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• W2122486687 abstract "Bax inhibitor-1 (BI-1) is a cell death suppression factor widely conserved in higher plants and animals. Overexpression of Arabidopsis BI-1 (AtBI-1) in plants confers tolerance to various cell death-inducible stresses. However, apart from the cell death-suppressing activity, little is known about the physiological roles of BI-1-overexpressing plants. In this study, we evaluated the effects of AtBI-1 overexpression on the rice metabolome in response to oxidative stress. AtBI-1-overexpressing rice cells in suspension displayed enhanced tolerance to menadione-induced oxidative stress compared with vector control cells, whereas AtBI-1 overexpression did not influence the increase of intracellular H(2)O(2) concentration or inhibition of oxidative stress-sensitive aconitase activity. Capillary electrophoresis-mass spectrometry (CE-MS)-based metabolome analysis revealed dynamic metabolic changes in oxidatively stressed rice cells, e.g. depletion of the central metabolic pathway, imbalance of the redox state and energy charge, and accumulation of amino acids. Furthermore, comparative metabolome analysis demonstrated that AtBI-1 overexpression did not affect primary metabolism in rice cells under normal growth conditions but significantly altered metabolite composition within several distinct pathways under cell death-inducible oxidative stress. The AtBI-1-mediated metabolic alteration included recovery of the redox state and energy charge, which are known as important factors for metabolic defense against oxidative stress. These observations suggest that although AtBI-1 does not affect rice metabolism directly, its cell death suppression activity leads to enhanced capacity to acclimate oxidative stress." @default.
• W2122486687 created "2016-06-24" @default.
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• W2122486687 date "2009-11-16" @default.
• W2122486687 modified "2023-09-25" @default.
• W2122486687 title "Metabolome Analysis of Response to Oxidative Stress in Rice Suspension Cells Overexpressing Cell Death Suppressor Bax Inhibitor-1" @default.
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• W2122486687 doi "https://doi.org/10.1093/pcp/pcp162" @default.
• W2122486687 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19919949" @default.
• W2122486687 hasPublicationYear "2009" @default.
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