Abstract

Molecular mechanisms of the toxic action of moniliformin, an extremely toxic fungal metabolite produced by Fusarium moniliforme, were investigated. Exceedingly low concentrations of moniliformin (<5 μM) selectively inhibited mitochondrial pyruvate and α-ketoglutarate oxidations by 50 per cent. It is suggested that these inhibitory effects could constitute the major molecular mechanism of toxic action and could largely, if not exclusively, account for the clinical symptoms of moniliformin poisoning.

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