Pretreatment of low dose radiation reduces radiation-induced apoptosis in mouse lymphoma (EL4) cells
Pretreatment of low dose radiation reduces radiation-induced apoptosis in mouse lymphoma (EL4) cells
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DOI：
10.1007/bf02976147
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发表时间：
1997-06-01
影响因子：
6.7
通讯作者：
Yoo, SY
中科院分区：
文献类型：
--
作者：
Kim, JH;Hyun, SJ;Yoo, SY
以细胞存活率和凋亡核小体DNA片段化为生物学终点，研究了电离辐射诱导小鼠淋巴瘤（EL 4）细胞的适应性反应。在高剂量γ射线（4、8和12戈伊用于细胞存活分数分析; 8戈伊用于DNA片段化分析）照射之前4或20小时，将早期对数期的细胞预暴露于低剂量γ射线（0.01戈伊）。然后测量细胞存活分数和DNA片段化程度。低、高剂量γ射线照射间隔4小时，可诱导细胞产生明显的适应性反应，细胞存活率增加，DNA断裂程度降低，在适应期、低剂量γ射线照射到高剂量γ射线照射之间、能够抑制适应性反应的诱导，适应性反应是辐射EL 4细胞中DNA片段化程度的降低。这些数据表明，诱导适应性反应的电离辐射在EL 4细胞需要蛋白质和RNA的合成。
Induction of an adaptive response to ionizing radiation in mouse lymphoma (EL4) cells was studied by using cell survival fraction and apoptotic nucleosomal DNA fragmentation as biological end points. Cells in early log phase were pre-exposed to low dose of gamma-rays (0.01 Gy) 4 or 20 hrs prior to high dose gamma-ray (4, 8 and 12 Gy for cell survival fraction analysis; 8 Gy for DNA fragmentation analysis) irradiation. Then cell survival fractions and the extent of DNA fragmentation were measured. Significant adaptive response, increase in cell survival fraction and decrease in the extent of DNA fragmentation were induced when low and high dose gamma-ray irradiation time interval was 4 hr. Addition of protein or RNA synthesis inhibitor, cycloheximide or 5,6-dichloro-1-beta-d-ribofuranosylbenzimidazole (DRFB), respectively during adaptation period, the period from low dose gamma-ray irradiation to high dose gamma-ray irradiation, was able to inhibit the induction of adaptive response, which is the reduction of the extent DNA fragmentation in irradiated EL4 cells. These data suggest that the induction of adaptive response to ionizing radiation in EL4 cells required both protein and RNA synthesis.