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Can hydrogen peroxide induce DSBs through a long-term cellular response?
https://repo.qst.go.jp/records/69475
https://repo.qst.go.jp/records/694756ed9ed11-76bd-4bdd-b892-25273c7561ff
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2008-09-26 | |||||
| タイトル | ||||||
| タイトル | Can hydrogen peroxide induce DSBs through a long-term cellular response? | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_c94f | |||||
| 資源タイプ | conference object | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Katsube, Takanori
× Katsube, Takanori× Mori, Masahiko× Tsuji, Hideo× Shiomi, Tadahiro× Onoda, Makoto× 勝部 孝則× 森 雅彦× 辻 秀雄× 塩見 忠博× 小野田 眞 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Reactive oxygen species (ROS) are generated within cells by ionizing radiation via primary ionizing events as well as through secondary amplification systems including metabolic synthesis. Mediating oxidation of cell components, ROS not only cause dysfunction of the target molecules but also perturb intra- and inter-cellular signal transduction pathways. Our ultimate aim is to elucidate the contribution of ROS in cellular events, especially DNA damages, elicited by ionizing radiation. In the current study, we compared cellular responses to hydrogen peroxide (H2O2) and X-rays in DNA repair-deficient cells. XRCC4-deficient mutant cells exhibited lower survival rates than XRCC4-proficient parental cells after exposure to either H2O2 or X-irradiation. The LD37 values of the XRCC4-/- and parental cells after a 1-hr treatment with H2O2 were 8.5 and 11.1 µM and those for X-irradiation were 0.5 and 1.7 Gy, respectively. XRCC4 is a component of the non-homologous end-joining, a predominant repair pathway for DNA double-strand breaks (DSBs). To date, no other functions of XRCC4 have not been reported yet. Thus, marked increases in death of the XRCC4-/- cells exposed to H2O2 or X-irradiation must be attributed to DSBs. Consistently, gammaH2AX staining revealed a dose-dependent formation of DSBs in the X-irradiated cells (~50 DSBs/cell/Gy). However, the formation of DSBs was not so significant just after a 1-hr exposure to 0-50 µM H2O2 in both the mutant and parental cells. DSBs might be formed at later stages in the H2O2-treated cells through some long-term cellular response. | |||||
| 会議概要（会議名, 開催地, 会期, 主催者等） | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 日本放射線影響学会 第50回大会 | |||||
| 発表年月日 | ||||||
| 日付 | 2007-11-17 | |||||
| 日付タイプ | Issued | |||||
