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作 者:邹仲敏[1] 陈兆珍[2] 罗成基[1] 李才安[2] 郭朝华[1] 王延江[1] 施炎[1]
机构地区:[1]第三军医大学防原医学教研室,重庆400038 [2]第三军医大学中心实验室,重庆400038
出 处:《细胞生物学杂志》1998年第1期34-38,共5页Chinese Journal of Cell Biology
摘 要:以4—10Gy射线在体损伤的小鼠为模型,应用DNA电泳和流式细胞术等方法证实细胞凋亡是射线损伤在体骨髓造血细胞的途径之一,发现射线诱导的造血细胞凋亡有明显的量效和时效关系。4、6、8和10Gy照射后,细胞凋亡发生率均表现为升高-降低过程,各剂量诱导的凋亡发生率峰值分别出现在照后12、8、4和4h,6和8Gy诱导的凋亡发生率已达最高水平,约为30%,10Gy诱导的凋亡反而要低。上述结果表明,诱导细胞凋亡是射线损伤骨髓造血细胞的一个重要途径,而且凋亡的发生率受照射剂量和照后时间的影响。因此,深入研究射线诱导的细胞凋亡,将有助于揭示射线损伤造血功能的机理。By means of flow cytometry and DNA electrophoresis, in this experiment we investigate that in what extent apoptosis was taken by the radiation injured-bone marrow hematopoietic cells(BMHCs)of 4-10Gy 7-ray irradiated-mice. The significant time-and dose-effect relationships of radiation-induced apoptosis of BMHCs was found. The peakvalues of apoptosis induced by 6Gy and 8Gy radiation were about 30%, and by 4Gy and 10Gy radiation 20%. The time needed to reach the peak was shortened correspondingly when dose inereased, shown as 12,8.4 and 4h for 4,6,8 and 10Gy irradiation respectively. The results demonstrate that apoptosis is an important cell death pathway taken by the radiation-injured BMHCs in vivo, so further investigation on the regulation of apoptosis would highlight the mechanism of radiation-induced hematopoiesis dysfunction.
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