Abstract
The metabolism of methyl parathion and of Sumithion®, O,O-dimethyl O-(3-methyl-4-nitrophenyl) phosphorothioate, by mouse liver and fat body from the American cockroach, Periplaneta Americana (L.), was compared, in an effort to find the reason for the comparatively low mammalian toxicity of Sumithion. Fat body activated both compounds while mouse liver slices activated methyl parathion but not Sumithion. Isolated liver microsomes were able to activate either of the 2 substances, an observation indicating that the absence of activation in the case of Sumithion incubated with liver slices was not due to any difference in the specificity of the activating system as such. A comparative study of the degrading ability of liver revealed a distinetly more efficient breakdown of Sumithion. The enzyme system(s) responsible for this differential rate of detoxification was localized in the supernatant fraction of a mouse liver homogenate. The hypothesis is proposed that the ability of liver tissue to degrade Sumithion faster than methyl parathion is, at least partly, the reason for the extremely low mammalian toxicity exhibited by the former substance.