Molecular mechanisms of fumonisin B1-induced toxicities and its applications in the mechanism-based interventions

Fumonisin B1 (FB1), the most toxic member of fumonisins, is one of the most common mycotoxins contaminating feed and food. It has been shown to produce pleiotropic toxicities in animals including neurotoxicity, hepatotoxicity and nephrotoxicity, and with highly potential impact on human health. Proposed mechanisms include disruption of sphingolipid metabolism, induction of oxidative stress, activation of endoplasmic reticulum (ER) stress and MAPKs, modulation of autophagy and alteration of DNA methylation. These mechanistic findings provide the theoretical basis for effectively managing FB1-induced adverse health effects. In this review, we will summarize the present understanding of the molecular basis underlying FB1-mediated toxicities, discuss the feasibility of developing mechanism-based approach to prevent FB1-induced toxicities, and suggest the issues that need to be addressed in the future in the field of FB1 toxicity-related studies.