Fumonisin B1 neurotoxicity: Preclinical evidence, biochemical mechanisms and therapeutic strategies

The neurotoxic effects of fungal toxins in both humans and animals have been well documented. Fumonisin B1 (FB1), a mycotoxin produced by fungi of the Fusarium species, is the most toxic fumonisin variant whose neurotoxic effect is still being elucidated. This review highlights the biochemical aspects of FB1 neurotoxicity, such as its mechanisms of action as well as therapeutic strategies. Both in vitro and in vivo studies have demonstrated that alteration in sphingolipid metabolism is a major event in FB-induced neurotoxicity. Studies have also shown that neurotoxicity due to FB1 involves dysregulation of several biochemical events in the brain, such as induction of oxidative stress and inflammation, mitochondrial dysfunction and associated programmed cell death, inhibition of acetylcholinesterase and alteration of neurotransmitter levels, decreased activity of Na + K + ATPase, as well as disruption of blood-brain barrier. This review highlights the potential public health effects of FB1-induced neurotoxicity and the need to limit human and animal exposure to FB1in order to prevent its neurotoxic effect. Moreover, it is hoped that this review would stimulate studies aimed at filling the current research gaps such as delineating the effect of FB1 on the blood-brain barrier and appropriate therapies for neurotoxicity caused by FB1. • Fumonisin B1 (FB1) is the most toxic fumonisin • Humans and animals become exposed to FB1 mainly through diet, mostly cereals • FB1 inhibits ceramide synthesis, thereby disrupting ceramide functions • Bioactive compounds are able to inhibit FB1 neurotoxicity