Radiation induced bystander signals are independent of DNA damage and DNA repair capacity of the irradiated cells
Radiation induced bystander signals are independent of DNA damage and DNA repair capacity of the irradiated cells
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DOI：
10.1016/j.mrfmmm.2007.02.005
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发表时间：
2007-06-01
影响因子：
2.3
通讯作者：
Prise, Kevin M.
中科院分区：
文献类型：
--
作者：
Kashino, Genro;Suzuki, Keiji;Prise, Kevin M.
越来越多的证据表明，受辐射的细胞会产生信号，这些信号会与同一群体中未受辐射的细胞相互作用。在这里，我们分析了旁观者信号在野生型CHO细胞和修复缺陷型细胞中产生的机制，重点是DNA修复能力和受辐射细胞中产生的旁观者信号之间的关系。为了研究旁观者效应，我们在X射线照射后进行了培养基转移实验，在非靶向DSB修复缺陷xrs 5细胞中对微核进行评分。当条件培养基从照射细胞转移到未照射xrs 5细胞，诱导的水平是独立的培养基是否来自照射野生型，ssb或dsb修复缺陷细胞。这一结果表明，旁观者信号的激活是独立的辐射细胞的DNA修复能力。此外，用0.5% DMSO预处理辐照细胞（可抑制CHO中的微核诱导，但不抑制xrs 5细胞中的微核诱导）完全抑制了两种条件培养基中的旁观者效应，表明DMSO可有效抑制辐照细胞中独立于DNA损伤而产生的旁观者信号。总的来说，这里提出的工作增加了这样的理解，即它是接收旁观者信号的细胞的修复表型，它决定了整体反应，而不是产生旁观者信号的细胞的反应。(c)2007 Elsevier B.V.保留所有权利。
Evidence is accumulating that irradiated cells produce signals, which interact with non-exposed cells in the same population. Here, we analysed the mechanism for bystander signal arising in wild-type CHO cells and repair deficient varients, focussing on the relationship between DNA repair capacity and bystander signal arising in irradiated cells. In order to investigate the bystander effect, we carried out medium transfer experiments after X-irradiation where micronuclei were scored in non-targeted DSB repair deficient xrs5 cells. When conditioned medium from irradiated cells was transferred to unirradiated xrs5 cells, the level of induction was independent of whether the medium came from irradiated wild-type, ssb or dsb repair deficient cells. This result suggests that the activation of a bystander signal is independent of the DNA repair capacity of the irradiated cells. Also, pre-treatment of the irradiated cells with 0.5% DMSO, which suppresses micronuclei induction in CHO but not in xrs5 cells, suppressed bystander effects completely in both conditioned media, suggesting that DMSO is effective for suppression of bystander signal arising independently of DNA damage in irradiated cells. Overall the work presented here adds to the understanding that it is the repair phenotype of the cells receiving bystander signals, which determines overall response rather than that of the cell producing the bystander signal. (c) 2007 Elsevier B.V. All rights reserved.