【作者】 赵卫东；

【导师】 王开运；

【作者基本信息】 山东农业大学 ， 农药学， 2002， 硕士

【摘要】 本研究利用10种不同类型的药剂对二斑叶螨山东省烟台市和寿光市两个种群进行抗药性测定，明确了其田间抗药性状况；研究了卵和雌成螨对药剂敏感度的差异；测定了药剂混用对二斑叶螨的联合毒力；测定了增效剂对药剂的增效作用，并用阿维菌素、甲氰菊酯和哒螨灵3种药剂对二斑叶螨进行抗性选育，明确了各自的抗性发展动态，探讨了二斑叶螨的抗性机理。结果表明： 1．二斑叶螨山东省烟台市种群（R₂）和寿光市种群（R₁）雌成螨对水胺硫磷、甲氰菊酯、哒螨灵和高效氟氯氰菊酯均已产生了明显的抗性，R₁种群的抗性倍数分别为17.7、10.4、6.67和6.63倍，R₂种群的抗性倍数分别为10.9、31.3、9.36和15.5倍。 2．二斑叶螨山东省烟台市种群（R₂）卵对甲氰菊酯和高效氟氯氰菊酯也已经产生了一定程度的抗药性，抗性倍数分别为2.99和2.08倍，对其他几种杀螨剂尚未产生明显的抗性。 3．二斑叶螨不同发育阶段对药剂的敏感度有明显的差异，卵对药剂的敏感度显著高于雌成螨，且对不同的药剂其敏感度差异不同，抗性种群的卵和雌成螨的敏感度差异更加明显。 4．药剂对二斑叶螨的联合毒力测定结果表明：甲氰菊酯与哒螨灵、双甲脒和三氯杀螨醇混合使用，对二斑叶螨有非常明显的增效作用，甲氰菊酯与虫螨腈、三唑锡和高效氟氯氰菊酯混合使用则有一定程度的拮抗作用；哒螨灵与甲氰菊酯和双甲脒混用有显著的增效作用，哒螨灵与三唑锡、高效氟氯氰菊酯和阿维菌素混用也有一定程度的增效作用，哒螨灵与虫螨腈、氧乐果、三氯杀螨醇和水胺硫磷混用则有明显的拮抗作用。 5．药剂对二斑叶螨抗性种群室内控制效果表明：虫螨腈和阿维菌素对二斑叶螨的室内控制效果最好，其次是三唑锡和哒螨灵，其余的几种杀螨剂对二斑叶螨的室内控制效果相对较差，不但用量大大超出了田间推荐用药量，而且持效期短，速效性差，不适宜用于田间二斑叶螨的防治。 6．药剂对二斑叶螨的抗性选育结果显示：室内选育至12代，对阿维菌素的抗性增加至6.72倍，对甲氰菊酯的抗性增加至19.8倍，对哒螨灵的抗性增加至12.1倍，已经形成稳定的抗性品系。 7．二斑叶螨的抗药性机理研究表明：对阿维菌素的抗性主要是由于药剂对害螨体壁穿透性降低、螨体内多功能氧化酶和谷胱甘肽—S—转移酶代谢解毒能力的增强引起的；对哒螨灵的抗性是由于多功能氧化酶和羧酸酯酶活性的增强引起的；对甲氰菊酯的抗性与螨体内谷胱甘肽—S—转移酶和羧酸酯酶代谢解毒能力的增强有关。生化测定结果显示：甲氰菊酯品系和哒螨灵品系羧酸酯酶的量与敏感品系相比有所增加，而且亲和力也比敏感品系的高，证明它们不但有量的差异，也有质的区别；阿维菌素的抗性与羧 2 赵卫东 二斑叶螨的抗药性及其机理研究酸酯酶无关：乙酞胆碱酯酶比活力的提高和谷肮甘肽－卜转移酶解毒能力的增强是二斑叶螨对甲氰菊酯和阿维菌素产生抗药性的主要原因；而二斑叶螨对呸螨灵抗性的产生与其没有关系。 8．酯酶同工酶电泳酶谱显示，敏感品系与阿维菌素、甲氰菊酯和啦螨灵抗性品系均有比较明显的三条酶带，四个品系中相同同工酶谱带的Rr基本相同，只是颜色深浅不一，其中一条颜色较深，RFO．4886，另外两条颜色较浅，分别为0．4355和0．5402。说明二斑叶螨对阿维菌素、甲氰菊酯和啦螨灵抗性品系的抗性对酯酶来说只有量的不同，没有质的改变。更多还原

