LH, FSH, and testosterone, which was associated with the downregulation of testicular 3beta-hydroxysteroid dehydrogenase (3β-HSD) and 17beta-hydroxysteroid dehydrogenase(17β-HSD) activities. Furthermore, BPF induced testicular inflammation, redox imbalance, and apoptosis, accompanied by elevated xanthine oxidase activity and uric acid concentration. Again, the observed toxic effects of BPF were dose-dependent and not reversed by BPF exposure withdrawal.CONCLUSION: Bisphenol F-induced gonadotoxicity by down-regulating the activities of steroidogenic enzymes and upregulation of xanthine oxidase/uric acid signalling.

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