Introduction
Fumonisins are produced by species of Fusarium (See Fusarium and its toxins).  In the U.S. the the ingestion of moldy corn was first associated with adverse health affects in farm animals.  Examples are: Horses (sloughing of  of hooves liquefaction of the cerebral hemisphere white matter, aka equine leukoencephalomalacia); and pigs (Porcine pulmonary edema). Laboratory  treatment of a a variety of animals (rats, mice, sheep, baboons) caused hepatosis, nephrosis, congestive heart failure and cholangiocarcinoma (Nelson et al, 1993; Dragan  et al, 2001; Masas, 2001; Gelderblom et al, 2002; Riley et al, 2001;Lemmer et al, 2004 ). In humans Fumonisins have been associated with esophageal cancer from ingested contaminated corn (Marsas, 2001).  More recently the have been implicated in birth defects (Neural Tube) in humans and animals (See Neurotoxicity of Mycotoxins). In addition, Fumonisins are liver and kidney toxins and carcinogenic  in rodents (Dragan  et al, 2001; Masas, 2001; Gelderblom et al, 2002; Riley et al, 2001).  The chemical mechanism of the toxic action of fumonisin B1 will be briefly reviewed below.

Fumonisin B1 (FB 1) inhibits the production of Ceramide by inhibiting the enzyme, ceramide synthase.This disrupts the sphingolipid pathway  leading to intracellular and extracellular accumulation of toxic by-products of the pathway.  The sphingolipids  are cell membrane structures, providing integrity of the membranes
 
 

This figure was taken from Riley et al 2001.  It outlines the pathways of Sphingolipid biosynthesis.

FB 1 inhibits the enzyme ceramide synthase preventing the formation of ceramide.  This disrupts the synthesis of critical sphingolipids downstream of ceramide, e.g. Sphingomyelin and glycosphingolipids.  In the process precursors of ceramide increase in concentration, e.g. sphinganine, sphingosine1-phosphate as as deoxysphinganine and other deoxyspingoid bases (Riley et al, 2001; He t al, 2006 Zitomer et al, 2009).  The accumulated metabolites are highly toxic causing cytotoxicity and cell death (apoptosis) (Yoo et al,  1996; Desai et al, 2002).  In addition reactive oxygen species (ROS) have

been shown to be active in apoptosis and damage to DNA (Stockman-Juvala et al, 2004; Domijan et al, 2007).

Finally, the disruption of sphingolipid metabolism has been associated with neural tube defects (NTBs) in animal models in vivo and intro as well was in humans living along the Texas-Mexico border.  The NTBs are discussed in the section on neurotoxicity and mycotoxins mentioned above (Marasas et al, 2003; Gelineau-van Waes et al, 2005, 2009; Missmer et al, 2006).  In addition, intracerebroventricular administration of FB 1to mice caused neurodegeneration, disruption of sphingolipid metabolism, stimulation of astrocytes and release of pro-inflammatory cytokines: TNF-α, IL1 beta, IL6 and IF- gamma (Osuchowski et al, 2005)