浓缩铀诱发细胞凋亡的形态及基因调控  

Study on Apoptosis of Human Leukemia Cells and Its Related Genes Regulation Induced by ^(235) U

作　　者：朱寿彭[1] 肖东[1] 吴越[1] 

机构地区：[1]苏州大学放射医学研究所,江苏苏州215007

出　　处：《工业卫生与职业病》2003年第2期68-71,共4页Industrial Health and Occupational Diseases

摘　　要：目的　研究浓缩铀诱发人白血病HL 6 0细胞凋亡的电镜形态特征 ,以及对相关基因bcl 2和bax的调控作用。方法　探讨受浓缩铀内照射不同时间 ,诱发HL 6 0细胞凋亡的电镜形态 ;运用免疫组织化学技术探讨浓缩铀对HL 6 0细胞bcl 2和bax蛋白的表达 ,运用RNA分子杂交技术探讨浓缩铀对HL 6 0细胞bcl 2mRNA的转录水平表达的影响。结果　人白血病HL 6 0细胞在浓缩铀辐照作用下 ,可呈现核断裂和核染质边聚。对照的HL 6 0细胞中bcl 2蛋白呈高度表达 ,为 (88± 7) % ,而受浓缩铀辐照下 ,可下调至(6 1± 5 ) %。bax在对照细胞中表达很低 ,在浓缩铀作用下 ,未见明显改变。经浓缩铀辐照后 ,可使HL 6 0细胞中的bcl 2mRNA表达呈明显下调。结论　浓缩铀内照射可诱发人白血病HL 6 0细胞凋亡发生 ,且其诱发HL 6 0细胞的凋亡作用与其下调凋亡相关基因bclObjective To study morphological characteristics of apoptosis of human leukemia HL 60 cells under electron microscope and regulation effects of its related genes bcl 2 and bax induced by enriched uranium. Methods Electron microscopic morphology was studied to show the apoptosis of HL 60 cells induced by internal radiation of enriched uranium for different time periods.Immuno histo chemical technique was used to identify the expression of bcl 2 and bax proteins in HL 60 cells.RNA dot blot hybridization was also used to show the expression of bcl 2 mRNA in HL 60 cells.Results Nuclear fragmentation and nuclear marginality could be seen in apoptotic HL 60 cells after irradiated by 235 U.Compared with bcl 2 high expression in the control HL 60 cells,which was as high as (88±7)%, bcl 2 protein expression could be lowered to (61±5)% after exposure to enriched 235 U.As to the expression of bax protein,no significant changes could be seen between the control and the irradiation group,however,significantly decreased bcl 2 mRNA expression was found in 235 U irradiated HL 60 cells.Conclusions 235 U could induce apoptosis of HL 60 cell,which might be associated with the lowered expression of apoptotic related gene bcl 2.

关 键 词：浓缩铀^235U HL-60细胞 凋亡 基因 

分 类 号：R811.3[医药卫生—放射医学]