Important insecticide resistance mechanisms in the dengue vector Aedes aegypti are mutations of voltage-gated sodium channel (VGSC) genes or knockdown resistance (kdr) and increased activity of metabolic enzymes. The objective of this study was to determine activity of mixed-function oxidases (MFO), esterases and glutathione-s-transferases (GSTs) in two strains of Ae. aegypti. The UPK-R strain, which harbors S989P and V1016G homozygous mutations in the VGSC, was compared with the wild-type PMD strain. Adult bioassays revealed that the UPK-R was resistant to DDT, permethrin, deltamethrin and malathion, whereas the PMD was resistant to only DDT. Enzyme activity in larvae, pupae and adults of the UPK-R strain was statistically higher than that observed in the PMD strain (mostly 1-2 fold). The current work supports previous studies which have suggested that increased MFO activity plays a partial role in pyrethroid resistance, whereas kdr is the major mechanism. Resistance to organophosphates and DDT is probably due to cross-resistance of MFO or increased activities of esterases and GSTs, respectively. Metabolic resistance combined with kdr may complicate insecticide-based control of dengue vectors in Thailand.