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item Voss, Kenneth
item Riley, Ronald
item Bacon, Charles
item Chamberlain, William
item Norred, William

Submitted to: Natural Toxins
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/6/1995
Publication Date: N/A
Citation: N/A

Interpretive Summary: Fusarium moniliforme is a mold that commonly grows on corn and is a suspected cause of cancer in humans. Fumonisins are toxins produced by this mold and one fumonisin, fumonisin B1, causes fatal brain disease in horses, fatal lung disease in pigs, and liver cancer in rats. Fumonisins also increase the amount of sphinganine, an important structural and functional component of cells, in animal tissues. In a series of studies we fed F. moniliforme or fumonisins to rats and mice. We found that F. moniliforme and fumonisin B1 caused similar kidney disease in rats and similar liver disease in both species. We also found that fumonisin B1 increaased liver and kidney sphinganine levels in rats at doses which were otherwise not toxic. This information is vital for understanding how fumonisin exerts its affects; for understanding the relationship between fumonisins, toxicity and cancer; and for designing future studies of fumonisin toxicity so that, ultimately, safe levels of this toxin in feeds and foods can be determined.

Technical Abstract: Fumonisins are mycotoxins produced by Fusarium species including F. moniliforme and F. proliferatum. They cause the fatal diseases of horses and pigs known as equine leukoencephalomalacia and porcine pulmonary edema, respectively. They are also liver toxins and, in rats, are nephrotoxic. F. moniliforme and fumonisins are suspected human carcinogens because of their prevalence on moldy corn, a dietary staple, in areas of China and southern Africa where the rate of human esophageal cancer is extraordinarily high. The effects of F. moniliforme and fumonisin B1 were studied in rats and mice. The liver is a target organ in both species. In rats, the kidney is also a target organ and renal lesions develop at lower dosages than liver lesions. Other findings suggest that toxigenesis may be mediated by disruption sphingolipid biosynthesis since liver and kidney sphinganine to sphingosine ratios were altered in rats fed fumonisin B1 at levels which did not cause other evidence of toxicity.