Abstract
The hepatotoxic and cancerogenic N-methyl- N-formyl hydrazine (MFH), which is formed from the mushroom poison, gyromitrin, by hydrolytic cleavage in vivo and in vitro during food processing, loses its hepatotoxicity and its influence on the renal function of rats after acetylation at the free NH 2-moiety. The importance of MFH-acetylation with regard to an inhibition of microsomal conversion of MFH into a toxic nitrosamide is considered. The known genetically determined heterogeneity of the acetylation rate for hydrazine derivates in man may explain the observed differences in sensitivity towards the mushroom toxins.
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