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Abstract
Fumonisins are mycotoxins produced worldwide by Fusarium fungi, principally F. moniliforme. While this fungus can be cultured from virtually all harvested corn, fumonisin production is highly variable. Fumonisin ingestion induces a number of fatal diseases in animals, with the organ specificity being species dependent. The first animal toxicoses to be characterized were leukoencephalomalacia (‘‘moldy corn poisoning’’) in equines and pulmonary edema in swine. Fumonisins additionally produce mild to fatal toxicity in liver, kidney and heart in horses, pigs, cattle, sheep, chickens, ducks, rabbits, rats and mice. Prolonged administration of high doses of fumonisin B1 causes carcinoma of hepatocytes and bile ducts in rats. In man, habitual ingestion of corn products that contain a high concentration of fumonisins is associated epidemiologically with cancer of the esophagus.
The pathogenesis of injury to target organs is not understood completely. Affected kidneys and livers are characterized by individual cell death through apoptosis, with the degree of injury being related to dose and time of exposure. Fumonisins decrease sphingolipid synthesis through inhibition on sphinganine N-acetyltransferase (ceramide synthetase). This inhibition results in the accumulation of intracellular sphinganine and sphingosine. Excretion of sphinganine and sphingosine into the serum and urine of animals serves as a biomarker of fumonisin exposure. Inhibition of the ceramide synthase also results in decreased synthesis of complex sphingolipids and ceramide, a potent regulator of cell growth, cell differentiation, mitogenesis and apoptosis. The most sensitive target organs presumably are less tolerant of sphingolipid dysregulation.
Because fumonisins occur worldwide in livestock feed and human foods and are potent hepatotoxic and nephrotoxic compounds, investigators and clinicians are prudent to remain alert to possible fumonisin-related toxicity to these organs in both livestock and humans.