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适应性反应:第二部分。剂量率和时间影响的进一步建模

Adaptive response: Part II. Further modeling for dose rate and time influences.

作者信息

Leonard Bobby E

机构信息

International Academy, Severna Park, Maryland 21146, USA.

出版信息

Int J Radiat Biol. 2007 Jun;83(6):395-408. doi: 10.1080/09553000701326995.

Abstract

PURPOSE

For adaptive response (AR) behavior, to model and analyze the dose rate dependence of AR. To examine and to model the influence of time interval between primer and challenge dose on the magnitude of radioprotection.

METHOD AND MATERIALS

Microdosimetry is used to examine effects of rate of critical volume specific energy depositions on activation of AR and induction of deleterious damage. The dose rate dependent adaptive response data, Shadley and Wiencke and Shadley et al. on AR fading, are analyzed.

RESULTS

We obtain good agreement with observed AR behavior. The 4-6 hour activation time for AR is from time necessary for the accumulation of enzymatic resources from the increased radioprotective capability for the recognition and repair of deleterious DNA damage and perhaps resources for reduction of RSO. The Shadley and Wiencke data, for the low 1.0 cGy primer dose, is as a result of a minimum rate of specific energy depositions (hits) for adaptive response to become operative and become fully activated. Increased deleterious damage with increased dose rate for a high 50 cGy primer dose is from a reduction in dose rate sparing as the rate approaches acute exposure.

CONCLUSIONS

The microdosimetric model substantiates the prior observations in Part I that only several radiation-induced charged particle cell nucleus traversals are sufficient to activate adaptive response. Further however we find here that a minimum dose rate threshold is necessary. The model shows promise to provide insight into adaptive response time and dose rate behavior.

摘要

目的

针对适应性反应(AR)行为,对AR的剂量率依赖性进行建模和分析。研究并模拟引发剂量与激发剂量之间的时间间隔对辐射防护程度的影响。

方法和材料

运用微剂量学来研究关键体积比能沉积速率对AR激活和有害损伤诱导的影响。分析了剂量率依赖性适应性反应数据,以及Shadley和Wiencke以及Shadley等人关于AR消退的数据。

结果

我们得到的结果与观察到的AR行为高度吻合。AR的4 - 6小时激活时间源于从增强的辐射防护能力中积累酶资源所需的时间,这些资源用于识别和修复有害的DNA损伤,或许还包括用于减少辐射敏感性氧效应(RSO)的资源。对于低1.0 cGy的引发剂量,Shadley和Wiencke的数据是由于适应性反应开始起作用并完全激活所需的比能沉积(击中)的最小速率。对于高50 cGy的引发剂量,随着剂量率增加有害损伤增加,这是因为当剂量率接近急性暴露时剂量率节省效应降低。

结论

微剂量学模型证实了第一部分中的先前观察结果,即仅几次辐射诱导的带电粒子穿过细胞核就足以激活适应性反应。然而,我们在此进一步发现需要一个最小剂量率阈值。该模型有望为适应性反应时间和剂量率行为提供深入见解。

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