The relationship of carbon disulfide metabolism to development of toxicity.
The metabolism of CS2 proceeds by two distinct metabolic pathways, direct reaction with amine or thiol functions of cellular constituents, and microsomal oxidation to reactive intermediates that covalently bind to cell macromolecules. Reaction with amines or thiols may alter protein function by two primary mechanisms: formation of dithiocarbamate metabolites capable of inactivating metalloenzymes by chelation of metal ions such as copper and zinc, and direct reaction with such functional groups on proteins. Both of these mechanisms may contribute to CS2-induced neurotoxicity. Formation of reactive intermediates catalyzed by microsomal metabolism is clearly important in mediating CS2-induced hepatotoxicity. Its role in catalyzing neurotoxicity is less certain, however, since the mixed function oxidase activity of the central and peripheral systems has not been well characterized.
D000818:Animals; D001369:Axons / Q000201:enzymology; D001923:Brain Chemistry; D002246:Carbon Disulfide / Q000378:metabolism / Q000633:toxicity*; D002395:Catecholamines / Q000032:analysis; D002412:Cations / Q000378:metabolism; D002614:Chelating Agents; D008862:Microsomes, Liver / Q000378:metabolism; D009419:Nerve Tissue Proteins; D009422:Nervous System Diseases / Q000139:chemically induced* / Q000378:metabolism; D011485:Protein Binding; D051381:Rats; D013859:Thiocarbamates / Q000096:biosynthesis; D013871:Thiones / Q000378:metabolism; D014018:Tissue Distribution; D026681:Vitamin B 6 Deficiency / Q000139:chemically induced
D002395:Catecholamines; D002412:Cations; D002614:Chelating Agents; D009419:Nerve Tissue Proteins; D013859:Thiocarbamates; D013871:Thiones; C013321:trithiocarbonic acid; D002246:Carbon Disulfide