Characteristics of resistance in house flies subjected to long-term concurrent selection with malathion and permethrin

Abstract

A laboratory strain of the house fly ( Musca domestica L.) subjected to long-term concurrent selection with permethrin and malathion demonstrated substantial levels of resistance to the selecting agents. These insects were also cross-resistant to other anticholinesterase insecticides (dimethoate, methyl parathion, stirofos, propoxur), as well as to fenvalerate and DDT. Coadministration of the microsomal oxidase inhibitor piperonyl butoxide substantially increased the toxicity of permethrin to both susceptible (S) and resistant (R) house flies, but had little if any effect on the toxicity of malathion. The esterase inhibitor DEF caused moderate increases in the toxicity of both insecticides. Studies of the post-treatment fate of 14C-labeled malathion and trans-permethrin indicated that, with both compounds, there was a generally slower rate of cuticular penetration and internal accumulation and a more rapid rate of excretion of absorbed toxicants and their metabolites by R house flies. In vivo studies indicated that metabolic degradation was enhanced in R insects in the case of trans-permethrin, but not with malathion. Comparative in vitro studies of enzymes in homogenate preparations of S and R house flies demonstrated that in R insects acetylcholinesterase (AChE) was definitely less sensitive to inhibition by malaoxon, and microsomal oxidase and GSH-transferase activities were higher. In vitro studies of the interaction of [ 3H]saxitoxin with nerve membrane receptors indicated decreased binding in R house fly brains. The evidence thus suggests that resistance to malathion in this R strain of the house fly is associated primarily with a reduction in the sensitivity of AChE to inhibition, and that permethrin resistance is attributable to decreased target site sensitivity and enhanced capability for metabolic degradation. Minor modifying factors most likely are involved in both cases.