通过对活体增效作用进行测定和生化分析，探讨了甜菜夜蛾对氰戊菊酯和顺式氯氰菊酯的抗性机理.结果表明：增效醚（PBO）、增效磷（SV1）、磷酸三苯酯（TPP）和顺丁烯二酸二乙酯（DEM）对甜菜夜蛾抗氰戊菊酯品系（Fen-R）和敏感品系（S）的增效倍数之比分别为10.2、7.8、12.5和1.1，对抗顺式氯氰菊酯品系（Cyp-R）和敏感品系（S）的增效倍数之比分别为21.6、15.5、8.6和1.2.PBO、SV1和TPP对氰戊菊酯和顺式氯氰菊酯均有显著增效作用，表明多功能氧化酶和羧酸酯酶均参与了甜菜夜蛾对氰戊菊酯和顺式氯氰菊酯的抗性.Fen-R品系和Cyp-R品系4龄幼虫羧酸酯酶的活性分别是S品系的1.9和2.2倍，而谷胱甘肽-S-转移酶活性与S品系差异不显著，表明羧酸酯酶活性的提高是甜菜夜蛾对氰戊菊酯和顺式氯氰菊酯产生抗性的重要原因，谷胱甘肽-S-转移酶与两种药剂的抗性无关.Fen-R品系和Cyp-R品系的Na-K-ATPase活性与S品系均无显著差异，但在相同浓度下氰戊菊酯和顺式氯氰菊酯对S品系Na-K-ATPase的抑制作用显著高于抗性品系，表明抗性品系Na-K-ATPase对杀虫剂的敏感性已明显降低.
By using synergist bioassay and biochemical analysis, this paper approached the resistance mechanisms of Spodoptera exigua (Hübner) to fenvalerate and alpha-cypermethrin. The synergistic ratios of piperonyl butoxide (PBO), o,o-diethyl-o-phenyl-thiophosphate (SV1), triphenyl phosphate (TPP), and diethyl maleate (DEM) between fenvalerate-resistant strain (Fen-R) and susceptible strain were 10.2, 7.8, 12.5, and 1.1, and those between alpha-cypermethrin resistant strain (Cyp-R) and susceptible strain were 21.6, 15.5, 8.6, and 1.2, respectively. Significant synergisms of PBO, SV1, and TPP to fenvalerateand alpha-cypermethrin wereobserved, implying that multifunctional oxidase and carboxylesterase were involved in the resistance to fenvalerate and alpha-cypermethrin. The carboxylesterase activities in the fourth instar larvae of Cyp-Rand Fen-R strains were 1.9 and 2.2 folds of the corresponding susceptible strains, respectively, but no differences were found in the glutathione-S-transferase activities between the resistant and susceptible strains, which indicated that carboxylesterase played an important role in the resistance of S. exigua to fenvalerate and alpha-cypermethrin, while glutathione-S-transferase contributed little to the resistance. There were no significant differences in the Na-K-ATPase activities between the resistant and susceptible strains, but the inhibition of fenvalerate and alpha-cypermethrin on Na-K-ATPase was higher in the susceptible strains than in the resistant strains, indicating the decreased sensitivity of Na-K-ATPase in resistant strains.