Journal of experimental pharmacology · 2026
Hesperidin Mitigates Bisphenol-A Induced Oxidative Stress, Endocrine Disruption and Testicular Damage in Adult Male Wistar Rats.
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Oviosun Augustine, Oviosun Ezinne Chidinma, Usman Ibe Micheal, Anyanwu Chinyere Nkemjika, Ojiakor Vivian Onyinye, Esom Emmanuel Anayochukwu, Anyanwu Emeka Godson
Аннотация
INTRODUCTION: Bisphenol A (BPA), a well-known endocrine disruptor, is newly emerging as causing male infertility by endocrine disturbances, induction of oxidative stress and testicular toxicity. This study investigates the protective role of hesperidin against BPA-induced testicular toxicity in male Wistar rats.
METHODOLOGY: The rats were divided into six groups (n=7): control (normal saline); BPA-only (50 mg/kg); hesperidin-only at 50 mg/kg and 100 mg/kg; and two pre-treated groups receiving hesperidin (50 and 100 mg/kg) followed by BPA (50 mg/kg). All treatments were administered orally for 8 weeks. Post-treatment analyses included testicular weight, volume, and diameter measurements; serum testosterone, FSH, and LH levels; oxidative stress markers (MDA, SOD, CAT, GPx, and GSH); and histological and morphometric evaluation of the testis.
RESULT AND DISCUSSION: BPA exposure significantly reduced testicular dimensions, decreased serum testosterone, FSH, and LH. Histopathological examination revealed degeneration of seminiferous tubules, germ-cell depletion, reduced counts of spermatogonia, spermatocytes, spermatids, Sertoli and Leydig cells. BPA significantly induced oxidative stress, evidenced by increased MDA and decreased SOD, CAT, GPx, and GSH. Hesperidin significantly mitigated these effects by restoring testicular morphology, hormonal profiles, enhancing oxidative stress markers, improving histology and cell populations.
CONCLUSION: Hesperidin demonstrates protective properties against BPA-induced testicular and endocrine toxicity in rats, likely as a result of its antioxidant properties.
METHODOLOGY: The rats were divided into six groups (n=7): control (normal saline); BPA-only (50 mg/kg); hesperidin-only at 50 mg/kg and 100 mg/kg; and two pre-treated groups receiving hesperidin (50 and 100 mg/kg) followed by BPA (50 mg/kg). All treatments were administered orally for 8 weeks. Post-treatment analyses included testicular weight, volume, and diameter measurements; serum testosterone, FSH, and LH levels; oxidative stress markers (MDA, SOD, CAT, GPx, and GSH); and histological and morphometric evaluation of the testis.
RESULT AND DISCUSSION: BPA exposure significantly reduced testicular dimensions, decreased serum testosterone, FSH, and LH. Histopathological examination revealed degeneration of seminiferous tubules, germ-cell depletion, reduced counts of spermatogonia, spermatocytes, spermatids, Sertoli and Leydig cells. BPA significantly induced oxidative stress, evidenced by increased MDA and decreased SOD, CAT, GPx, and GSH. Hesperidin significantly mitigated these effects by restoring testicular morphology, hormonal profiles, enhancing oxidative stress markers, improving histology and cell populations.
CONCLUSION: Hesperidin demonstrates protective properties against BPA-induced testicular and endocrine toxicity in rats, likely as a result of its antioxidant properties.