Mechanistic Insights Into Aflatoxin B1-Induced Histopathology in the Gill, Liver, and Kidney Tissues and Immune Dysregulation by Altering the Expression of Cytokine Genes in Channa punctata.

Abstract

Aflatoxin B1 (AFB1) is one of the most potent mycotoxins and poses substantial health concerns to humans and other animals, including aquatic organisms. Addressing the increasing AFB1 contamination in aquaculture due to the utilization of plant-based ingredients for aquafeed formulations. In this study, we investigated the impact of sublethal doses of Aflatoxin B1 (11.4, 22.8, and 45.5 μg) on the multiple tissue histology and hepatic cytokine gene expression in Channa punctata after 28 days of exposure. Dose-dependent histological alterations were seen in the gill, liver, and kidney tissues. Gill tissues exhibited epithelial lifting, hyperplasia, lamellar fusion, and shortening of secondary lamellae. Liver sections showed hepatic tissue alterations, including cytoplasmic vacuolation, congestion, and necrosis, particularly at medium and high doses. Renal tissue displayed glomerular atrophy, hyperplasia in the Bowman's capsule, and tubular necrosis. Furthermore, AFB1 exposure modulated hepatic cytokine gene expression. At a low AFB1 concentration, a significant upregulation of both pro-inflammatory (TNF-α, INF-γ, and IL-6) and anti-inflammatory (IL-10) cytokine expression was observed, suggesting a regulatory inflammatory response. As the concentration was increased, the anti-inflammatory cytokine mRNA expression was downregulated, indicating immunotoxic stress. Overall, the study suggests that AFB1 induces multiorgan histopathology and also immune dysregulation by modulating the hepatic cytokine gene expression. To our best knowledge, this research draft may represent one of the earliest findings that provide comprehensive evidence of multiorgan histopathology and immune alterations induced by AFB1 in Channa punctata.