Hydrogen peroxide production and mitochondrial dysfunction contribute to the fusaric acid-induced programmed cell death in tobacco cells
文献类型: 外文期刊
第一作者: Jiao, Jiao
作者: Jiao, Jiao;Sun, Ling;Hao, Yu;Zhu, Xiaoping;Liang, Yuancun;Zhou, Benguo;Gao, Zhengliang
作者机构:
关键词: Fusaric acid;Programmed cell death;Hydrogen peroxide;Mitochondrion;Tobacco suspension cells
期刊名称:JOURNAL OF PLANT PHYSIOLOGY ( 影响因子:3.549; 五年影响因子:4.164 )
ISSN: 0176-1617
年卷期: 2014 年 171 卷 13 期
页码:
收录情况: SCI
摘要: Fusaric acid (FA), a non-specific toxin produced mainly by Fusarium spp., can cause programmed cell death (PCD) in tobacco suspension cells. The mechanism underlying the FA-induced PCD was not well understood. In this study, we analyzed the roles of hydrogen peroxide (H2O2) and mitochondrial function in the FA-induced PCD. Tobacco suspension cells were treated with 100 mu M FA and then analyzed for H2O2 accumulation and mitochondrial functions. Here we demonstrate that cells undergoing FA-induced PCD exhibited H2O2 production, lipid peroxidation, and a decrease of the catalase and ascorbate peroxidase activities. Pre-treatment of tobacco suspension cells with antioxidant ascorbic acid and NADPH oxidase inhibitor diphenyl iodonium significantly reduced the rate of FA-induced cell death as well as the caspase-3-like protease activity. Moreover, FA treatment of tobacco cells decreased the mitochondrial membrane potential and ATP content. Oligomycin and cyclosporine A, inhibitors of the mitochondrial ATP synthase and the mitochondrial permeability transition pore, respectively, could also reduce the rate of FA-induced cell death significantly. Taken together, the results presented in this paper demonstrate that H2O2 accumulation and mitochondrial dysfunction are the crucial events during the FA-induced PCD in tobacco suspension cells. (C) 2014 Elsevier GmbH. All rights reserved.
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