Mechanisms of methyl and ethyl parathion resistance in the western corn rootworm (Coleoptera: Chrysomelidae)

Abstract The mechanisms of methyl parathion and ethyl parathion resistance were studied in two populations (Phelps and York) of western corn rootworm adults ( Diabrotica virgifera virgifera Le Conte). Results of these studies indicate that the resistance is due to the combined effects of metabolic detoxification and target site insensitivity and that different processes are involved in conferring resistance in the two resistant populations. Resistance to methyl parathion is partially suppressible by the hydrolytic enzyme inhibitor DEF in both resistant populations, suggesting involvement of hydrolytic enzymes, and is in agreement with the increased general esterase activity toward naphtholic ester substrates observed in both resistant populations. Resistance was also partially suppressed by the monooxygenase inhibitor piperonyl butoxide (PBO), but only in the York population. This suppression of the resistance by PBO is consistent with the significantly higher cytochrome P-450-dependent activities (epoxidation and N -demethylation) that were observed in the York population. In vivo metabolism experiments with 14 C-labeled ethyl parathion confirm involvement of metabolic detoxification in the resistance based on differences in the rates of metabolite formation in both resistant populations. However, the York and Phelps populations again displayed significant differences in the overall pharmacokinetics and profiles of metabolite formation, indicating that the two populations employ different resistance mechanisms. Comparison of acetylcholinesterase inhibition by methyl paraoxon among the resistant and susceptible populations indicated that only the Phelps population possessed a decrease in sensitivity to inhibition (twofold). Therefore, we conclude that increased metabolic detoxification by NADPH-dependent monooxygenases and general esterases confers resistance to the York population, while acetylcholinesterase insensitivity and hydrolytic metabolism interact to confer resistance in the Phelps population.