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moniliformin
Editor	Kerstin Gross
Entity code	MONIL
CAS registry No.	71376-34-6
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Last updated	30/7/2004

Fate
Moliniformin is a mycotoxin produced by a number of Fusarium species including F. avenaceum. F. subglutinans, and F. proliferatum. These fungi also commonly produce other important mycotoxins so that moniliformin is frequently present in a mixture of mycotoxins.

Data on the occurrence of moniliformin in food is scarce. It has been detected in cereals such as wheat, rye, rice and maize. Gutema et al (2000) analysed 100 food-grade maize and maize-based food products intended for human consumption. Fifty percent of the samples contained moniliformin with concentrations ranging from 26 to 774 microg/kg. In Poland, fusarium-damaged maize kernels contained an average of 130.9 mg/kg of moniliformin, rangeing between 4.2 mg/kg and 530 mg/kg in individual samples each year Lew et al 1996.
Moliniformin occurs as the sodium or potassium salt of 1-hydroxycyclobut-1-ene-3,4-dione. It is an ionic compound and is soluble in water and polar solvents. On heating, moniliformin decomposes at 150-153° C without melting.

Its stability and fate during processing is still poorly studied so that the degree of consumer exposure is uncertain.

Toxicology
The mechanism of moniliformin action consists of the suppression of the pyruvate dehydrogenase enzymatic system. Thus, the Krebs cycle is inhibited, consequently hampering cellular respiration. Primary histopathological lesions in animals are described as acute myocardial degeneration and infarction (Conková et al 2003).

Experiments have been conducted to determine the effects of moniliformin on animals. Feeding chickens mixtures contaminated by moniliformin producing Fusarium fujikuroi resulted in their death (Harvey et al 1997). Toxic manifestations included cardiac dysfunction leading to depression, dyspnoea, cyanosis, and sudden death. Necropsy revealed lesions and dilatation of the right atrium and bilateral myocardial hypertrophy. Microscopic findings included acute myocardial degeneration with necrosis, fibrosis, and hypertrophy (Ledoux et al 1995). When feeding 100 mg moniliformin per kilogram of diet to growing turkeys from one to 21 days of age resulted in significantly reduced food intake and weight gain. Necropsy showed an absolute increase in heart and kidney weights, renal lesions, and an increased variation in the size of the nuclei of cardiomyocytes, with numerous giant nuclei, and a generalized loss of cardiomyocyte cross-striation. Engelhardt et al (1989) studied the effects of moniliformin produced by F. moniliforme var. subglutinas in chickens, ducklings, and turkeys. Ducklings were found to be the most sensitive. Mild diffuse mineralization was found in renal tubules (Morris et al 1999). In broiler chickens, a single dose of moniliformin (1 mg kg-1 b.w.) resulted in bradycardia 15 min after administration. The toxic dose of moniliformin in chickens was reported to be 5 mg kg-1 b.w. (Burmeister et al 1979).

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