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Redox regulation in radiation-induced cytochrome c release from mitochondria of human lung carcinoma A549 cells.

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Title: Redox regulation in radiation-induced cytochrome c release from mitochondria of human lung carcinoma A549 cells.
Other Titles: Redox regulation in radiation-induced cytochrome-c release from mitochondria of human lung carcinoma A549 cells.
Authors: Ogura, Aki Browse this author
Oowada, Shigeru Browse this author
Kon, Yasuhiro Browse this author →KAKEN DB
Hirayama, Aki Browse this author
Yasui, Hironobu Browse this author →KAKEN DB
Meike, Syunsuke Browse this author
Kobayashi, Saori Browse this author
Kuwabara, Mikinori Browse this author
Inanami, Osamu Browse this author →KAKEN DB
Keywords: Radiation
Reactive oxygen species (ROS)
Redox regulation
Electron spin resonance (ESR)
Issue Date: 8-May-2009
Publisher: Elsevier
Journal Title: Cancer Letters
Volume: 277
Issue: 1
Start Page: 64
End Page: 71
Publisher DOI: 10.1016/j.canlet.2008.11.021
PMID: 19117669
Abstract: Mitochondria in mammalian cells were well-known to play an important role in the intrinsic pathway of genotoxic-agent-induced apoptosis by releasing cytochrome c into cytosol and to be a major source of reactive oxygen species (ROS). The aim of this study is to examine whether mitochondrial ROS involved in radiation-induced apoptotic signaling in A549 cells. The post-irradiation-treatment of N-acetyl-L-cystein (NAC) inhibited cytochrome c release from mitochondria but did not affect expression level of Bcl-2, Bcl-XL and Bax, suggesting late production of ROS triggered cytochrome c release. The experiments using DCFDA (a classical ROS fluorescence probe) and MitoAR (a novel mitochondrial ROS probe) demonstrated that intracellular and mitochondrial ROS were enhanced 6 h after X irradiation. Furthermore, the O2^[-.] production ability of mitochondria isolated from A549 cells was evaluated by ESR spectroscopy combined with a spin-trapping reagent (CYPMPO). When isolated mitochondria were incubated with NADH, succinate and CYPMPO, the ESR spectrum due to CYPMPO-OOH was detected. This NADH/succinate-dependent O2^[-.] production from mitochondria of irradiated cells was significantly increased in comparison with that of unirradiated cells. These results indicated that ionizing radiation enhanced O2^[-.] production from mitochondria to trigger cytochrome c release in A549 cells.
Type: article (author version)
Appears in Collections:獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 稲波 修

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