The role of acrylonitrile metabolism in the mechanism of its toxic effect
Gigiena Truda i Professional'nye Zabolevaniya (9): 48-50
ISSN/ISBN: 0016-9919 Accession: 006756427
The high toxicity of acrylonitrile [AN], its mutagenic effect and the possibility of carcinogenic effects were discussed. The question of whether the whole molecule or products of its metabolism were responsible for the high toxicity was also discussed. In rats, the microsomal oxidase system [MOS] intensified the hepatotoxicity of AN. Inhibition of this enzymic system activity blocked the damaging effects. The transformation of AN in the MOS led to the formation of highly active products (differing from cyanide products) that caused the damaging effect of this industrial monomer. The mutagenic effect of AN was detected only in the presence of liver microsomes and NADPH, confirming the highly toxic effect of products of AN metabolism.