【Abstract】 Laboratory measurement of resistance of two Tetranychus urticae populations to ten kinds of acaricides was carried out. The susceptibility difference of eggs and adults to ten acaricides was tested. The joint-toxicity of several acaricides and the synergism of five synergists were studied. The resietance selection of Tetranychus urticae to abamectin, fenpropathrin and pyridaben were carried out. The resistance mechanism was evaluated. Besides , the measuring method to eggs and larves was improved.The results could be summarized as follows:1. The resistance of T.urticae Ri population(sampled from Shouguang City, Shandong Province) was 17. 7-fold, 10. 4-fold, 6. 67-fold and 6.63-fold to isocarbophos , fenpropathrin, pyridaben and cyhalothrin ,respectively. The resistance of T. urticae R2 population(sampled from Yantai City, Shandong Proprince) was 10. 9-fold, 31. 3-fold, 9. 36-fold and 15. 5-fold to the four kinds of acaricides.2. Moderate resistance had been occurred in the eggs of T. urticae R: population(sampled from Yantai City, Shandong Province). The resistance ratios were 2.99-fold and 2.08-fold to fenpropathrin and cyhalothrin, respectively.3. The susceptibility of eggs and adults to ten kinds of acaricides was different. Eggs were much more susceptible than adults and have different susceptibility to different acaricides. what is more,the degree of difference of resistant population was more striking than that of susceptible population.4. The results of joint-toxicity measurement showed that the combined application of fenpropathrin with pyridaben , amitraz and dicofol were synergisted, co-toxicity coefficience were 377> 342 and 184. While antagoism were expressed by joint-using fenpropathrin with chlorfenapyr, azocyclotin and cyhalothrin. The synergism was evident for the pyridaben combining with fenpropathrin and amitraz, co-toxicity coefficience were 377 and 249.But when pyridaben was jointly used with chlorfenapyr, omethoate , azocyclotin and isocarbophos, they expressed antagoism.5. The controlling effects of acaricides to T. urticae R2 population in laboratory showed that chlorfenapyr and abamectin had the best effect to T. urticae, azocyclotin and pyridaben were secondary, the others had little effect to T. urticae at the recommending doses in the field. So, they were not fit for the measurment of T.urticae.6. The studies of resistance selection showed that the resistance of T. urticae had reached 6. 72-fold to abamectin, 19. 8-fold to fenpropathrin and 12. 1-fold to pyridaben after treated 12 times in the laboratory, which had formed stabled resistant strains.7. The rise of resistance of T. urticae to abamectin is polyfactorial , which mainly caused by the increased activities of microsomal oxidase -. acetylcholinesterase and glutathione S-transferase, in addition, decreased cuticular penetration is also one of factors. T. urticae is highly resistant to pyridaben because of increased activities of carboxy lesterase and microsomal oxidase. The main cause resistance to fenpropathrin is the increased activities of carboxy lesterase and glutathione S-transferase. In addition, the increased activities of acetylcholinesterase is related to the resistance of T. urticae to fenpropathrin.8. The zymogram of esterase isodyna electrophoresis demonstrated that susceptible strain and three resistance strains all have three obvious enzyme bands. The difference of the color on the bands shows that the resistance of T.urticae to abamectin> pyridaben and fenpropathrin is all concerned with the changes of esterase.更多还原