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Metabolic mechanisms of resistance to spirodiclofen and spiromesifen in Iranian populations of Panonychus ulmi
Crop Protection ( IF 2.8 ) Pub Date : 2020-08-01 , DOI: 10.1016/j.cropro.2020.105166
Fahimeh Badieinia , Jahangir Khajehali , Ralf Nauen , Wannes Dermauw , Thomas Van Leeuwen

Abstract The European red mite, Panonychus ulmi (Koch), is one of the major pests of apple trees worldwide. Cyclic keto-enol compounds such as spirodiclofen and spiromesifen are frequently used to control phytophagous spider mites in agricultural crops, including P. ulmi on apple trees. Spider mites, however, can rapidly develop resistance against acaricides and, in this study, multiple P. ulmi populations from apple orchards in Iran were monitored for spirodiclofen and spiromesifen resistance. The Urmia and Shahin Dej population showed the highest spirodiclofen resistance ratio (more than 150-fold) compared to the susceptible Ahar population. Toxicity bioassays also revealed the presence of moderate cross-resistance between spiromesifen and spirodiclofen, but not towards the chitin synthase inhibitor etoxazole. As a first step towards elucidating spirodiclofen resistance mechanisms, the role of detoxification enzymes (cytochrome P450 monooxygenases, carboxyl/choline esterases and glutathione S-transferases) was investigated by in vivo synergism and in vitro enzyme assays. PBO pretreatment synergized spirodiclofen toxicity in the populations of Urmia and Shahin Dej to a higher extent than in the susceptible Ahar population. Furthermore, enzyme activity measurements showed relatively higher activity of detoxifying enzymes in the resistant populations. In conclusion, increased detoxification is most likely underlying spirodiclofen resistance and results in limited cross-resistance to spiromesifen.

中文翻译:

伊朗全爪螨种群对螺双氯芬和螺螨酯耐药的代谢机制

摘要 欧洲红螨 Panonychus ulmi (Koch) 是世界范围内苹果树的主要害虫之一。环状酮-烯醇化合物,如螺双氯芬和螺螨酯,经常用于控制农作物中的植食性红蜘蛛,包括苹果树上的紫菀。然而,红蜘蛛可以迅速产生对杀螨剂的抗药性,在本研究中,监测了伊朗苹果园的多个 P. ulmi 种群对螺螨酯和螺螨酯的抗药性。与易感 Ahar 人群相比,Urmia 和 Shahin Dej 人群表现出最高的螺二氯芬耐药率(超过 150 倍)。毒性生物测定还显示螺美昔芬和螺二氯芬之间存在中等交叉耐药性,但对几丁质合成酶抑制剂依托恶唑不存在交叉耐药性。作为阐明螺双氯芬耐药机制的第一步,通过体内协同作用和体外酶测定研究了解毒酶(细胞色素 P450 单加氧酶、羧基/胆碱酯酶和谷胱甘肽 S 转移酶)的作用。PBO 预处理在 Urmia 和 Shahin Dej 人群中协同螺二氯芬毒性的程度高于易感 Ahar 人群。此外,酶活性测量显示抗性群体中解毒酶的活性相对较高。总之,增加的解毒作用很可能是螺二氯芬耐药的潜在原因,并导致对螺麦昔芬的交叉耐药性有限。通过体内协同作用和体外酶分析研究了羧基/胆碱酯酶和谷胱甘肽 S-转移酶。PBO 预处理在 Urmia 和 Shahin Dej 人群中协同螺二氯芬毒性的程度高于易感 Ahar 人群。此外,酶活性测量显示抗性群体中解毒酶的活性相对较高。总之,增加的解毒作用很可能是螺二氯芬耐药的潜在原因,并导致对螺麦昔芬的交叉耐药性有限。通过体内协同作用和体外酶分析研究了羧基/胆碱酯酶和谷胱甘肽 S-转移酶。PBO 预处理在 Urmia 和 Shahin Dej 人群中协同螺二氯芬毒性的程度高于易感 Ahar 人群。此外,酶活性测量显示抗性群体中解毒酶的活性相对较高。总之,增加的解毒作用很可能是螺二氯芬耐药的潜在原因,并导致对螺麦昔芬的交叉耐药性有限。酶活性测量显示抗性群体中解毒酶的活性相对较高。总之,增加的解毒作用很可能是螺二氯芬耐药的潜在原因,并导致对螺麦昔芬的交叉耐药性有限。酶活性测量显示抗性群体中解毒酶的活性相对较高。总之,增加的解毒作用很可能是螺二氯芬耐药的潜在原因,并导致对螺麦昔芬的交叉耐药性有限。
更新日期:2020-08-01
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