Occurrence and Toxicology

Investigation of the association of human esophageal cancer and the consumption of Fusarium verticillioides (formerly called F. moniliforme) infested maize by South African Researchers suggested that fumonisins were a new group of mycotoxins (Bezuidenhout et al. 1988; Gelderblom et al. 1988). Even though the fumonisins were originally identified from F. verticillioides, these toxins have been reported in cultures of F. anthophilum, F. dlamini, F. napiforme, F. oxysporum, and F. proliferatum (Desjardins et al. 2000; Munkvold and Desjardins 1997; Musser and Plattner 1997; Seo et al. 1996). No other genera have been reported to produce fumonisins other than fungi. Production of fumonisins by Alternaria has also been reported (Mirocha et al. 1992; Mirocha et al. 1996. Some fumonisin-producing Fusaria have been known to produce AAL toxins, a compound with its structure closely related to fumonisins (Mirocha et al. 1992). The Alternaria alternata, a tomato pathogen, was found to produce AAL toxin (Wang et al. 1996). The fumonisins produced by F. verticillioides and F. proliferatum pose the greatest health hazard to human and animals since these species readily colonize corn all over the world (Bhatnagar et al. 2002; Dutton 1996; Proctor 2000; Riley et al. 1996; Scott 1993).

Nine structurally related fumonisins, including FB1, FB2, FB3, FB4, FA1, and FA2, have been identified. Fumonisin B1 (FB1) is the most abundant in maize. Chemically, FB1 is a derivative (diester) of propane-1,2,3-tricarboxylic acid of 2-amino-12,16-dimethyl-3,5,10,14,15-pentahydroxyicosane (Gelderblom et al. 1988; 1992a,b; Marasas 1995; Nelson et al. 1993; Riley etal. 1996; Scott 1993; Shier 1992). Other B series fumonisins such as fumonisin B2 (FB2), B3 (FB3), and (FB4), occur at low levels. Related structurally to B series fumonisins, the four other series of fumonisins (A, AK, C, and P) also occur at low levels (Proctor 2000). The other fumonisins are resulted from removal of tricarballylic acid and other ester groups (Musser et al. 1996; Seo et al. 1996).

Fumonisins have been shown to have diverse biological and toxicological effects. The mechanism of fumonisin toxicity is not well understood. Studies have shown that fumonisins inhibit ceramide synthase. Fumonisins have been shown to be hepatotoxic and carcinogenic in rats resulting in liver cirrhosis and hepatic nodules, adenofibrosis, hepato-cellular carcinoma, ductular carcinoma, and cholangio-carcinoma (Gelderblom et al. 1988; 1991; 1992b; 1993; 1994; Marasas 1996). Studies on rats by Riley et al. (1996) suggested that fumonisin B1 (FB1) might act primarily as a tumor promoter. The tumor promoting activity of fumonisins has also been proposed by Huang et al. (1995), Wattenberg et al. (1996) to have been resulted from the stimulation or suppression of signal transduction enzymes, the mitogen-activated protein kinase and protein kinase C. The mechanism of toxicological effect is a subject of intense study.

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