They are toxic to animals and exert their effects through mechanisms involving disruption of sphingolipid metabolism.
Fumonisin B₁ (FB₁) is the predominant fumonisin in this family. FB₁ is converted to its hydrolyzed analogs HFB₁, by alkaline cooking (nixtamalization) or through enzymatic degradation.
The toxicity of HFB₁ is poorly documented especially at the intestinal level.
The objectives of this study were to compare the toxicity of HFB₁ and FB₁ and to assess the ability of these toxins to disrupt sphingolipids biosynthesis. HFB₁ was obtained by a deesterification of FB₁ with a carboxylesterase. Piglets, animals highly sensitive to FB₁, were exposed by gavage for 2 weeks to 2.8 μmol FB₁ or HFB₁/kg body weight/day. FB₁ induced hepatotoxicity as indicated by the lesion score, the level of several biochemical analytes and the expression of inflammatory cytokines. Similarly, FB₁ impaired the morphology of the different segments of the small intestine, reduced villi height and modified intestinal cytokine expression.
By contrast, HFB₁ did not trigger hepatotoxicity, did not impair intestinal morphology and slightly modified the intestinal immune response.
This low toxicity of HFB₁ correlates with a weak alteration of the sphinganine/sphingosine ratio in the liver and in the plasma.
Taken together, these data demonstrate that HFB₁ does not cause intestinal or hepatic toxicity in the sensitive pig model and only slightly disrupts sphingolipids metabolism.
This finding suggests that conversion to HFB₁ could be a good strategy to reduce FB₁ exposure.