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塞拉菲尔德周边儿童的DNA不稳定性、父系辐射与白血病

DNA instability, paternal irradiation and leukaemia in children around Sellafield.

作者信息

Baverstock K F

机构信息

MRC Radiobiology Unit, Chilton, Didcot, UK.

出版信息

Int J Radiat Biol. 1991 Oct;60(4):581-95. doi: 10.1080/09553009114552421.

DOI:10.1080/09553009114552421
PMID:1680140
Abstract

The chemical instability of DNA under physiological conditions requires that cells have highly developed processes for repairing stochastic single-strand damage. It is proposed here that provided ionizing-radiation-induced single-strand damage does not occur at a rate sufficient to perturb the dynamic steady state between degradation and repair, it can be regarded as "irrelevant' to biological effect, leaving double-strand damage and DNA-protein crosslinks as "relevant' damage to biological effect. At dose rates of approximately 0.05 Gy/min low-LET radiation the rate of induced single-strand damage equals that of the spontaneous damage, and in this region a transition, with increasing dose-rate, from constant effect to increasing effect, will be expected. This is observed in studies of specific locus mutation by radiation in the male mouse. The application of this biophysical principle governing the influence of radiation dose-rate, to the association observed between paternal preconceptional dose to Sellafield workers and childhood leukaemia in their offspring, shows that the likelihood of a causal relationship is extremely remote.

摘要

在生理条件下,DNA的化学不稳定性要求细胞具备高度发达的机制来修复随机的单链损伤。本文提出,如果电离辐射诱导的单链损伤发生速率不足以扰乱降解与修复之间的动态稳态,那么就可以将其视为对生物效应“无关”,而双链损伤和DNA-蛋白质交联则作为对生物效应“相关”的损伤。在低传能线密度辐射剂量率约为0.05 Gy/分钟时,诱导单链损伤的速率与自发损伤的速率相等,在这个区域,随着剂量率增加,预计会出现从效应恒定到效应增加的转变。这在对雄性小鼠进行辐射诱导的特定基因座突变研究中得到了观察。将这一控制辐射剂量率影响的生物物理原理应用于塞拉菲尔德核电站工人受孕前的辐射剂量与其后代儿童白血病之间的关联研究中,结果表明因果关系的可能性极其微小。

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