Abstract

Investigations of pyrethroid resistant (R) and susceptible (S) house flies ( Musca domestica L.) provided conclusive evidence that a high level of cross-resistance to fenvalerate in the laboratory-selected R strain was influenced by an enhanced capability for metabolic degradation of the toxicant. Comparative studies of the in vitro metabolism of [ 14C]fenvalerate by homogenate preparations of S and R house flies, in the presence or absence of the mixed function oxidase (mfo) inhibitor piperonyl butoxide (PBO) or the esterase inhibitor S,S,S-tributylphosphorothioate (DEF), indicated that elevation of mfo activity was a major component of enhanced metabolism and that there also was enhancement of esterases associated with both the microsomal and cytosolic subcellular fractions of homogenate preparations of R insects. In vitro studies of the effects of coad-ministered PBO or DEF on the absorption and metabolism of topically applied [ 14C]fenvalerate in R insects demonstrated that both synergists slowed the rate at which the toxicant penetrated the cuticle; PBO significantly reduced the metabolic degradation of fenvalerate, but effects of DEF on metabolism were less conclusive.

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