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First published online April 9, 2002; 10.1104/pp.010999

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Plant Physiol, April 2002, Vol. 128, pp. 1271-1281

Oxidative Stress Increased Respiration and Generation of Reactive Oxygen Species, Resulting in ATP Depletion, Opening of Mitochondrial Permeability Transition, and Programmed Cell Death1

Budhi Sagar Tiwari, Beatrice Belenghi, and Alex Levine*

Department of Plant Sciences, Silberman Institute of Life Sciences, The Hebrew University of Jerusalem, Givat-Ram, Jerusalem 91904, Israel

Mitochondria constitute a major source of reactive oxygen species and have been proposed to integrate the cellular responses to stress. In animals, it was shown that mitochondria can trigger apoptosis from diverse stimuli through the opening of MTP, which allows the release of the apoptosis-inducing factor and translocation of cytochrome c into the cytosol. Here, we analyzed the role of the mitochondria in the generation of oxidative burst and induction of programmed cell death in response to brief or continuous oxidative stress in Arabidopsis cells. Oxidative stress increased mitochondrial electron transport, resulting in amplification of H2O2 production, depletion of ATP, and cell death. The increased generation of H2O2 also caused the opening of the MTP and the release of cytochrome c from mitochondria. The release of cytochrome c and cell death were prevented by a serine/cysteine protease inhibitor, Pefablock. However, addition of inhibitor only partially inhibited the H2O2 amplification and the MTP opening, suggesting that protease activation is a necessary step in the cell death pathway after mitochondrial damage.


1 This work was supported by the Israel Science Foundation.

* Corresponding author; e-mail alexlevine{at}huji.ac.il; fax 972-2-658-4425.

© 2002 American Society of Plant Physiologists



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