Acetamiprid is widely used in paddy fields for controlling Nilaparvata lugens (Stål). However, the risk of resistance development, the cross-resistance pattern and the resistance mechanism of acetamiprid in this pest remain unclear. In this study, an acetamiprid-resistant strain (AC-R) was originated from a field strain (UNSEL) through successive selection with acetamiprid for 30 generations, which reached 60.0-fold resistance when compared with a laboratory susceptible strain (AC-S). The AC-R strain (G₃₀) exhibited cross-resistance to thiamethoxam (25.6-fold), nitenpyram (21.4-fold), imidacloprid (14.6-fold), cycloxaprid (11.8-fold), dinotefuran (8.7-fold), sulfoxaflor (7.6-fold) and isoprocarb (8.22-fold), while there was no cross-resistance to etofenprox, buprofezin and chlorpyrifos. Acetamiprid was synergized by the inhibitor piperonyl butoxide (2.2-fold) and the activity of cytochrome P450 monooxygenase was significantly higher in the AC-R strain compared with the AC-S strain, suggesting the critical role of P450. The gene expression results showed that the P450 gene CYP6ER1 was significantly overexpressed in AC-R compared with the AC-S and UNSEL strains. In addition, the RNA interference (RNAi) of CYP6ER1 significantly increased the susceptibility of AC-R to acetamiprid. Molecular docking predicted that acetamiprid and CYP6ER1 had close binding sites, and the nitrogen atoms had hydrogen bond interactions with CYP6ER1. These results demonstrated that the overexpression of CYP6ER1 contributed to acetamiprid resistance in N. lugens.

Clothianidin is a second-generation neonicotinoid insecticide that can effectively prevent piercing-sucking pests, such as white-backed planthopper (WBPH), Sogatella furcifera (Horváth). In this study, the sublethal effects of clothianidin on the biological traits of S. furcifera were evaluated via the age-stage, two-sex life table procedure. Our results exhibited that the female adult longevity, fecundity and hatchability of F₀ generation were significantly decreased after LC₁₀ and (or) LC₃₀ of clothianidin exposure compared to the control. Transgenerational effects showed that the pre-adult period, female adult longevity, total longevity, oviposition days (Od), fecundity and mean generation time (T) of F₁ generation were significantly decreased in the LC₁₀ and LC₃₀ groups compared to the control. Moreover, the development times of the third- and fifth-instar nymphs, total preoviposition period (TPOP) and doubling time (DT) were significantly shorter in the LC₁₀ group than in the control and LC₃₀ groups. Furthermore, the intrinsic rate of increase (r_i) and finite rate of increase (λ) values of the LC₁₀ group were significantly higher than those of the control group. However, there was no significant difference in the male adult longevity, adult preoviposition period (APOP) and net reproductive rate (R₀) between the treated groups and the control. Enzyme activity and gene expression results showed that the P450 enzyme activity and mRNA levels of many P450 genes were significantly increased by clothianidin treatment. In addition, the knockdown of CYP4CE3 and CYP6FJ3, which showed the highest inducing levels, by RNA interference (RNAi) dramatically increased the toxicity of clothianidin against S. furcifera. These results indicated that sublethal concentrations of clothianidin showed a stimulatory effect on the development, but it could adversely affect the survival and reproduction of S. furcifera. Additionally, CYP4CE3 and CYP6FJ3 might play an important role in the detoxification and evolution of clothianidin resistance in S. furcifera.