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Mechanisms underlying biological effects of low dose radiation: Mutagenic adaptive response to high-LET radiation in human lymphoblastoid cells
https://repo.qst.go.jp/records/64093
https://repo.qst.go.jp/records/6409314e14c81-1d1b-4f0d-98bc-756a26d5985b
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2010-11-12 | |||||
| タイトル | ||||||
| タイトル | Mechanisms underlying biological effects of low dose radiation: Mutagenic adaptive response to high-LET radiation in human lymphoblastoid cells | |||||
| 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 |
Vares, Guillaume
× Vares, Guillaume× Bing, Wang× Nenoi, Mitsuru× Ｇｕｉｌｌａｕｍｅ Ｖａｒｅｓ× 王 冰× 根井 充 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Recent developments in the low dose radiation research suggest that cellular response to low doses of ionizing radiation (IR) cannot necessarily be directly extrapolated from responses to high doses [Mullenders, et al., Nat. Rev. Cancer. 9 (2009) 596-604, Averbeck, Health. Phys. 97 (2009) 493-504.]. Specific phenomena associated with low dose IR include bystander effect, low-dose hyper-radiosensitivity, genomic instability and adaptive response (AR). The ability of cells to adapt to low-dose or low-dose rate IR has been well documented both in vitro and in vivo, where pre-exposure of cells to low levels of radiation is responsible for decreased biological effects of challenging high doses [Vares, et al., Indian. J. Radiat. Res. 3 (2006) 16-34]. High-LET radiation has unique characteristics, and the question of whether AR could be observed when using such radiation is of great interest for both the basic radiation research and the clinical fields. Unlike low-LET radiation, high-LET heavy-ion radiation produces non-randomly distributed DNA damage in the form of clusters, which are generally considered as non-easily repairable [Hada, et al., J. Radiat. Res. 49 (2008) 203-210]. Recent advances in cancer radiotherapy include the use of high-LET heavy-ion beams, which have over the last few years produced very promising clinical results. To date, not much is known about potential AR-related effects in relationship with high-LET radiation, let alone possible implications of this phenomenon for radiation therapy. Space research is another field showing strong interest in high-LET-related radio-adaptation, because long-term space journeys would involve exposure to various kinds of high-LET radiation. The precise molecular mechanisms involved in AR remain elusive, but DNA repair and p53-related pathways are considered important effectors. It was suggested that repression of p53-dependent responses to radiation might be one of the mechanisms associated with AR, both in in vitro and in vivo models [Ohnishi, et al., Radiat. Res. 151 (1999) 368-372., Takahashi, et al., Int. J. Radiat. Biol. 77 (2001) 939-945]. Involvement of p53 pathways in AR might lead to the induction of several proteins associated with DNA repair, such as RAD51, RAD54 and BRCA1. The existence of an AR to mutation induction with low-LET radiation was demonstrated in different models, including lymphoblastoid cells, by several authors [Rigaud, et al., Mutat. Res. 358 (1996) 127 - 134., Hafer, et al., Radiat. Res. 168 (2007) 168-174., Lu, et al., Int. J. Radiat. Biol. 85 (2009) 532-537., Zhou, et al., Mutagenesis. 8 (1993) 109-111.]. They observed decreased mutation frequencies after irradiation when cells had previously been conditioned by low doses of low-LET radiation. In this study, we assessed in vitro the ability of low doses of X-rays to induce an AR to a subsequent challenging dose of heavy-ion radiation. Lymphoblastoid cells (TK6, AHH-1, NH32) were exposed to priming 0.02-0.1 Gy X-rays, followed 6 hours later by challenging 1 Gy heavy-ion radiation (carbon-ion: 20 and 40 keV/µm, neon-ion: 150 keV/µm). Pre-exposure of p53-competent cells resulted in decreased mutation frequencies at Hypoxanthine-guanine phosphoribosyl transferase (HPRT) locus and different H2AX phosphorylation kinetics, as compared to cells exposed to challenging radiation alone. This phenomenon did not seem to be linked with cell cycle effects or radiation-induced apoptosis. Taken together, our results suggested the existence of an AR to mutagenic effects of heavy-ion radiation in lymphoblastoid cells and the involvement of double-strand break repair mechanisms. |
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| 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 | ー放医研ワークショップー放射線医学・安全研究分野の国際展開に向けて-NIRS-Workshop as an IAEA Collaborationg Centre- | |||||
| 発表年月日 | ||||||
| 日付 | 2010-11-12 | |||||
| 日付タイプ | Issued | |||||
