The mechanisms and genetics of chlorpyrifos resistance were studied in a strain (Dursban-R) of the German cockroach displaying 20-fold levels of resistance by topical application compared to a susceptible laboratory strain (CSMA). Dursban-R was equally resistant to both chlorpyrifos and chlorpyrifos oxon. Penetration rates of [14C]chlorpyrifos were similar for both strains. In vivo metabolism studies employing [14C]chlorpyrifos indicate that chlorpyrifos oxon was present at reduced levels in the resistant strain relative to the susceptible strain, and that elevated levels of the hydrolysis product, 3,5,6-trichloropyridinol, were also associated with resistance. Resistance to chlorpyrifos was partially suppressed by both piperonyl butoxide and DEF suggesting the involvement of both cytochrome P450-dependent monooxygenases (MFOs) and hydrolytic enzymes in the resistance mechanism. In vitro, the Dursban-R strain displayed higher rates of NADPH-dependent microsomal metabolism of [14C]chlorpyrifos associated with the formation of chlorpyrifos oxon, trichloropyridinol, and unknown metabolites, further implicating the monooxygenase system in the resistance. In vitro metabolism of [14C]-chlorpyrifos with cytosolic fractions was not detected. However, higher levels of hydrolysis were detected in the Dursban-R strain when [14C]chlorpyrifos oxon was used as substrate. These results indicate that increased levels of monooxygenase activity as well as increased hydrolysis of chlorpyrifos oxon are mainly responsible for resistance to chlorpyrifos in this strain. Reciprocal crosses of the resistant and susceptible strains and backcrosses of the F1 progeny to the parental CSMA strain indicate that resistance is incompletely dominant, autosomal, and associated with more than one genetic factor.
All Science Journal Classification (ASJC) codes
- Agronomy and Crop Science
- Health, Toxicology and Mutagenesis