Wu_1998_Pestic.Biochem.Physiol_61_53

The Munsyana strain of German cockroach, originally collected in Muncie, Indana, was found to have high-level resistance to fenvalerate, displaying 825-fold levels of resistance by topical application compared to a susceptible laboratory strain (Johnson Wax). Pretreatment with the cytochrome P450 monooxygenase inhibitors piperonyl butoxide (PBO) or MGK-264, or the esterase inhibitorS,S,S-tributyl phosphorotrithioate (DEF), reduced fenvalerate LD50resistance ratios by 12-fold, 55-fold, and 10-fold, respectively. Detoxication enzyme assays revealed elevated activity of microsomal oxidases (N-demethylation), esterases (PNPA hydrolysis), and glutathione-S-transferases (CDNB conjugation).In vivopenetration studies employing [14C]fenvalerate indicated reduced accumulation in the resistant strain relative to the susceptible strain.In vitrometabolism of [14C]fenvalerate by 105,000-g supernatant fractions with and without DEF inhibition suggested that hydrolysis was occurring. In the microsomal fraction, PBO also reduced the quantity of metabolitesin vitro. Overall, results suggest that monooxygenase, hydrolase, glutathione-S-transferase and decreased cuticular penetration are involved in fenvalerate resistance in the Munsyana strain. However, resistance to fenvalerate was not completely eliminated by either PBO, MGK-246, or DEF, suggesting that additional mechanisms, possibly including sodium channel insensitivity, are involved in this resistance.