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Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine >
Peer-reviewed Journal Articles, etc >
Redox regulation in radiation-induced cytochrome c release from mitochondria of human lung carcinoma A549 cells.
| 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 | | Mitochondria | | 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) |
| URI: | http://hdl.handle.net/2115/38355 |
| 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)
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Submitter: 稲波 修
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