Cr(Ⅵ)染毒对小鼠肝脏细胞凋亡以及凋亡相关蛋白的影响  

Exposure to Cr(Ⅵ) leads to increased apoptosis and concomitant changes of apoptosis-related proteins in mice liver

作　　者：王晓峰[1] 徐立红[1] 

机构地区：[1]浙江大学医学院生物化学与遗传学系,杭州310058

出　　处：《环境科学学报》2008年第3期540-543,共4页Acta Scientiae Circumstantiae

基　　金：国家自然科学基金重点项目(No.20137010)~~

摘　　要：为研究六价铬(Cr(VI))对生物体的细胞凋亡以及凋亡相关蛋白的改变,用0、25、50和100mg.kg-1的重铬酸钾(K2Cr2O7)对小鼠进行1d或持续5d灌胃,检测肝脏细胞凋亡以及p53、Bcl-2、Bax蛋白表达水平和caspase-3酶的激活.实验结果显示,Cr(VI)染毒1d或5d后,小鼠肝细胞凋亡率随染毒剂量的增加而增加,并呈明显的剂量-反应关系;p53、Bax蛋白表达升高,Bcl-2蛋白表达下降,caspase-3酶激活增加,且p53、Bcl-2蛋白表达水平和caspase-3酶激活水平在100mg.kg-1剂量组的2个染毒时间段与对照组相比均具有显著性差异,Bax蛋白表达水平仅在100mg.kg-1染毒5d的实验组与对照组相比具有显著性差异.结果表明,Cr(VI)能诱导小鼠肝脏细胞凋亡,p53、Bcl-2、Bax和caspase-3在这个过程中可能起重要作用.To explore apoptosis and the change of apoptosis-related proteins in organisms induced by hexavalent chromium, mice were administered by oral garage with potassium dichromate at a dose of 0, 25, 50 or 100 mg·kg^-1 once daily for 5 consecutive days. One day and five days after treatment the animals were sampled and the changes of apoptosis as well as p53, Bcl-2, Bax protein expression and caspase-3 activation in the liver were measured. Results showed that dose- dependent increased apoptotic rates were observed after 1 day or 5 days of Cr（Ⅵ） exposure. Expression of p53 and Bax protein and activation of caspase-3 increased, and expression of Bcl-2 protein decreased after 1 day or 5 days of exposure. Furthermore, significant differences were observed on the p53, Bcl-2 expression level and caspase-3 activation level at 100 mg·kg^-1 at both timepoints as compared to the control animals. A significant increase in Bax protein expression level was observed only at 100 mg·kg^-1 after 5 days of exposure. Results indicated that Cr（Ⅵ） could induce apoptosis in mice liver, and p53, Bcl-2, Bax, caspase-3 may play an important role in this process.

关 键 词：Cr(Ⅵ) 细胞凋亡 p53 Bcl-2 BAX CASPASE-3 

分 类 号：X171.5[环境科学与工程—环境科学]