METABOLISM OF ACRYLONITRILE TO CYANIDE INVITRO STUDIES

  • 1 January 1980
    • journal article
    • research article
    • Vol. 8  (6) , 376-379
Abstract
In liver fractions from Sprague-Dawley rats, metabolism of acrylonitrile (VCN) to cyanide (CN-) was localized in microsomal fraction, and required NADPH and O2 for maximal activity. Biotransformation of VCN to CN- was characterized with respect to time, microsomal protein concentration, pH and temperature. Metabolism of VCN was increased in microsomes obtained from phenobarbital-, Aroclor 1254 or 3-methylcholanthrene-treated rats (479, 414 and 142% of control, respectively), and decreased with CoCl2 treatment (54% of control). KM estimated for VCN with phenobarbital (54.8 .+-. 9.5 mM) or Aroclor 1254 (40.9 .+-. 4.1 mM) preparation was lower than control (190.7 .+-. 19.7 mM). Addition of SKF 525-A [proadifen hydrochloride] or CO to incubation mixtures inhibited VCN metabolism. Addition of epoxide hydratase inhibitor.sbd.1,1,1-trichloropropane 2,3-oxide.sbd.decreased formation of CN- from VCN. Addition of glutathione Cys, D-penicillamine or 2-mercaptoethanol enhanced release of CN- from VCN. VCN was metabolized to CN- via a cytochrome P-450-dependent mixed-function oxidase system.

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