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Mechanistic basis for nonlinear dose-response relationships for low-dose radiation-induced stochastic effects.低剂量辐射诱发随机效应的非线性剂量-反应关系的机制基础。
Nonlinearity Biol Toxicol Med. 2003 Jan;1(1):93-122. doi: 10.1080/15401420390844492.
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Neoplastic transformation in vitro after exposure to low doses of mammographic-energy X rays: quantitative and mechanistic aspects.低剂量乳腺X线摄影能量X射线照射后体外肿瘤转化:定量与机制方面
Radiat Res. 2004 Dec;162(6):646-54. doi: 10.1667/rr3277.
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The linear no-threshold model does not hold for low-dose ionizing radiation.线性无阈模型不适用于低剂量电离辐射。
Radiat Res. 2004 Oct;162(4):447-52. doi: 10.1667/rr3228.
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The bystander response in C3H 10T1/2 cells: the influence of cell-to-cell contact.
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Low-dose hyper-radiosensitivity: a consequence of ineffective cell cycle arrest of radiation-damaged G2-phase cells.低剂量超放射敏感性:辐射损伤的G2期细胞细胞周期阻滞无效的结果。
Radiat Res. 2004 Mar;161(3):247-55. doi: 10.1667/rr3130.
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Adaptive response in embryogenesis: V. Existence of two efficient dose-rate ranges for 0.3 Gy of priming irradiation to adapt mouse fetuses.胚胎发生中的适应性反应:V. 对0.3 Gy预照射使小鼠胎儿产生适应性反应存在两个有效剂量率范围。
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A reanalysis of thyroid neoplasms in the Israeli tinea capitis study accounting for dose uncertainties.对以色列头癣研究中甲状腺肿瘤进行的再分析,其中考虑了剂量不确定性。
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Cancer risks attributable to low doses of ionizing radiation: assessing what we really know.低剂量电离辐射所致癌症风险:评估我们真正了解的情况。
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Interaction between radiation-induced adaptive response and bystander mutagenesis in mammalian cells.哺乳动物细胞中辐射诱导的适应性反应与旁观者诱变之间的相互作用。
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低剂量低传能线密度辐射后肿瘤转化的非线性反应。

Nonlinear response for neoplastic transformation following low doses of low let radiation.

作者信息

Redpath J Leslie

机构信息

Department of Radiation Oncology, University of California Irvine, Irvine, CA.

出版信息

Nonlinearity Biol Toxicol Med. 2005 Jan;3(1):113-24. doi: 10.2201/nonlin.003.01.007.

DOI:10.2201/nonlin.003.01.007
PMID:19330158
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2657837/
Abstract

There are now several independent studies that indicate that the dose-response for the endpoint of radiation-induced neoplastic transformation in vitro is non-linear for low linear energy transfer (LET) radiation. At low doses (<10 cGy) the transformation frequency drops below that seen spontaneously. Importantly, this observation has been made using fluoroscopic energy x-rays, a commonly used modality in diagnostic radiology, the practice of which is responsible for the majority of radiation exposure to the general public. Since the transformation frequency is reduced over a large dose range (0.1 to 10cGy) it is likely that multiple mechanisms are involved and that the relative contribution of these may vary with dose. These include the killing of a subpopulation of cells prone to spontaneous transformation at the lowest doses, and the induction of DNA repair at somewhat higher doses. Protective effects of low doses of low LET radiation on other cancer-relevant endpoints in vitro and in vivo have also been observed by several independent laboratories. These observations strongly suggest that the linear-nonthreshold dose-response model is unlikely to apply to the induction of cancer by low doses of low LET radiation in humans.

摘要

现在有几项独立研究表明,对于低线性能量传递(LET)辐射,体外辐射诱导肿瘤转化终点的剂量反应是非线性的。在低剂量(<10 cGy)时,转化频率低于自发出现的频率。重要的是,这一观察结果是使用荧光透视能量X射线得出的,荧光透视能量X射线是诊断放射学中常用的一种方式,而这种方式导致了普通公众大部分的辐射暴露。由于在较大剂量范围(0.1至10 cGy)内转化频率降低,可能涉及多种机制,并且这些机制的相对贡献可能随剂量而变化。这些机制包括在最低剂量时杀死易于自发转化的细胞亚群,以及在稍高剂量时诱导DNA修复。几个独立实验室还观察到低剂量低LET辐射在体外和体内对其他癌症相关终点的保护作用。这些观察结果强烈表明,线性无阈剂量反应模型不太可能适用于低剂量低LET辐射对人类癌症的诱导。