氧化砷促进食管癌细胞增殖  被引量:1

ARSENIC TRIOXIDE ENHANCES PROLIFERATION OF ESOPHAGEAL CARCINOMA CELLS

在线阅读下载全文

作  者:沈健[1] 吴敏华[1] 陈铭华[1] 郑瑞明[1] 沈忠英[1] 

机构地区:[1]汕头大学医学院肿瘤病理研究室,广东汕头515031

出  处:《癌变.畸变.突变》2002年第3期159-163,共5页Carcinogenesis,Teratogenesis & Mutagenesis

基  金:广东省中医药局资助科研课题 (10 0 0 83 )

摘  要:目的 :三氧化二砷 (As2 O3 )已被证实对治疗某些白血病有效 ,引起白血细胞和某些实体瘤细胞凋亡。本文着重观察小剂量As2 O3 (0 .1μmol/L和 0 .5 μmol/L)对食管癌细胞SHEEC1的作用。方法 :食管癌细胞于瓶中培养 ,以 0 .1μmol/L ,0 .5 μmol/L和 5 .0 μmol/LAs2 O3 处理。结果 :大剂量 (5 .0 μmol/L)As2 O3 引起SHEEC1凋亡和生长的抑制。小剂量As2 O3 (0 .5 μmol/L)提高核分裂指数 ,DNA荧光定量检测可见DNA合成增加 ,电镜下可见SHEEC1细胞处于增殖状态 ,出现细胞质线粒体和多聚核糖体增多 ,细胞核中可见多个核仁。结论 :低剂量As2 O3 可促进食管癌细胞增殖和DNA合成 ,因此As2 O3 具有促细胞分裂作用的特性。Purpose: Arsenic trioxide(As\-2O\-3) has proved to be effective in the treatment of some leukemias and caused apoptosis in leukinua cells and some solid tumor cells. This study focused on the effects of low dosage of As\-2O\-3 on the esophageal carcinoma cells(SHEEC1). Methods: Esophageal carcinoma cells were cultured in flasks and treated with As\-2O\-3 in concentration of 0.1 μmol/L, 0.5 μmol/L and 5.0 μmol/L, respectively. Results: The high dose(5 μmol/L) of As\-2O\-3 induced apoptosis and inhibited proliferation of SHEEC1 cells, and the low doses(0.1μmol/L or 0.5 μmol/L) of As\-2O\-3 enhanced the mitotic index and DNA synthesis(in 0.5 μmol/L), which was determined by quantitative fluorescent cytometry. In transmitted electron microscope(EM), it was showed that SHEEC1 cells treated with As\-2O\-3 in low doses displayed proliferative status with increasing mitochondria and poly ribosomes in cytoplasm and multiple nucleoli in nucleus. Conclusion: The results suggest that As\-2O\-3 in low dosage promotes the proliferation of esophageal carcinoma cells and increament of DNA synthesis. As a conclusion, As\-2O\-3 has the characteristics of mitogenic effects.

关 键 词:砷剂 食管癌 细胞增殖 DNA合成 

分 类 号:R735.1[医药卫生—肿瘤]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象