The effects of chlordane, DDT, and 3-methylcholanthrene upon the metabolism and toxicity of diethyl-4-nitrophenyl phosphorothionate (Parathion)

Abstract

In rats, (1) DDT and chlordane cause equal stimulation of both pathways of parathion metabolism, similar to phenobarbital, and (2) 3-methylcholanthrene treatment results in preferential enhancement of the pathway leading to the formation of paraoxon. With mice, (1) DDT treatment results in greater enhancement of the pathway responsible for diethyl hydrogen phosphorothionate than of that producing paraoxon, (2) chlordane equally enhances both pathways of parathion metabolism, and (3) 3-methylcholanthrene treatment results in a repression of diethyl hydrogen phosphorothionate production. The differential inductive effects are discussed in terms of the hypothesis that two separate enzyme systems are involved in the metabolism of parathion. Results from toxicity studies in mice indicate that (1) no significant change in parathion toxicity results from DDT treatment, (2) toxicity is not altered significantly after treatment with 3-methylcholanthrene, and (3) chlordane treatment affords protection against the toxicity of parathion. The lack of correlation between the toxicity studies and the metabolic studies suggests that factors other than metabolism contribute to toxicity.