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A model of radiation action based on nanodosimetry and the application to ultra-soft X-rays.
Radiation and Environmental Biophysics ( IF 1.5 ) Pub Date : 2020-04-10 , DOI: 10.1007/s00411-020-00842-1
Uwe Schneider 1, 2 , Fabiano Vasi 1, 2 , Kevin Schmidli 1, 2 , Jürgen Besserer 1, 2
Affiliation  

A radiation action model based on nanodosimetry is presented. It is motivated by the finding that the biological effects of various types of ionizing radiation lack a consistent relation with absorbed dose. It is postulated that the common fundamental cause of these effects is the production of elementary sublesions (DSB), which are created at a rate that is proportional to the probability to produce more than two ionisations within a volume of 10 base pairs of the DNA. The concepts of nanodosimetry allow for a quantitative characterization of this process in terms of the cumulative probability F2. The induced sublesions can interact in two ways to produce lethal damage. First, if two or more sublesions accumulate in a locally limited spherical volume of 3–10 nm in diameter, clustered DNA damage is produced. Second, consequent interactions or rearrangements of some of the initial damage over larger distances (~ µm) can produce additional lethal damage. From the comparison of theoretical predictions deduced from this concept with experimental data on relative biological effectiveness, a cluster volume with a diameter of 7.5 nm could be determined. It is shown that, for electrons, the predictions agree well with experimental data over a wide energy range. The only free parameter needed to model cell survival is the intersection cross-section which includes all relevant cell-specific factors. Using ultra-soft X-rays it could be shown that the energy dependence of cell survival is directly governed by the nanodosimetric characteristics of the radiation track structure. The cell survival model derived in this work exhibits exponential cell survival at a high dose and a finite gradient of cell survival at vanishing dose, as well as the dependence on dose-rate.



中文翻译:

基于纳米剂量学的辐射作用模型及其在超软X射线中的应用。

提出了基于纳米剂量的辐射作用模型。发现的动机是,各种类型的电离辐射的生物学效应与吸收剂量缺乏一致的关系。据推测,这些效应的常见根本原因是基本亚病变(DSB)的产生,其速率与在10个碱基对的DNA中产生两个以上电离的概率成比例。纳米剂量学的概念允许根据累积概率F 2对该过程进行定量表征。。诱发的皮损可以两种方式相互作用以产生致命伤害。首先,如果两个或多个皮损聚集在直径为3-10 nm的局部有限球形体积中,则会产生聚集的DNA损伤。其次,在较大距离(〜μm)上,某些初始损伤的后续相互作用或重新排列可能产生额外的致命损伤。通过从该概念得出的理论预测与相对生物学有效性的实验数据进行比较,可以确定直径为7.5 nm的簇体积。结果表明,对于电子,预测结果与较宽的能量范围内的实验数据吻合良好。建模细胞存活所需的唯一自由参数是相交横截面,其中包括所有相关的细胞特异性因子。使用超软X射线,可以证明细胞存活的能量依​​赖性直接受辐射径迹结构的纳米剂量特性支配。在这项工作中得出的细胞存活模型在高剂量下表现出指数细胞存活率,在消失剂量下表现出有限的细胞存活率梯度,以及对剂量率的依赖性。

更新日期:2020-04-23
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