THE ROLE OF A-ESTERASE IN THE ACUTE TOXICITY OF PARAOXON, TEPP, AND PARATHION

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Abstract
The liver and serum A-esterase activity was determined in normal rats and in rats which four days previously had been fed a massive sublethal dose of aldrin. Aldrin pretreatment doubled the A-esterase activity in the liver and halved it in the serum. The intravenous toxicity of paraoxon increased slightly following aldrin pretreatment, while the oral toxicity decreased threefold. These results indicated that the A-esterase activity of the liver mediates the oral toxicity, and that the serum activity influences the intravenous toxicity. The latter conclusion was verified by the preparation of a partially purified concentrate of rabbit serum A-esterase. The concentrate was intravenously injected into rats. The serum A-esterase activity increased three- to five-fold, and the acute toxicity of paraoxon decreased significantly. Following aldrin pretreatment the oral toxicity of TEPP decreased slightly, while the intravenous toxicity remained unaltered. This result is explained by the relative activity of A-esterase toward paraoxon and TEPP. Parathioa intravenous toxicity increased two- to three-fold following aldrin pretreatment. Comparison of paraoxon with parathion experiments suggested that aldrin pretreatment results in the inhibition of the 'in vivo' conversion of parathion to paraoxon. The serum esterase hydrolyzing phenylbenzoate in rat and rabbit was found to be the B-type esterase of Aldridge.