Inhibition of the glutathione biosynthetic pathway increases phytochemical toxicity to Spodoptera litura and Nilaparvata lugens

Inhibition of the glutathione biosynthetic pathway increases phytochemical toxicity to Spodoptera litura and Nilaparvata lugens
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抑制谷胱甘肽生物合成途径会增加对斜纹夜蛾和褐飞虱的植物化学毒性

DOI:
10.1016/j.pestbp.2020.104632
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发表时间:
2020-09-01
影响因子:
4.7
通讯作者:
Zheng, Sichun
Zheng, Sichun
中科院分区:
农林科学1区
文献类型:
--
作者:
Cen, Yongjie;Zou, Xiaopeng;Zheng, Sichun

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植物化学物质对昆虫有毒,但与合成杀虫剂相比,它们的杀虫效率通常较低。了解昆虫对植物化学物质的适应机制将为提高植物化学物质的药效提供指导。还原型谷胱甘肽(GSH)是植物化学物质诱导的活性氧自由基(ROS)的清除剂。然而,在昆虫中,响应于植物化学物质的GSH生物合成途径尚不清楚。我们发现,暴露于0.5%吲哚-3-甲醇(I3 C),黄毒素,鱼藤酮(ROT)显着延迟的Spodoptera linfra幼虫的生长。研究了S. Linfra幼虫暴露于植物化学物质的增加。谷氨酸半胱氨酸连接酶而不是谷胱甘肽还原酶的上调表明,从头合成途径是负责谷胱甘肽合成在植物化学品处理的幼虫。γ-谷氨酰半胱氨酸合成酶(gcic)抑制剂(BSO)处理后,I3 C处理的幼虫体内GSH水平和GST活性下降,ROS水平升高,最终导致幼虫中肠坏死和死亡。单独用BSO或I3 C处理不会导致幼虫死亡。GSH的加入可部分降低I3 C和BSO对S.林弗拉生长褐飞虱gcic RNAi证实了BSO处理的结果。斜纹。N. lugens gcic RNAi显著增加了喷施ROT的N.褐飞虱,其中ROS水平显著增加。所有数据表明gcic参与昆虫对植物化学处理的反应。用dsgcic处理将增加植物衍生化合物的杀虫功效。
Phytochemicals are toxic to insects, but their insecticidal efficiencies are usually low compared to synthetic insecticides. Understanding the mechanism of insect adaptation to phytochemicals will provide guidance for increasing their efficacy. Reduced glutathione (GSH) is a scavenger of reactive oxygen species (ROS) induced by phytochemicals. However, in insects, the pathway of GSH biosynthesis in response to phytochemicals is unclear. We found that exposure to 0.5% indole-3-methanol (I3C), xanthotoxin, and rotenone (ROT) significantly retarded the growth of Spodoptera linfra larvae. The oxidative stress in S. linfra larvae exposed to phytochemicals was increased. The up-regulation of glutamate cysteine ligase but not glutathione reductase revealed that the de novo synthesis pathway is responsible for GSH synthesis in phytochemical-treated larvae. Treatment with the inhibitor (BSO) of gamma-glutamylcysteine synthetase (gcic), a subunit of glutamate cysteine ligase, resulted in decreases of GSH levels and GST activities, increases of ROS levels in I3C-treated larvae, which finally caused midgut necrosis and larval death. Treatment with BSO or I3C alone did not cause larval death. The addition of GSH could partly reduce the influence of I3C and BSO on S. linfra growth. Nilaparvata lugens gcic RNAi confirmed the result of BSO treatment in S. litura. N. lugens gcic RNAi significantly increased the mortality of ROT-sprayed N. lugens, in which ROS levels were significantly increased. All data indicate that gcic is involved in insect response to phytochemical treatment. Treatment with dsgcic will increase the insecticidal efficacy of plant-derived compounds.