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Fumonisins (Fums) are mycotoxins widely distributed in crops and feed, and ingestion of Fums-contaminated crops is harmful to animal health. The purpose of this study is to explore the effect of Fum B 1 (FB 1 ) on barrier functions of porcine intestinal epithelial cells, IPEC-J2, to clarify the intestinal toxicity of Fums in pigs. The results showed that the persistent treatment of FB 1 significantly decreased the viability of IPEC-J2. Moreover, the expressions of Claudin 1, Occludin, Zonula Occluden-1 (ZO-1) on the messenger RNA (mRNA), and protein levels and MUC1 on the mRNA level were significantly inhibited after FB 1 treatment, while the mRNA relative expression level of MUC2 was clearly increased. FB 1 also enhanced the monolayer cell permeability of IPEC-J2. Importantly, FB 1 promoted the expression of phosphorylated extracellular regulated protein kinase (p-ERK 1/2 ). These data suggest that long-term treatment of FB 1 can suppress IPEC-J2 proliferation, damage tight junctions of IPEC-J2, and regulate expression of mucins to induce the damage of barrier functions of porcine intestinal epithelial cells, which may be associated with the ERK 1/2 phosphorylation pathway., (© 2019 Wiley Periodicals, Inc.)

The fumonisins are a group of common mycotoxins found around the world that mainly contaminate maize. As environmental toxins, they pose a threat to human and animal health. Fumonisin B1 (FB1) is the most widely distributed and the most toxic. FB1 can cause pulmonary edema in pigs. However, the current toxicity mechanism of fumonisins is still in the exploratory stage, which may be related to sphingolipid metabolism. Our study is designed to investigate the effect of FB1 on the cell proliferation and barrier function of swine umbilical vein endothelial cells (SUVECs). We show that FB1 can inhibit the cell viability of SUVECs. FB1 prevents cells from entering the S phase from the G1 phase by regulating the expression of the cell cycle-related genes cyclin B1, cyclin D1, cyclin E1, Cdc25c, and the cyclin-dependent kinase-4 (CDK-4). This results in an inhibition of cell proliferation. In addition, FB1 can also change the cell morphology, increase paracellular permeability, destroy tight junctions and the cytoskeleton, and reduce the expression of tight junction-related genes claudin 1, occludin, and ZO-1. This indicates that FB1 can cause cell barrier dysfunction of SUVECs and promote the weakening or even destruction of the connections between endothelial cells. In turn, this leads to increased blood vessel permeability and promotes exudation. Our findings suggest that FB1 induces toxicity in SUVECs by affecting cell proliferation and disrupting the barrier function. [ABSTRACT FROM AUTHOR]

Fumonisins (Fums) are mycotoxins widely distributed in crops and feed, and ingestion of Fums‐contaminated crops is harmful to animal health. The purpose of this study is to explore the effect of Fum B1 (FB1) on barrier functions of porcine intestinal epithelial cells, IPEC‐J2, to clarify the intestinal toxicity of Fums in pigs. The results showed that the persistent treatment of FB1 significantly decreased the viability of IPEC‐J2. Moreover, the expressions of Claudin 1, Occludin, Zonula Occluden‐1 (ZO‐1) on the messenger RNA (mRNA), and protein levels and MUC1 on the mRNA level were significantly inhibited after FB1 treatment, while the mRNA relative expression level of MUC2 was clearly increased. FB1 also enhanced the monolayer cell permeability of IPEC‐J2. Importantly, FB1 promoted the expression of phosphorylated extracellular regulated protein kinase (p‐ERK1/2). These data suggest that long‐term treatment of FB1 can suppress IPEC‐J2 proliferation, damage tight junctions of IPEC‐J2, and regulate expression of mucins to induce the damage of barrier functions of porcine intestinal epithelial cells, which may be associated with the ERK1/2 phosphorylation pathway. [ABSTRACT FROM AUTHOR]

Fumonisins (Fums) are types of mycotoxin that widely contaminante feed material crops, and can trigger potential biological toxicities to humans and various animals. However, the toxicity of Fums on porcine blood vessels has not been fully explored. Fumonisin B1 (FB1) is the main component of Fums. Therefore, the aim of this study was to explore the effects of FB1 on the oxidative stress and tight junctions of the pig iliac endothelial cells (PIECs) in vitro. The results showed that FB1 reduced the viability of PIECs, increased the contents of lipid peroxidation product malondialdehyde (MDA), decreased the activities of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and thioredoxin reductase (TrxR), and decreased the level of glutathione (GSH). In addition, the barrier functions were destroyed, along with the down-regulations on Claudin 1, Occludin and ZO-1 and the increase of paracellular permeability. Thus, this research indicates that FB1 facilitates oxidative stress and breaks barrier functions to damage pig iliac endothelium cells. [ABSTRACT FROM AUTHOR]