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原文

电离辐射产生的生物效应主要表现为直接的染色体和DNA损伤。但有证据表明也可以诱导基因组不稳定性,即辐射产生的损伤使整个基因组处于一种“临界”状态,并且通过某种机制传递到子代中,在细胞复制许多代后产生滞后的遗传改变[1]。可共检测的生物学终点有染色体改变、多倍体数的改变、微核形成、基因突变和扩增、小卫星和微卫星不稳定性以及克隆形成率的下降等。基因组不稳定性是许多癌症的一个特点[2],它可能是肿瘤形成的驱动力[3]。在某些辐射诱导的肿瘤形成过程中,越来越多的证据表明,不稳定性可能是一个关键的步骤[4]。许多文献都提出了这样的一种假说,即辐射诱导的基因组不稳定性为辐射致癌作用提供了一种模型。因此,研究辐射诱发的基因组不稳定性,将为辐射有关的健康危险和一般的致癌过程提供有价值的见解。

 

虽然很多生物学终点可用于检测基因组不稳定性,但由于其主要是以自发突变的形式表现出来,不仅所需观察时间长,而且发生率低,利用一些常规的放射生物学终点检测方法直接检测基因组不稳定性存在一定的困难。因此,本研究根据多级致癌理论中二次事件的推动作用,采用二次照射的方法,对60Co-γ射线照射人正常肝细胞后诱发的基因组不稳定性进行检测,从而为与肝脏辐射有关的辐射损伤与防护研究提供一定的理论依据。

翻译改写稿

Biological effects of ionized radiation include gene mutation, chromosomal rearrangement, cellular transformation, apoptosis, and radiation carcinogenesis; and DNA is the target of these biological effects. Increasing evidence demonstrates that these effects can occur in progeny of irradiated cells at delayed time points, and these damage effects could emerge in some single cell first, then spread and cause whole genome instability (Huang et al., 2003).

It has been known that genome instability exists in many cancers, and it can be a potential cause in tumorigenesis. More and more evidence indicates that genome instability is a crucial step in the tumorigenesis for some cases induced by ionized radiation (Yokota et al., 2010). Thus, it has been proposed in some studies (Oikawa et al., 2011) that by introducing ionized radiation experimentally, those genome instability induced by irradiation can serve as a model for research in radiation related carcinogenesis, which will provide valuable reference for risk evaluation of public health imposed by radiation and for better understanding of radiation related carcinogenesis.

Some detectable biological endpoints have been utilized for genomic studies, such as point mutation, chromosomal rearrangement, micronucleus formation, accelerating cellular differentiation, and decreasing cloning rate (Yokota et al., 2010). However, some of these biological endpoints occur in form of spontaneous mutation, for which a prolonged time period is needed for observation, and their prevalence is too low to study. Thus, difficulties may be encountered when common approaches are used for direct detection of genome instability. In our present study, in light of the hypothesis of second-hit promotion in multiple-stage of carcinogenesis, 60Co- ray induced genome instability has been investigated

with introduction of a second irradiation in human normal liver cells, which will render unique evidence experimentally to radiation related studies in the liver and its protection.

 

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