Biochemical mechanisms of insecticide resistance in the diamondback moth (DBM), Plutella xylostella L. (Lepidopterata: Yponomeutidae), in the Sydney region, Australia
Article first published online: 16 NOV 2009
© 2009 The Authors. Journal compilation © 2009 Australian Entomological Society
Australian Journal of Entomology
Volume 48, Issue 4, pages 321–327, November 2009
How to Cite
Eziah, V. Y., Rose, H. A., Wilkes, M. and Clift, A. D. (2009), Biochemical mechanisms of insecticide resistance in the diamondback moth (DBM), Plutella xylostella L. (Lepidopterata: Yponomeutidae), in the Sydney region, Australia. Australian Journal of Entomology, 48: 321–327. doi: 10.1111/j.1440-6055.2009.00723.x
- Issue published online: 16 NOV 2009
- Article first published online: 16 NOV 2009
- Accepted for publication 22 March 2009.
- cytochrome P450 monooxygenases;
- glutathione S-transferases;
- Plutella xylostella;
Following the detection of resistant diamondback moth (DBM) populations to synthetic pyrethroid, organophosphorus and indoxacarb insecticides in the Sydney Basin, a study of the major biochemical mechanisms was conducted to determine the type of resistance in these populations. The activity of cytochrome P450 monooxygenases increased two- to sixfold when compared with the susceptible strain. Up to a 1.9-fold increase in esterase activity in resistant strains compared with the susceptible strain was observed. In vitro inhibition studies showed that profenofos, methamidophos and chlorpyrifos strongly inhibited the esterases while permethrin and esfenvalerate resulted in less than 30% inhibition. Qualitative analysis of the esterases using native polyacrylamide gel electrophoresis showed four bands in both the susceptible and resistant individuals with more intense staining in the resistant individuals. The development of these bands was inhibited by methamidophos and chlorpyrifos pretreatment of the protein extract while permethrin and esfenvalerate did not exhibit this effect. Glutathione S-transferase (GST) activity was significantly higher in two field populations compared with the remaining populations. Overall, the study showed that the mechanisms of insecticide resistance in the DBM populations in the area studied were due to cytochrome P450 monooxygenases, esterase and GSTs, and possibly other non-metabolic mechanisms that were not investigated in the present study.