Ultrastructural and Immunohistochemical Alterations in Renal Tissue of Rats Exposed to Aflatoxin <scp>B1</scp> : Glomerular Barrier Disruption and Cytoskeletal Remodeling

Aflatoxin B1 (AFB1), a potent mycotoxin, poses significant health risks to humans and animals, with the kidney emerging as a secondary target organ beyond its well-documented hepatotoxicity. Cytoskeletal components are essential for proper podocyte, mesangial cell morphology, and glomerular function. This study investigated the histopathological and ultrastructural changes induced by AFB1 on renal tissues, focusing on glomerular filtration barriers, renal tubules, interstitial telocytes, and β-tubulin expression. Adult female Wistar rats were administered 250 μg/kg/day of AFB1 for 8 weeks, and kidney tissues were analyzed using toluidine blue staining, transmission electron microscopy (TEM), and immunohistochemistry. AFB1 exposure induced severe glomerular atrophy, thickened Bowman's capsules, widened Bowman's spaces, and tubular epithelial vacuolation. Telocytes exhibited necrotic changes, TEM confirmed podocyte foot process effacement, mitochondrial damage, and autophagic vacuole formation in proximal and distal tubules. Additionally, telocytes displayed fragmented telopodes and nuclear condensation, suggesting impaired tissue repair mechanisms, while immunohistochemistry revealed upregulated β-tubulin expression in glomeruli and tubules, indicating cytoskeletal disruption. These findings highlight AFB1-induced nephrotoxicity through oxidative stress, cytoskeletal remodeling, and interstitial inflammation, which in turn affect the glomerular filtration, underscoring the kidney's vulnerability to mycotoxin exposure. This study provides novel insights into the role of telocytes and β-tubulin dysregulation in AFB1-induced renal injury, offering a foundation for future research on therapeutic interventions.