Department of Radiation Medicine, Georgetown University Medical Center, USA.
J Radiat Res. 2011;52(3):309-19. doi: 10.1269/jrr.10147.
Cells exposed to densely ionizing radiation (high-LET) experience more severe biological damage than do cells exposed to sparsely ionizing radiation (low-LET). The prevailing hypothesis is that high-LET radiations induce DNA double strand-breaks (DSB) that are more complex and clustered, and are thereby more challenging to repair. Here, we present experimental data obtained by atomic force microscopy imaging, DNA-dependent protein kinase (DNA-PK) activity determination, DNA ligation assays, and genomic studies to suggest that short DNA fragments are important products of radiation-induced DNA lesions, and that the lengths of DNA fragments may be significant in the cellular responses to ionizing radiation. We propose the presence of a subset of short DNA fragments that may affect cell survival and genetic stability following exposure to ionizing radiation, and that the enhanced biological effects of high-LET radiation may be explained, in part, by the production of increased quantities of short DNA fragments.
细胞暴露于高传能线密度（high-LET）辐射下会经历比低传能线密度（low-LET）辐射更严重的生物损伤。主流假说是高 LET 射线诱导的 DNA 双链断裂（DSB）更复杂且更聚集，因此更难修复。在这里，我们通过原子力显微镜成像、DNA 依赖性蛋白激酶（DNA-PK）活性测定、DNA 连接测定和基因组研究提供了实验数据，表明短 DNA 片段是辐射诱导的 DNA 损伤的重要产物，并且 DNA 片段的长度在细胞对电离辐射的反应中可能具有重要意义。我们提出存在一小部分短 DNA 片段，这些片段可能会影响细胞在暴露于电离辐射后的存活和遗传稳定性，并且高 LET 辐射的增强的生物学效应部分可以通过产生更多数量的短 DNA 片段来解释。
