Dimethoate (Rogor) (0,0-Dimethyl S~-[N-methylcarbamoylmethyl] phosphoro- 
dithioate) 
Male rats were orally administered labeled dimethoate in corn oil via 
stomach tube. Using ion exchange chromatography, 0,0-dimethyl phosphoric 
acid, 0,0-dimethyl phosphorothioic acid, and two unidentified compounds 
were isolated from urine samples. When the carboxy derivative was admin- 
istered, 0,0-dimethyl phosphorodithioic, 0,0-dimethyl phosphorothioic, and 
0,0-dimethyl phosphoric acids were found. Highest levels of radioactivity 
persisted in the liver, skin, and bone. Dimethoate residues were present 
as long as 672 hours after administration (Dauterman et al., 1959; Krueger 
et al., 1960; Plapp and Casida, 1958b; Uchida et al., 1964; Sanderson and 
Edson, 1964). 
From urine samples from a steer treated with labeled dimethoate, the 
following metabolites were isolated and identified: 0,0-dimethyl S-carboxy- 
methyl phosphorodithioate, O-methyl S-(N-methylcarbamoylmethyl) phosphoro- 
thioic acid, 0,0-dimethyl phosphoric acid, 0,0-dimethyl phosphorothioic 
acid, and 0,0-dimethyl phosphorodithioic acid. Of 34 tissues tested for 
residue levels, liver and kidney. contain the greatest amount of total 
dimethoate equivalents and of actual dimethoate (Dauterman et al., 1959; 
Kaplanis et al., 1959b). Similar results were obtained with sheep (Cham- 
berlain et-al., 1961). Other mammalian studies nee indicated that the 
predominant path was dependent on species, sex, and concentration of the 
dimethoate. In the pheasant, the toxic thiolate analog tends to accumulate 
(Sanderson and Edson, 1964).and its conversion to one of the other metabo- 
lites is much slower than in mammals. This probably explains the greater 
susceptibility of the pheasant. 
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