DNA断裂损伤在抗癌药物诱导肝癌细胞凋亡反应中的作用  

Role of DNA breaks in hepatoma cells apoptotic response induced by anti cancer drugs

作　　者：马运国[1] 王文亮[1] 

机构地区：[1]第四军医大学病理学教研室

出　　处：《第四军医大学学报》1997年第3期207-210,共4页Journal of the Fourth Military Medical University

基　　金：国家自然科学基金

摘　　要：目的：探讨抗癌药物等对ＤＮＡ直接损伤因素所致的ＤＮＡ断裂损伤在凋亡反应中所起的作用．方法：采用定量原位缺口平移技术检测阿霉素等抗癌药物诱导的肝癌细胞凋亡反应中的单位细胞ＤＮＡ断裂损伤程度．结果：高浓度（大于２０μｍｏｌ／Ｌ）阿霉素在凋亡反应的早期无可检测的ＤＮＡ断裂，也无凋亡细胞产生；较低浓度（２μｍｏｌ／Ｌ）阿霉素在药物作用早期有可检测的ＤＮＡ断裂，同时也有凋亡细胞产生；而５－氟尿嘧啶在检测浓度范围内（０．２～１００ｍｍｏｌ／Ｌ）均有ＤＮＡ断裂损伤，但无凋亡细胞产生．结论：ＤＮＡ断裂损伤可能并非诱导凋亡反应所必须．Objective: To investigate the role of DNA breaks in hepatoma cells apoptotic response induced by anticancer drugs. Methods: Quantitative in situ nick translation assays. Results: DNA breaks and the induction of apoptosis were not induced by adriamycin with higher concentrations (>20 μmol/L) but by adriamycin with lower concentrations (2 μmol/L) at the third hours. In contrast, 5 fluorouracil showed higher levels of DNA breaks but no apoptosis at the third hours. Conclusions: Our data suggest that DNA breaks induced directly by anticancer drugs may be not a neccesary step in apoptotic response.

关 键 词：肝肿瘤 抗癌药物 DNA断裂 细胞凋亡 

分 类 号：R735.705[医药卫生—肿瘤]