Possible Protective Role of Selenium on Adverse Effect of Bisphenol A on the Adrenal Cortex in Adult Male Albino Rats: A Histological, Immunohistochemical, and Biochemical Study

Document Type : Original Article

Authors

Department of Anatomy and Embryology, Faculty of Medicine, Cairo University, Egypt.

Abstract

Background: Bisphenol A (BPA) is a common endocrine disruptor that induces oxidative stress and apoptosis in endocrine organs. The adrenal cortex, essential for stress hormone regulation, may be particularly vulnerable. Selenium, a potent antioxidant, has been proposed as a protective agent. Methods: Twenty-one adult male albino rats were randomized into three groups (n = 7 each): control, BPA (10 mg/kg/day), and BPA + sodium selenite (0.5 mg/kg/day). Adrenal tissues were evaluated histologically, immunohistochemically   (caspase-3), and    biochemically
(Malondialdehyde, Glutathione Peroxidase, Adrenocorticotropic Hormone corticosterone). Morphometric analyses quantified cortical thickness, collagen deposition, and apoptotic index. Results: BPA exposure disrupted adrenocortical architecture, with cytoplasmic vacuolations, capsular fibrosis, and significant reduction in zone thickness (ZG: 68.14 ± 1.91 µm; ZF: 256.54 ± 12.51 µm; ZR: 100.61 ± 6.52 µm, p < 0.001). Caspase-3 expression and collagen deposition increased markedly (23.41 ± 2.54%). Biochemically, BPA elevated MDA (167.23 ± 3.84) and ACTH (385.03 ± 6.44), while reducing GPx (59.97 ± 4.55) and corticosterone (51.07 ± 1.38). Selenium co-treatment significantly reversed these effects: cortical thickness improved, caspase-3 and fibrosis were reduced (3.02 ± 0.63%), MDA decreased (61.07 ± 3.02), and GPx activity increased (112.11 ± 3.37). Hormone levels normalized toward control values. Conclusion: Se Supplementation significantly attenuates BPA-induced oxidative stress, fibrosis, and apoptosis in the adrenal cortex, thereby restoring both structural and functional integrity. These findings support selenium’s potential as a protective agent against endocrine disruptor–induced adrenal injury, although further studies on dosing, duration, and clinical translation are warranted.

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