The intestine as a possible target for fumonisin toxicity

Furnonisins constitute a family of toxic and carcinogenic mycotoxins produced by Fusarium verticilloides (formerly F mondiforme), a common fungal contaminant of corn. Contamination with fumonisin B-1 (FBI) is of concern as this mycotoxin causes various animal diseases. The gastrointestinal tract represents the first barrier against ingested chemicals, food contaminants, and natural toxins. Following ingestion of fumomsin-contarninated food or feed, intestinal epithelial cells could be exposed to a high concentration of toxin. In this review, we have summarized the data dealing with the impact of FBI on the intestine. Although FBI is poorly absorbed and metabolized in the intestine, it induces intestinal disturbances (abdominal pain or diarrhea) and causes extra-intestinal organ pathologies (pulmonary edema, leukoencephalomalacia, or neural tube defects). The main toxicological effect of FBI reported in vivo and in vitro is the accumulation of sphingoid bases associated with the depletion of complex sphingolipids. This disturbance of the sphingolipid biosynthesis pathway could explain the other observed toxicological effects such as an alteration in intestinal epithelial cell viability and proliferation, a modification of cytokine production, and a modulation of intestinal physical barrier function.