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镉暴露通过激活 ROS/CnCC 信号通路介导的 P450 解毒来赋予舞毒蛾对β-氯氰菊酯的耐受性。

Cd exposure confers β-cypermethrin tolerance in Lymantria dispar by activating the ROS/CnCC signaling pathway-mediated P450 detoxification.

机构信息

School of Forestry, Northeast Forestry University, Harbin 150040, PR China; Key Laboratory of Sustainable Forest Ecosystem Management-Ministry of Education, Northeast Forestry University, Harbin 150040, PR China.

Forest Botanical Garden of Heilongjiang Province, Harbin 150040, PR China.

出版信息

J Hazard Mater. 2024 Oct 5;478:135566. doi: 10.1016/j.jhazmat.2024.135566. Epub 2024 Aug 16.

DOI:10.1016/j.jhazmat.2024.135566
PMID:39173384
Abstract

Heavy metal pollutants are important abiotic environmental factors affecting pest habitats. In this study, Cd pre-exposure significantly increased the tolerance of Lymantria dispar larvae to β-cypermethrin, but did not significantly alter their tolerance to λ-cyhalothrin and bifenthrin. The activation of P450 by Cd exposure is the key mechanism that induces insecticide cross-tolerance in L. dispar larvae. Both before and after β-cypermethrin treatment, Cd exposure significantly increased the expression of CYP6AB224 and CYP6AB226 in L. dispar larvae. Silencing CYP6AB224 and CYP6AB226 reduced the tolerance of Cd-treated L. dispar larvae to β-cypermethrin. Transgenic CYP6AB224 and CYP6AB226 genes significantly increased the tolerance of Drosophila and Sf9 cells to β-cypermethrin, and the recombinant proteins of both genes could significantly metabolise β-cypermethrin. Cd exposure significantly increased the expression of CnCC and Maf. CnCC was found to be a key transcription factor regulating CYP6AB224- and CYP6AB226-activated insecticide cross-tolerance in Cd-treated larvae. Decreasing reactive oxygen species (ROS) levels in the Cd-treated larvae or increasing ROS levels in the untreated larvae reduced or enhanced the expression of CnCC, CYP6AB224 and CYP6AB226 and β-cypermethrin tolerance in L. dispar larvae, respectively. Collectively, Cd exposure confers β-cypermethrin tolerance in L. dispar larvae through the ROS/CnCC signalling pathway-mediated P450 detoxification.

摘要

重金属污染物是影响害虫栖息地的重要非生物环境因素。本研究中,Cd 预暴露显著提高了舞毒蛾幼虫对β-氯氰菊酯的耐受性,但对 λ-氯氟氰菊酯和联苯菊酯的耐受性没有显著改变。Cd 暴露对 P450 的激活是诱导舞毒蛾幼虫杀虫剂交叉耐受性的关键机制。β-氯氰菊酯处理前后,Cd 暴露均显著增加了舞毒蛾幼虫中 CYP6AB224 和 CYP6AB226 的表达。沉默 CYP6AB224 和 CYP6AB226 降低了 Cd 处理的舞毒蛾幼虫对β-氯氰菊酯的耐受性。转 CYP6AB224 和 CYP6AB226 基因显著提高了果蝇和 Sf9 细胞对β-氯氰菊酯的耐受性,且这两个基因的重组蛋白均能显著代谢β-氯氰菊酯。Cd 暴露显著增加了 CnCC 和 Maf 的表达。发现 CnCC 是调节 Cd 处理幼虫中 CYP6AB224 和 CYP6AB226 激活的杀虫剂交叉耐受性的关键转录因子。降低 Cd 处理幼虫中的活性氧(ROS)水平或增加未处理幼虫中的 ROS 水平,分别降低或增强了舞毒蛾幼虫中 CnCC、CYP6AB224 和 CYP6AB226 的表达以及对β-氯氰菊酯的耐受性。总之,Cd 暴露通过 ROS/CnCC 信号通路介导的 P450 解毒作用赋予舞毒蛾幼虫对β-氯氰菊酯的耐受性。

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