WEKO3
アイテム
DNA double-strand break induction in Ku80-deficient CHO cells following Boron Neutron Capture Reaction
https://repo.qst.go.jp/records/46186
https://repo.qst.go.jp/records/46186abab4891-6d8d-4b4c-b0f6-c910ad1f39ab
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2011-10-25 | |||||
| タイトル | ||||||
| タイトル | DNA double-strand break induction in Ku80-deficient CHO cells following Boron Neutron Capture Reaction | |||||
| 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_6501 | |||||
| 資源タイプ | journal article | |||||
| 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 |
Kinashi, Yuko
× Kinashi, Yuko× Takahashi, Sentaro× Kashino, Genro× Okayasu, Ryuichi× Masunaga, Shinichiro× Suzuki, Minoru× Ono, Koji× 高橋 千太郎× 岡安 隆一× 増永 慎一郎× 小野 公二 |
|||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | BACKGROUND: Boron neutron capture reaction (BNCR) is based on irradiation of tumors after accumulation of boron compound. 10B captures neutrons and produces an alpha (4He) particle and a recoiled lithium nucleus ( 7Li ). These particles have the characteristics of high linear energy transfer (LET) radiation and have marked biological effects. The purpose of this study is to verify that BNCR will increase cell killing and slow disappearance of repair protein-related foci to a greater extent in DNA repair-deficient cells than in wild-type cells. \nMETHODS: Chinese hamster ovary (CHO-K1) cells and a DNA double-strand break (DSB) repair deficient mutant derivative, xrs-5 (Ku80 deficient CHO mutant cells), were irradiated by thermal neutrons. The quantity of DNA-DSBs following BNCR was evaluated by measuring the phosphorylation of histone protein H2AX (gamma-H2AX) and 53BP1 foci using immunofluorescence intensity. \nRESULTS: Two hours after neutron irradiation, the number of gamma-H2AX and 53BP1 foci in the CHO-K1 cells was decreased to 36.542.8% of the levels seen 30 min after irradiation. In contrast, two hours after irradiation, foci levels in the xrs-5 cells were 58.469.5% of those observed 30 min after irradiation. The number of gamma-H2AX foci in xrs-5 cells at 60120 min after BNCT correlated with the cell killing effect of BNCR. However, in CHO-K1 cells, the RBE (relative biological effectiveness) estimated by the number of foci following BNCR was increased depending on the repair time and was not always correlated with the RBE of cytotoxicity. \nCONCLUSION: Mutant xrs-5 cells show extreme sensitivity to ionizing radiation, because xrs-5 cells lack functional Ku-protein. Our results suggest that the DNA-DSBs induced by BNCR were not well repaired in the Ku80 deficient cells. The RBE following BNCR of radio-sensitive mutant cells was not increased but was lower than that of radio-resistant cells. These results suggest that gamma-ray resistant cells have an advantage over gamma-ray sensitive cells in BNCR. |
|||||
| 書誌情報 |
Radiation Oncology (Online only URL:http://www.ro-journal.com/) 巻 6, p. 106, 発行日 2011-09 |
|||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 1748-717X | |||||
| 関連サイト | ||||||
| 識別子タイプ | URI | |||||
| 関連識別子 | http://www.ro-journal.com/content/6/106 | |||||
| 関連名称 | http://www.ro-journal.com/content/6/106 | |||||
