Turning point in apoptosis/necrosis induced by hydrogen peroxide |
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Authors: | Saito Yoshiro Nishio Keiko Ogawa Yoko Kimata Junko Kinumi Tomoya Yoshida Yasukazu Noguchi Noriko Niki Etsuo |
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Affiliation: | a National Institute of Advanced Industrial Science and Technology (AIST), Human Stress Signal Research Center (HSSRC), Osaka, Ikeda, Japanb Thermo Electron KK, Yokohama, Japanc Department of Environmental Systems Science, Faculty of Engineering, Doshisha University, Kyoto, Japan |
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Abstract: | The turning point between apoptosis and necrosis induced by hydrogen peroxide (H2O2) have been investigated using human T-lymphoma Jurkat cells. Cells treated with 50 μM H2O2 exhibited caspase-9 and caspase-3 activation, finally leading to apoptotic cell death. Treatment with 500 μM H2O2 did not exhibit caspase activation and changed the mode of death to necrosis. On the other hand, the release of cytochrome c from the mitochondria was observed under both conditions. Treatment with 500 μM H2O2, but not with 50 μM H2O2, caused a marked decrease in the intracellular ATP level; this is essential for apoptosome formation. H2O2-reducing enzymes such as cellular glutathione peroxidase (cGPx) and catalase, which are important for the activation of caspases, were active under the 500 μM H2O2 condition. Prevention of intracellular ATP loss, which did not influence cytochrome c release, significantly activated caspases, changing the mode of cell death from necrosis to apoptosis. These results suggest that ATP-dependent apoptosome formation determines whether H2O2-induced cell death is due to apoptosis or necrosis. |
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Keywords: | 3-ABA 3-aminobenzamide AcOr acridime orange Apaf-1 apoptotic protease activating factor-1 cGPx cellular glutathione peroxidase 2D gel two-dimentinal gel GSH glutathione H2O2 hydrogen peroxide PARP poly (ADP-ribose) polymerase pI isoelectric point PI propidium iodide Prx peroxiredoxin PS phosphatidylserine ROS reactive oxygen species |
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