Selenium ameliorates fumonisin B₁-induced mitochondrial dysfunction and barrier impairment in porcine intestinal...

This study reveals for the first time that selenium (Se) antagonizes Fumonisin B₁ (FB₁)-induced damage in porcine intestinal epithelial cells (IPEC-J2) by modulating mitochondrial biogenesis and dynamics. Fumonisins (FBs) are mycotoxins that are widely distributed in crops and feed, and ingestion of FBs-contaminated crops is harmful to animal health especially in intestine. Se has a protective effect on mycotoxin-induced tissue and cell toxicity. Nevertheless, whether Se can antagonize FB₁-induced intestinal epithelium injury, and underlying role of Se in FB₁-induced intestinal epithelium cell damage remains unclear. Our study was aimed to investigate the role of Se in FB₁-induced intestinal epithelium cell damage and underlying possibly mechanism, investigated whether Se could alleviate intestinal epithelium injury, and mitochondrial dysfunction by FB₁ in IPEC-J2. The results indicated that Se alleviated the FB₁-induced abnormal intestinal barrier function, the disturbance of reactive oxygen species (ROS), increased mitochondrial membrane potential (MMP), mitochondrial DNA (mtDNA), and mRNA expression of genes related to mitochondrial function. These showed Se alleviated FB₁-induced abnormal intestinal barrier function might related with the destroyed mitochondrial homestasis. We concluded that Se enhances mitochondrial function by regulating mitochondrial biogenesis and dynamics to antagonize FB₁-reduced the damage to the intestinal epithelial barrier and protect intestinal barrier integrity. Overall, our study provides promising insights into the protective role of Se in FB₁-induced intestinal epithelial cell damage.