Shim Grace, Ricoul Michelle, Hempel William M, Azzam Edouard I, Sabatier Laure
Mutat Res Rev Mutat Res. 2014 Jan 31. doi: 10.1016/j.mrrev.2014.01.001.
It is well established that ionizing radiation induces chromosomal damage, both following direct radiation exposure and via non-targeted (bystander) effects, activating DNA damage repair pathways, of which the proteins are closely linked to telomeric proteins and telomere maintenance. Long-term propagation of this radiation-induced chromosomal damage during cell proliferation results in chromosomal instability. Many studies have shown the link between radiation exposure and radiation-induced changes in oxidative stress and DNA damage repair in both targeted and non-targeted cells. However, the effect of these factors on telomeres, long established as guardians of the genome, still remains to be clarified. In this review, we will focus on what is known about how telomeres are affected by exposure to low- and high-LET ionizing radiation and during proliferation, and will discuss how telomeres may be a key player in the process of radiation-induced carcinogenesis.
众所周知，电离辐射会导致染色体损伤，无论是直接辐射暴露后还是通过非靶向（旁观者）效应，都会激活DNA损伤修复途径，其中的蛋白质与端粒蛋白和端粒维持密切相关。这种辐射诱导的染色体损伤在细胞增殖过程中的长期传播会导致染色体不稳定。许多研究表明，辐射暴露与靶向和非靶向细胞中氧化应激和DNA损伤修复的辐射诱导变化之间存在联系。然而，这些因素对长期以来被视为基因组守护者的端粒的影响仍有待阐明。在这篇综述中，我们将重点关注关于端粒如何受到低LET和高LET电离辐射暴露以及增殖过程影响的已知信息，并将讨论端粒如何可能在辐射诱导致癌过程中发挥关键作用。
