Multiple resistance mechanisms to abamectin in the two-spotted spider mite

Resistance mechanisms to abamectin in Iranian populations of the two-spotted spider mite, Tetranychus urticae Koch (Acari: Tetranychidae)

“…High resistance to abamectin in T. urticae has previously been demonstrated, 342-fold (Sato et al, 2005), 1132 and 4753-fold (Kwon et al, 2010a) and ≥3000-fold (Memarizadeh et al 2011). The estimated LC 50 value obtained using RCV method in the present study was 7.87 ppm for the susceptible population, and more than 100,000 ppm for ISR population, showing the highest level of resistance to abamectin in T. urticae (more than 12,755-fold).…”

“…Therefore, the role of GSTs has certain universality in the spider mites' resistance mechanism. However, Kwon et al (2010a) indicated no obvious role of GST in abamectin resistance.…”

“…The toxicity of abamectin to the GUS2 and ISR populations of two-spotted spider mite was assayed using the residual contact vial (RCV) bioassay (Kwon et al 2010a). For estimating LC 50 values, abamectin was dissolved in acetone to various concentrations (0.112 -100,000 ppm) and 4 replicates were used per concentration (5 concentrations for GUS2 population).…”

“…Since 1998, abamectin has been the most widely used acaricide in Iran, but recently it has failed to provide satisfactory T. urticae control on some crops in fields and greenhouses (Memarizadeh et al, 2011). Abamectin resistance in T. urticae was reported worldwide (Campos et al 1995, Stumpf and Nauen 2002, Kwon et al 2010a. Synergism studies by Stumpf and Nauen (2002) reported that in an abamectinresistant strain of T. urticae, piperonyl butoxide (PBO) and diethyl maleate (DEM) had enhanced activities of mixed function oxidases (MFO) and glutathione S-transferases (GST).…”

“…In addition to synergism studies, the involvement of GST and MFO in abamectin resistance was confirmed by direct measurement of the enzymatic activities of P 450 s and GSTs, revealing a 13-and 11-fold increase, respectively (Stumpf and Nauen 2002). Recently, Kwon et al (2010a) reported that MFO and esterase (Est) were associated with abamectin resistance in two resistant strains of T. urticae from South Korea. Investigation on the role of reduced penetration or adsorption and metabolic mechanisms in resistance to abamectin showed that resistant mites excreted more [3H]avermectin B1a after ingestion than their susceptible strain (Clark et al, 1995).…”