假设辐射的致癌作用是由组织反应引起的寿命缩短,对小鼠剂量率效应的检验。

Nori Nakamura
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引用次数: 0

摘要

目的:辐射暴露似乎不会增加小鼠死于肿瘤的比例,而是导致自发癌症的出现发生变化,使它们更早出现,从而产生缩短寿命的效果。这样,就有可能用缩短寿命的效应作为衡量标准来估计剂量率对辐射致癌效应的影响。结论:急性暴露条件下诱导寿命缩短的剂量反应是线性的,这表明慢性暴露条件下的剂量反应也可能是线性的,因此剂量率因子(DRF)在整个剂量下是恒定的。此外,随着暴露年龄的增加,寿命缩短效应急剧下降。为了将长期照射条件下的剂量率效应与年龄效应分离开来,设计了一项思想实验,其中包括8次急性1 Gy剂量的重复照射,间隔50天,假设该效应是可加性的,并将结果与慢性连续照射实验(每天20 mGy,持续400天,总共8 Gy: Tanaka et al. 2003)中观察到的结果进行比较。结果表明,前者缩短寿命211 d,后者缩短寿命120 d, DRF为1.8(211/120)。如果假设组织反应是辐射致癌的主要原因,那么对比鲜明的两个概念,即低剂量下的辐射激效和线性非阈值模型,将是相容的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
An examination of the dose rate effect in mice assuming that the carcinogenic effect of radiation is life shortening resulting from a tissue reaction.

Purpose: Radiation exposures do not seem to increase the proportion of mice dying from tumors, but rather cause a shift in the appearance of spontaneous cancers, allowing them to appear earlier, and hence produce a life shortening effect. Then, it was possible to estimate the effect of the dose rate on the carcinogenic effects of radiation using life shortening effects as a measure.

Conclusion: The dose response for the induction of life shortening was linear under acute exposure conditions, which indicates that the response under chronic exposure conditions is also likely to be linear, and hence the dose rate factor (DRF) would be constant throughout the dose. Furthermore, the life shortening effect decreased sharply with an increase in age at exposure. To separate the dose rate effect from the effects of age under long-term exposure conditions, a thought experiment was designed which consisted of 8 repeated exposures to an acute 1 Gy dose at intervals of 50 days with an assumption that the effect is additive, and the results were compared with those observed in a chronic continuous exposure experiment (20 mGy per day for 400 days, for a total of 8 Gy: Tanaka et al. 2003). The results showed 211 days of life shortening in the former and 120 days in the latter, which provided a DRF of 1.8 (211/120). If one assumes that a tissue reaction is the primary cause of radiation carcinogenesis, the contrasting two concepts, radiation hormesis and linear-non-threshold model at low doses, would become compatible.

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