Biochemical factors contributing to toxicity differences among chlorpyrifos, parathion, and methyl parathion in mosquitofish ( Gambusia affinis )

Biochemical systems in the mosquitofish were assayed in order to determine the factors contributing to the differences in toxicity among chlorpyrifos, parathion, and methyl parathion. In mosquitofish, chlorpyrifos was more toxic than parathion followed by methyl parathion. The brain cholinesterase (ChE) was more sensitive to chlorpyrifos-oxon than paraoxon followed by methyl paraoxon, assessed by the I 50 : 50nM for chlorpyrifos-oxon, 270nM for paraoxon, and 8400nM for methyl paraoxon. The muscle ChE was also more sensitive to chlorpyrifos-oxon than paraoxon followed by methyl paraoxon and was more sensitive to each compound than brain ChE; the I 50 's were: 6nM for chlorpyrifos-oxon, 60nM for paraoxon, and 540nM for methyl paraoxon. The hepatic aliesterases (AliE) were also more sensitive to chlorpyrifos-oxon than paraoxon followed by methyl paraoxon; the I 50 's were: InM for chlorpyrifos-oxon, 40nM for paraoxon, and 900nM for methyl paraoxon. Methyl parathion was activated by P450-mediated desulfuration in liver microsomes to the greatest extent followed by chlorpyrifos and parathion. Chlorpyrifos was detoxified by P450-mediated dearylation in liver microsomes more than parathion followed by methyl parathion. Hepatic A-esterases were capable of detoxifying chlorpyrifos-oxon, but had no significant effect on paraoxon or methyl paraoxon. The ChE sensitivity to oxon inhibition appears to reflect the toxicity levels of the parent insecticides, while metabolic factors are not predictions of toxicity levels.