Efficiency of naringin against reproductive toxicity and testicular damages induced by bisphenol A in rats.
Iran J Basic Med Sci. 2019 Mar ;22(3):315-523. PMID: 31156794
Objectives: Bisphenol A (BPA) as a synthetic compound is applied in many plastic industries. BPA has been reported to have endocrine-disrupting feature with cytotoxic effects. The study aimed to evaluate the efficiency of Naringin against testicular toxicity induced by BPA in adult rats.
Materials and Methods: The animals were assigned into six groups of control, BPA-treated (50 mg/kg), BPA+Naringin-administrated (40, 80, 160 mg/kg) and Naringin-treated (160 mg/kg) for 30 days. At the end of experiments, testicular weight, total testicular protein, epididymal sperm count, testicular enzymes, serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone and estradiol, testicular enzymatic and non-enzymatic antioxidants and histopathology of testis tissue were evaluated by their own methods.
Results: The results showed a reduction in testicular weight, total testicular protein, epididymal sperm count, testicular enzymes (alkaline phosphatase and lactate dehydrogenase) and decrease in the serum TSH, LH, testosterone and estradiol in BPA-administrated rats. Furthermore, BPA reduced the enzyme activities of glutathione peroxidase, superoxide dismutase, and catalase in testis tissue. Also, BPA caused an induction in lipid peroxidation and increase in reactive oxygen species levels, whereas it decreased the glutathione content of testis tissue. Histological findings exhibited seminiferous tubules vacuoles, atrophy and separation of the germinal epithelium in BPA-administrated rats. Oral administration of Naringin along with BPA normalized the biochemical, morphological and histological changes and reduced the testicular toxic condition.
Conclusion: These results demonstrated that Naringin significantly managed male reproductive toxicity by antioxidant capabilities, preventing morphological modifications and escalating defense mechanism, thereby reducing oxidative stress from BPA-induced damage.