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Abstract
1. The alkenyl phosphate insecticide, dimethylvinphos, is rapidly metabolized and eliminated by rats and dogs.
2. Metabolism proceeds via demethylation followed by the hydrolysis of desmethyl dimethylvinphos to 2,4-dichlorophenacyl chloride which is further metabolized mainly to 2,4-dichloromandelic acid, l-(2,4-dichlorophenyl)ethanol (glucuronide) and 2,4-dichlorophenylethanediol (glucuronide).
3. The dechlorination of 2,4-dichlorophenacyl chloride to 2,4-dichloroaceto-phenone proceeds via the spontaneous formation of S-(2,4-dichlorophenacyl) glutathione which is converted to the ketone by an enzyme-catalysed glutathione-dependent reaction.
4. Demethylation of dimethylvinphos occurs in liver fractions via the action of two enzymes: glutathione S-methyl transferase in the cytosol, and microsomal mono-oxygenase. The relatively high activities of both enzymes in dog liver (compared with rat liver) partly account for the observed differences in metabolism and toxicity of dimethylvinphos in the two species.
5. The glutathione transferase is enhanced twofold by pre-treatment of rats with 0–1% phenobarbital in their drinking water. This treatment also induces the microsomal demethylation 45-fold and results in a > 13-fold protective effect against the acute toxic effects of dimethylvinphos.