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A Paradigm Shift in the Understanding of Oxidative Stress and its Implications to Exposure of Low-level Ionizing Radiation
http://hdl.handle.net/10069/9314
http://hdl.handle.net/10069/9314a8f0ce5c-d1cf-4365-985f-d78d7dbdcc5c
名前 / ファイル | ライセンス | アクション |
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acta50_s1_63.pdf (811.3 kB)
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Item type | 紀要論文 / Departmental Bulletin Paper(1) | |||||
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公開日 | 2007-11-02 | |||||
タイトル | ||||||
タイトル | A Paradigm Shift in the Understanding of Oxidative Stress and its Implications to Exposure of Low-level Ionizing Radiation | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Oxidativestress | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Gapjunctionalintercellularcommunication | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Epigenetictoxicity | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Cancer | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | NADPHoxidase | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Signaltransduction | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | departmental bulletin paper | |||||
著者 |
L..Upham, Brad
× L..Upham, Brad× E..Trosko, James |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | For many years, research on oxidative stress focused primarily on determining how reactive oxygen species (ROS) damage cells by indiscriminate reactions with its macromolecular machinery, particularly lipids, proteins and DNA. However, many chronic diseases affiliated with oxidative stress are not always a consequence of tissue necrosis, DNA, or protein damage but rather to altered gene expression. Gene expression is highly regulated by the coordination of extra-, intra- and inter-cellular communication systems that typically maintain tissue homeostasis by sustaining a balance between proliferation, differentiation and apoptosis. Therefore, much research has shifted to the understanding of how ROS reversibly controls gene expression at noncytotoxic doses through cell signaling mechanisms. Cell proliferation typically involves a transient inhibition of gap junctional intercellular communication (GJIC) and the activation of mitogen activated protein kinase pathways (MAPK). We demonstrate that epidermal growth factor (EGF) inhibited GJIC in normal rat liver epithelial cells in addition to activating extracellular signal regulatory kinase, a MAPK. Inhibition of NADPH oxidase, which reduces oxygen to H2O2 with the very selective inhibitor diphenyleneiodonium, prevented EGF from inhibiting GJIC, suggesting that the generation of H2O2 is an essential component of the intracellular pathway controlling GJIC. We previously demonstrated that reduced-glutathione (GSH) was also a necessary cofactor of H2O2-induced inhibition of GJIC. These results demonstrate that ROS and GSH play essential roles in controlling EGF-dependent control of GJIC. Therefore, the overly simplistic approach of either preventing the generation of ROS or accelerate the removal by antioxidants could deleteriously alter normal signaling functions. | |||||
書誌情報 |
Acta medica Nagasakiensia 巻 50, 号 supl.1, p. 63-68, 発行日 2005-12 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 00016055 | |||||
書誌レコードID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA00508430 | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
関係URI | ||||||
関連名称 | http://joi.jlc.jst.go.jp/JST.JSTAGE/amn/50.S63 | |||||
sortkey | ||||||
P00063-P00068 | ||||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | Acta medica Nagasakiensia. 2005, 50(supl.1), p.63-68 |