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作 者:王小军[1] 包建红[1] 张燕娜[1] 祝儒伟 赵伊英[1] Wang Xiaojun Bao Jianhong Zhang Yanna Zhu Ruwei Zhao Yiying(College of Agriculture, Shihezi University, Shihezi 832000, Chin)
出 处:《植物保护》2017年第4期70-75,共6页Plant Protection
基 金:国家自然科学基金(31560532)
摘 要:为探索土耳其斯坦叶螨的抗药性及其生化机理,在室内对敏感系土耳其斯坦叶螨分别用螺螨酯、甲氰菊酯和阿维菌素逐代处理,选育出抗性种群。结果表明,选育至15代,土耳其斯坦叶螨对螺螨酯、甲氰菊酯和阿维菌素的抗性指数分别达到268.63、37.98和112.68倍。分别测定敏感品系(SS)、抗螺螨酯(RS)、抗甲氰菊酯(RF)、抗阿维菌素(RA)品系的解毒酶活性显示,3种不同抗性品系相对SS品系的羧酸酯酶(CarE)、谷胱甘肽S-转移酶(GSTs)和多功能氧化酶(MFO)的比活力均有不同程度的提高,差异均达到显著水平(P<0.05)。其中,RF品系的MFO比活力上升最快,是SS品系的12.7倍;RA品系的MFO比活力次之,是SS品系的5.76倍;RS品系的3种解毒酶比活力均增长较慢,其中CarE比活力上升最慢,是SS品系的1.31倍。由此表明,CarE、GSTs、MFO的活性增大可促进土耳其斯坦叶螨对3种杀虫剂的抗性形成;螺螨酯的抗性增强可能与CarE关系甚微;MFO活性的增加可能与甲氰菊酯抗性升高密切相关;GSTs、MFO的活性升高可能是土耳其斯坦叶螨对阿维菌素产生抗性的主要原因。In order to study the resistance and biochemical resistance mechanisms of Tetranychus turkestani to insecticides,the related susceptible strains of T.turkestani were separately treated with spirodiclofen,fenpropathrin and abamectin in order to select their resistance in the laboratory.The results showed that the resistance of T.turkestani reached 268.63 folds to spirodiclofen,37.98 folds to fenpropathrin and112.68 folds to abamectin after treatment for 15 generations.The resistance mechanism was evaluated by activity measurement of detoxification enzymes.The activities for susceptible strains(SS),resistant strains to spirodiclofen(RS),resistant strains to fenpropathrin(RF)and resistant strains to abamectin(RA)were measured,and compared with susceptible strains,the fastest growing activity was observed in the mixed function oxidase(MFO)of RF,reaching 12.7 folds;the MFO activity of RA reached5.76 folds,and the carboxylesterase(CarE)was the slowest in activity growth(1.31 folds for the 3 detoxification enzymes of RS).It was concluded that the increase in the activities of CarE,glutathione-S-transferase(GSTs)and MFO were induced by resistance to insecticides;the rise in resistance to spirodiclofen was not independent of carboxylesterase;the resistance to fenpropathrin was mainly associated with increased activity of mixed function oxidase;the main cause of resistance to abamectin was the increased activity of glutathione-S-transferase and mixed function oxidase.
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