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通过2,5 - 二羟基苯甲酸破坏细胞内谷胱甘肽稳态增强咯菌腈的杀菌活性。

Enhancement of fludioxonil fungicidal activity by disrupting cellular glutathione homeostasis with 2,5-dihydroxybenzoic acid.

作者信息

Kim Jong H, Campbell Bruce C, Mahoney Noreen, Chan Kathleen L, Molyneux Russell J, May Gregory S

机构信息

Plant Mycotoxin Research Unit, Western Regional Research Center, USDA-ARS, Albany, CA 94710, USA.

出版信息

FEMS Microbiol Lett. 2007 May;270(2):284-90. doi: 10.1111/j.1574-6968.2007.00682.x. Epub 2007 Mar 13.

DOI:10.1111/j.1574-6968.2007.00682.x
PMID:17355596
Abstract

The activity of fludioxonil, a phenylpyrrole fungicide, is elevated by coapplication of the aspirin/salicylic acid metabolite, 2,5-dihydroxybenzoic acid (2,5-DHBA). Fludioxonil activity is potentiated through a mitogen-activated protein kinase (MAPK) pathway that regulates osmotic/oxidative stress-responses. 2,5-DHBA disrupts cellular GSH (reduced glutathione)/GSSG (oxidized glutathione) homeostasis, further stressing the oxidative stress-response system. This stress enhances fludioxonil activity. 2,5-DHBA treatment also prevents tolerance of MAPK mutants resistant to fludioxonil.

摘要

咯菌腈是一种苯基吡咯类杀菌剂,与阿司匹林/水杨酸代谢物2,5 -二羟基苯甲酸(2,5 - DHBA)共同施用时,其活性会增强。咯菌腈的活性通过调节渗透/氧化应激反应的丝裂原活化蛋白激酶(MAPK)途径得到增强。2,5 - DHBA会破坏细胞内谷胱甘肽(还原型谷胱甘肽)/氧化型谷胱甘肽(GSSG)的稳态,进一步加重氧化应激反应系统的负担。这种应激增强了咯菌腈的活性。2,5 - DHBA处理还可防止对咯菌腈耐药的MAPK突变体产生耐受性。

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