Radiotherapy has been identified as a causative factor contributing to Premature Ovarian Failure (PMOF). The primary objective of the present investigation is to assess the mitigative effects of Genistein (GEN) and ethinyl Estradiol (E2) on the reserve of ovarian follicles after exposure to γ-radiation. Female albino Wistar rats underwent irradiation with 3.4 gray (γ-rays) to induce PMOF, followed by a ten-day administration of either GEN [5mg/kg] or E2 [0.2mg/kg]. GEN demonstrated the preservation of anti-Müllerian hormone levels and exhibited antioxidant activity. Moreover, GEN hindered apoptosis by downregulating the expression of the Bax gene. In synopsis, this study delineates the potential of GEN in safeguarding the ovaries against radiation-induced damage. The underlying mechanisms encompass its antioxidative capacity, promoting the proliferation of ovarian follicle cells, surpassing the potential of E2. Additionally, GEN induced the up-regulation of forkhead box protein L2 (FOXL-2), resulting in the downregulation of transforming growth factor beta (TGF-β). The approach elucidated in this study holds promise as a protective strategy against radiation-induced PMOF, with implications for future clinical applications.

Keywords:Genistein; Ethinyl estradiol; Ovaries; ER-β; FOXL-2