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ρ0 Cells Are Susceptible to X-Irradiation
https://repo.qst.go.jp/records/65443
https://repo.qst.go.jp/records/654438b42f9b1-c857-4c87-a908-4ec3a8c4fdc8
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2014-03-31 | |||||
| タイトル | ||||||
| タイトル | ρ0 Cells Are Susceptible to X-Irradiation | |||||
| 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 |
犬童, 寛子
× 犬童, 寛子× 鶴岡, 千鶴× 柿沼, 志津子× 鈴木, 雅雄× 松本, 謙一郎× 中西, 郁夫× Yen, Hsiu-Chuan× 松井, 裕史× 小澤, 俊彦× 馬嶋, 秀行× 犬童 寛子× 鶴岡 千鶴× 柿沼 志津子× 鈴木 雅雄× 松本 謙一郎× 中西 郁夫× 松井 裕史× 小澤 俊彦× 馬嶋 秀行 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Oxidative stress has been focused as cause of many diseases with chronic symptoms. In such diseases, mitochondria have been paid attention as the trigger of diseases. Mitochondria DNA (mtDNA) have 13 genes, which encode parts of electron transport chain (ETC). Previously we have reported evidence of reactive oxygen species (ROS) generation by mitochondria in cells with impaired electron transport chain and mitochondrial DNA damage. Inhibitors for ETC, or mitochondrial DNA damages generate more ROS from mitochondria (Indo et al. Mitochondrion 2007). Cells without mitochondrial DNA, ρ0 cells produce more ROS, lipid peroxidation, and pronounced more apoptosis at condition without uridine and pyruvate. ρ0 cells decrease in the red/green fluorescence intensity ratio, i.e., mitochondrial depolarization. The higher sensitivity to X-rays against ρ0 cells, higher rate of chromosomal aberration and larger amount of DNA double strand breaks indicated that pronounced radiation sensitive compared to the parental cells. Moreover ρ0 cells indicated less activity of manganese superoxide dismutase (MnSOD). These results indicate that ρ0 cells are radiation sensitive at the nuclear effects besides their mitochondria mediated apoptosis, and these results suggest mitochondria are the primary sites of X-irradiation-induced cellular injuries. | |||||
| 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 | 第32回Cytoprotection研究会 | |||||
| 発表年月日 | ||||||
| 日付 | 2014-03-23 | |||||
| 日付タイプ | Issued | |||||
