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 4 days previously were 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 injected intravenously into rats. The serum A-esterase activity increased 3- to 5-fold, and the acute toxicity of paraoxon decreased slightly, while the intravenous toxicity remained unaltered. This result is explained by the relative activity of A-esterase toward paraoxon and TEPP. Parathion intravenous toxicity increased 2- to 3-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.