摘要
辐射的剂量率能显著影响放射治疗的生物效应,降低剂量率就降低了生物效应。然而,当剂量率降低到一定阈值以下,DNA损伤不能激活细胞的探测器——共济失调毛细血管扩张症突变(ATM)基因以及ATM基因介导的损伤修复途径,因而出现细胞高的致死性,即“反剂量率效应”。在持续低剂量率照射下,主要有两条修复途径参与双链断裂(DSB)的修复,即非同源末端连接(NHEJ)修复和同源重组(HR)修复。这些修复系统在亚致死性损伤和产生剂量率效应中起重要作用,如果损伤得以完整和精确的修复,细胞的辐射敏感性就会发生改变;如果损伤不能被修复,则会诱导细胞凋亡。p53基因在低剂量率辐射引起的细胞周期阻滞和诱导细胞凋亡过程中起关键作用。
The dose rate with which radiation is delivered significantly affects the biological response to radiation and reducing the dose rate decreases the biological effect. However, DNA damage introduced at a reduced rate does not activate the DNA damage sensor ATM and that failure to activate ATM-associated repair pathways contributes to the increased lethality of continuous radiation exposures, which has been termed the “inverse dose rate effect”. Under continuous low dose rate irradiation, there are two major pathways by which DSB＇s can be repaired, nonhomologous end joining （NHEJ）, and homologous recombination（HR）, which play an important role in sublethal damage repair and the generation of dose-rate effect. A change in sensitivity is modified if DNA damage can be repaired with high fidelity. The cells will lead to apoptosis if the cell DNA damage is not sufficiently repaired. The p53 gene is a key factor in the radiation-induced the cell cycle arrest and the activation of apoptosis after exposure to low dose-rate irradiation.
出处
《国外医学（放射医学核医学分册）》
2005年第4期186-189,共4页
Foreign Medical Sciences(Section of Radiation Medicine and Nuclear Medicine)
