Hydrogen peroxide production and mitochondrial dysfunction contribute to the fusaric acid-induced programmed cell death in tobacco cells |
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Authors: | Jiao Jiao Ling Sun Benguo Zhou Zhengliang Gao Yu Hao Xiaoping Zhu Yuancun Liang |
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Affiliation: | 1. Department of Plant Pathology, Shandong Agricultural University, Taian 271018, Shandong Province, China;2. Tobacco Research Institute, Anhui Academy of Agricultural Sciences, Hefei 230031, Anhui Province, China |
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Abstract: | 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 μM 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. |
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Keywords: | APX, ascorbate peroxidase AsA, ascorbic acid CAT, catalase CsA, cyclosporine A DHR123, dihydrohodamine123 DPI, diphenyl iodonium FA, fusaric acid H2O2, hydrogen peroxide MDA, malondialdehyde MPTP, mitochondrial permeability transition pore NO, nitric oxide PBS, phosphate buffered saline ROS, reactive oxygen species PCD, programmed cell death |
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