The use of acaricide-resistant predatory mites is a key strategy for ensuring compatibility between biological and chemical control in integrated pest management (IPM) programs. This study aimed to quantify resistance to abamectin and bifenazate in a laboratory-selected resistant population of Amblyseius swirskii (Athias-Henriot) (Acari: Phytoseiidae) and to determine the contribution of metabolic detoxification pathways to resistance expression using synergist bioassays and enzyme activity measurements. To estimate LC50 values, concentration–mortality bioassays were conducted separately for abamectin and bifenazate on the resistant (RP) and the susceptible native populations (SP). To evaluate metabolic involvement, synergist bioassays were performed by co-applying piperonyl butoxide (PBO; monooxygenase inhibitor), S,S,S- tributyl phosphorotrithioate (DEF; esterase inhibitor), and diethyl maleate (DEM; glutathione S-transferase-GST- inhibitor) with each acaricide, and shifts in LC50 values and resistance ratios were determined. Detoxification capacity was further examined through biochemical assays measuring carboxylesterase, GST, and cytochrome P450 monooxygenase activities in both populations. Kinetic analyses were conducted to compare reaction rates between resistant and susceptible populations. LC50 values of bifenazate and abamectin in the RP of A. swirskii exhibited a significantly higher compared to the SP, resulting in a resistance ratio of 8.74 and 19.42, respectively. Synergist assays demonstrated that none of the inhibitors altered susceptibility in the SP. In the RP, co-application of PBO and DEF significantly suppressed resistance to bifenazate (reducing resistance ratios by 0.26- and 0.14- fold) and abamectin (by 0.14- and 0.08), indicating the involvement of cytochrome P450 monooxygenase- and carboxylesterase-mediated detoxification pathways. These enzymatic systems contributed only marginally to bifenazate resistance compared to abamectin. Biochemical profiling corroborated the functional assays, revealing a 2.59-fold increase in carboxylesterase activity and a 1.23-fold increase in cytochrome P450 monooxygenase activity in the resistant population relative to the native population. Kinetic analyses further showed significantly higher catalytic turnover rates for both carboxylesterase and cytochrome P450 monooxygenase systems in the resistant population, consistent with an enhanced metabolic detoxification phenotype. Collectively, these data indicate that abamectin resistance in A. swirskii is only weakly associated with elevated detoxification enzyme activity, whereas bifenazate resistance is predominantly mediated by upregulated monooxygenase- and esterase-dependent metabolic pathways. Future investigations integrating target-site mutation screening and transcriptomic or quantitative gene expression analyses will be critical to resolve the relative contributions of structural and regulatory mechanisms underlying resistance evolution in this predatory mite. This research was funded by TÜBITAK (Scientific and Technological Research Council of Türkiye) under grant number 123R080.