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Target-Site Resistance to Neonicotinoid Insecticides in the Brown Planthopper Nilaparvata lugens

机译:棕色Planthopper Nilaparvata Lugens的靶位耐药性对新霉素杀虫剂

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28.1 Introduction Neonicotinoid insecticides (Figure 1) are potent selective agonists of insect nicotinic acetylcholine receptors (nAChRs) and are used extensively for both crop protection and animal health applications. The use of neonicotinoids has grown considerably in recent years and annual worldwide sales are currently estimated to be approximately one billion US dollars [1-2]. Since the introduction of the first neonicotinoid insecticide (imidacloprid) in 1991, resistance has been slow to develop, but is now established in some insect field populations and is a major worldwide threat to the effective control of insect pests [3]. For several major insecticide classes (including organophosphates, carbamates, and pyrethroids), both target-site modifications and enhanced detoxification have been identified as being important resistance mechanisms. However, in most cases where mechanisms of resistance to neonicotinoid insecticides have been resolved, resistance has been attributed to enhanced oxidative detoxification of neonicotinoids by overexpression of mono-oxygenase enzymes [3].
机译:28.1介绍类新烟碱杀虫剂(图1)是昆虫烟碱乙酰胆碱受体(nAChRs)的有效的选择性激动剂和被广泛用于既作物保护和动物健康的应用中。近年来,使用Neonicotinoids的使用大大增加,目前估计每年全球销售额约为10亿美元[1-2]。自1991年推出第一烟碱类杀虫剂(吡虫啉)的,电阻一直发展缓慢,但目前已在一些领域的昆虫种群,并有效控制害虫[3]的主要全球性威胁。对于几种主要的杀虫剂类(包括有机磷酸盐,氨基甲酸酯和拟除虫菊酯),靶部位点修饰和增强的解毒都被鉴定为重要的阻力机制。然而,在对新烟碱类杀虫剂抗性的机制已经解决大多数情况下,电阻已经通过单加氧酶[3]的过表达归因于新烟碱类的增强的氧化解毒。

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