Submitted to: Food Safety
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 17, 2013
Publication Date: November 20, 2013
Repository URL: http://handle.nal.usda.gov/10113/58367
Citation: Voss, K.A., Riley, R.T. 2013. Fumonisin toxicity and mechanism of action: overview and current perspectives. Food Safety. 1(1):49-69. doi: 10.14252/foodsafetyfscj.2013006. Interpretive Summary: Fumonisins are mycotoxins that are produced by Fusarium verticillioides and Fusarium proliferatum. They are found in corn (maize) and in corn-based foods. This review highlights selected toxicological and related investigations that have characterized the liver and kidney toxicity, liver and kidney cancer, and birth defects known as neural tube defects in laboratory animal models that are caused by the most common fumonisin, fumonisin B1. The studies have also established that fumonisin B1 causes these effects by disrupting sphingolipid metabolism and signaling pathways involved in cell death and survival. Further, results of applied toxicology investigations have shown that the alkaline cooking method used to make tortillas and extrusion reduce the amount of fumonisin and the potential toxicity of cooked foods. Taken together, toxicology investigations have also contributed to the development of a biomarker of exposure based on the concentration of fumonisin B1 that is excreted in urine. Together, the results of these investigations have contributed to risk assessments of fumonisins and to development of a biomarker for epidemiological investigations that are needed to determine the potential risk of fumonisins to consumers.
Technical Abstract: Fumonisin B1 and other fumonisins are mycotoxins produced predominantly by Fusarium verticillioides and F. proliferatum. They contaminate maize and maize-based foods throughout the world. Fumonisin B1 is the most common. It causes species-specific toxicities in laboratory and farm animals including liver and kidney cancer in rodents. Inhibition of ceramide synthase and disruption of sphingolipid metabolism is the non-genotoxic mechanism underlying its toxicological and carcinogenic effects. The extent to which fumonisin B1 or other fumonisins impact human health remains poorly understood although epidemiological and experimental evidence implicate them as a risk factor for neural tube defects in populations consuming large amounts of contaminated maize-based foods. Selected toxicological investigations providing evidence for the above and serving as basis for applied studies to better understand the extent of human exposure are reviewed. The latter includes the use of kidney toxicity in rats as a bioassay showing that alkaline cooking (nixtamalization, the traditional method for making masa and tortillas) and extrusion effectively reduce the toxicity of fumonisin-contaminated maize and the development of robust exposure biomarkers for use in epidemiological studies. Future initiatives to better understand the relationship between fumonisins and human health should emphasize validation of biomarkers, such as urinary fumonisin B1 concentration, as well as comparative studies to determine which animal models are most relevant to humans.