|Voss, Kenneth - Ken|
|Gelineau-van waes, Janee|
Submitted to: Book Chapter
Publication Type: Book / chapter
Publication Acceptance Date: 1/10/2007
Publication Date: 9/1/2007
Citation: Voss, K.A., Riley, R.T., Gelineau-Van Waes, J.B. 2008. Toxicity of fumonisins, mycotoxins from Fusarium verticillioides. In: Wilson, C.L., editor. Microbial Food Contamination. Boca Raton, FL:CRC Press. p. 107-126. Interpretive Summary: Scientists at ARS, Russell Research Center are reviewing the recent research on the toxicity of the fumonisins, which are toxins that are produced by Fusarium molds and that are present in corn and feeds and food made from corn. Fumonisins are suspected of increasing the risk of esophageal cancer and neural tube defects in human populations that eat large amounts of foods made from moldy corn. The most common type of fumonisin, known as fumonisin B1(FB1) has been shown to cause diseases in farm and laboratory animals associated with Fusarium moldy corn. Fumonisins' effects on human health are unclear but they are suspected of increasing the risk of cancer and birth defects known as neural tube defects (NTDs). In cells, FB1 blocks an enzyme known as ceramide synthase and disrupts the metabolism of fats known as sphingolipids. Sphingolipids are involved in many cell processes including those involved in cell death, cell division, tissue integrity, and nutrient utilization and the evidence indicates that the imbalance in sphingolipids found in tissues of fumonisin exposed animals is an important factor contributing to toxicity. Accordingly, the development of NTDs in mice exposed to fumonisins is likely related to the changes in sphingolipids that are involved in the uptake of folate, an essential nutrient that protects against NTDs. Further studies on the mechanistic role of sphingolipids in NTDs and other fumonisin-induced animal diseases are needed to determine the extant to which fumonisins affect human health.
Technical Abstract: Fumonisins are mycotoxins produced by Fusarium, predominantly F. verticillioides. They are present in variable amounts in corn and corn-based feeds and food products. They are suspected risk factors for esophageal cancer and neural tube defects in some human populations depending on corn as a diet staple. The most prevalent fumonisin, fumonisin B1 (FB1), causes diseases in animals associated F. verticillioides, namely pulmonary edema in swine, leukoencephalomalacia in horses, and apoptosis and cancer in the liver and kidney of rodents. Fumonisins inhibit the enzyme ceramide synthase, thereby disrupting sphingolipid metabolism, leading to accumulations of sphinganine, sphingosine and their 1-phosphate metabolites in tissues and serum and to decreases in complex sphingolipids. Due to the involvement of sphigolipids in multiple physiological processes including apoptosis, mitosis, cell adhesion, pathogen recognition, and nutrient transport, it is likely that sphingolipid metabolism disruption underlies fumonisin-related diseases. This includes the induction of neural tube defects in mice, in which the uptake of folate, an essential nutrient that protects against neural tube defects, is inhibited due to a reduction in complex sphingolipids associated with lipid raft structures involved in folate transport. Further studies on the mechanistic role of sphingolipids as mediators of fumonisin-induced diseases in animal models are needed to elucidate the extant to which these mycotoxins affect human health.