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ARS Home » Southeast Area » Athens, Georgia » U.S. National Poultry Research Center » Toxicology & Mycotoxin Research » Research » Publications at this Location » Publication #275242

Research Project: Toxicology and Toxinology of Mycotoxins in Foods

Location: Toxicology & Mycotoxin Research

Title: Current perspectives on Fusarium mycotoxins: fumonisin and deoxynivalenol

item Voss, Kenneth - Ken
item Riley, Ronald
item Gelineau-van Waes, Janee
item Pestka, James

Submitted to: The Canadian Workshop on Fusarium Head Blight
Publication Type: Abstract Only
Publication Acceptance Date: 10/22/2011
Publication Date: 11/27/2011
Citation: Voss, K.A., Riley, R.T., Gelineau-Van Waes, J.B., Pestka, J.J. 2011. Current perspectives on Fusarium mycotoxins: fumonisin and deoxynivalenol [abstract]. 7th Canadian Workshop on Fusarium Head Blight Proceedings. p. 24

Interpretive Summary: Abstract - no summary required.

Technical Abstract: The trichothecene deoxynivalenol (DON) and the fumonisins (FBs) are among the structurally diverse mycotoxins produced by Fusarium species. DON is a contaminant of wheat, barley, and maize, FBs occur mainly in maize, and both are found in grain-based foodstuffs. Both cause diseases in farm animals and elicit various toxicities in laboratory animals; however, their impact on human health is unknown. To better understand the latter, mechanistic studies in animals with emphasis on effects considered to be potentially most relevant to humans are essential. These include growth suppression (DON) and neural tube defects (FBs). DON elicits a complex sequence of cytokine mediated signaling events in mice that involve upregulation of proinflammatory cytokines and suppressors of cytokine signaling, and reductions in plasma insulin-like growth factor 1 and insulin-like growth factor acid-labile substance. The net effect of these interrelated and other associated events is to perturb growth hormone signaling and impair growth. Fumonisin B1 (FB1) induces neural tube defects in the LM/Bc and CD1 mouse strains. Evidence suggests that the well characterized inhibition of ceramide and sphingolipid biosynthesis by FB1 leads to the loss of complex sphingolipids that are critical for the uptake and utilization of folate. This in turn increases the risk of neural tube defects. Other findings suggest that aberrant signaling by cytokines or sphingoid base 1-phosphates are also likely to be involved. These findings provide plausible mechanisms for DON and FB-mediated toxicities and a basis for further experiments to determine their relevance to humans.