Fumonisins are mycotoxins produced worldwide by Fusarium fungi, princi
pally F. moniliforme. While this fungus can be cultured from virtually
all harvested corn, fumonisin production is highly variable. Fumonisi
n ingestion induces a number of fatal diseases in animals, with the or
gan 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 pro
duce mild to fatal toxicity in liver, kidney and heart in horses, pigs
, cattle, sheep, chickens, ducks, rabbits, rats and mice. Prolonged ad
ministration of high doses of fumonisin B-1 causes carcinoma of hepato
cytes and bile ducts in rats. In man, habitual ingestion of corn produ
cts that contain a high concentration of fumonisins is associated epid
emiologically with cancer of the esophagus. The pathogenesis of injury
to target organs is not understood completely. Affected kidneys and l
ivers are characterized by individual cell death through apoptosis, wi
th the degree of injury being related to dose and time of exposure. Fu
monisins decrease sphingolipid synthesis through inhibition on sphinga
nine N-acetyltransferase (ceramide synthetase). This inhibition result
s in the accumulation of intracellular sphinganine and sphingosine. Ex
cretion of sphinganine and sphingosine into the serum and urine of ani
mals serves as a biomarker of fumonisin exposure. Inhibition of the ce
ramide synthase also results in decreased synthesis of complex sphingo
lipids and ceramide, a potent regulator of cell growth cell differenti
ation, mitogenesis and apoptosis. The most sensitive target organs pre
sumably are less tolerant of sphingolipid dysregulation. Because fumon
isins occur worldwide in livestock feed and human foods and are potent
hepatotoxic and nephrotoxic compounds, investigators and clinicians a
re prudent to remain alert to possible fumonisin-related toxicity to t
hese organs in both livestock and humans.