傅强,张澜生,朱寿彭.放线菌酮和放线菌素D对放射性核素235U诱发细胞凋亡的影响[J].中华放射医学与防护杂志,1999,19(5):325-327
放线菌酮和放线菌素D对放射性核素235U诱发细胞凋亡的影响
Effect of cycloheximide and actinomycin D on radionuclide 235 U induced apoptosis
投稿时间:1998-06-03  修订日期:1998-11-08
DOI:
中文关键词:  放线菌酮  放线菌素D  放射性核素235U  细胞凋亡
英文关键词:Cycloheximide  Actinomycin D  Radionuclide 235 U  Apoptosis
基金项目:
作者单位
傅强 200433 上海, 复旦大学遗传所 
张澜生 苏州医学院 
朱寿彭 苏州医学院 
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中文摘要:
      目的 对放射性核素235U内照射诱发细胞凋亡的机理进行探讨。方法 通过MTT和JAM实验,检测凋亡细胞存活率及DNA链断裂量。结果 蛋白质合成抑制剂放线菌酮(CHX)及RNA合成抑制剂放线菌素D(ActD)不能抑制235U诱导的细胞凋亡,但CHX具有部分抑制凋亡细胞DNA链断裂的作用。结论 放射性核素235U内照射诱导细胞凋亡途径与外照射不同,不需要蛋白质的合成,但需合成性核酸内切酶参与。
英文摘要:
      Objective The mechanism of apoptosis induced by radionuclide 235 U was studied.Methods MTT and JAM assay were used to analyse the cell viability and quantification of fragmented DNA. Results The inhibitor of protein cycloheximide (CHX), and the inhibitor of RNA synthesis, actinomycin D, cannot inhibit the apoptosis induced by 235 U, but CHX can partly inhibit apoptotic cells DNA fragmentation. Conclusion The pathway of apoptosis induced by radionuclide 235 U is different from X-and γ-ray external irradiation, protein synthesis is not essential for it,but synthetic endonuclease is necessary for DNA fragmentation of apoptotic cells.
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