镉致脾淋巴细胞功能抑制与细胞凋亡的关系

目的 采用体外作用的方式观察氯化镉引起的脾淋巴细胞功能抑制与镉诱导的细胞凋亡之间的关系。方法 在实验中选择了3．10、6．25、12．50、25．00、50．00μmol／L共5个浓度的氯化镉,在体外与小鼠淋巴细胞共育不同时间后,采用MTT颜色反应法观察淋巴细胞转化,用DNA凝胶电泳法及流式细胞仪法检测细胞凋亡。结果 25．00和50．00μmol／L氯化镉对小鼠脾淋巴细胞的转化功能产生明显抑制作用,并有剂量．反应关系,这两个浓度的氯化镉对淋巴细胞转化功能的抑制率：刀豆蛋白A刺激组分别为50％和78％,脂多糖刺激组分别为39％和55％;同时12．50-50．00μmol／L氯化镉可诱导脾淋巴细胞发生凋亡,流式细胞仪检测结果为30％-60％。在较高浓度下氯化镉还可以引起细胞存活率下降,并且氯化镉诱导细胞凋亡的作用与其抑制脾淋巴细胞功能的作用相比,作用时间短、作用浓度低。结论 氯化镉在体外可能以诱导细胞发生凋亡作为其抑制脾淋巴细胞功能的一种机制。

The relationship between cadmium-induced inhibition of splenic lymphocyte function and cell apoptosis

OBJECTIVE: To explore the relationship between cadmium-induced inhibition of splenic lymphocyte function and cell apoptosis in vitro. METHODS: The splenic lymphocytes of mice were exposed to 3.10, 6.25, 12.50, 25.00, 50.00 micromol/L of cadmiun chloride (CdCl(2)) for various time period, to measure the lymphocyte transformation by MTT colorimetric assay and to detect the apoptosis in splenocytes by DNA agarose electrophoresis and flow cytometry (FACS). RESULTS: CdCl(2) could significantly inhibit the function of lymphocyte transformation in a dose-response pattern at concentrations of 25.00 and 50.00 micromol/L, with inhibition rates of 50% and 78% in ConA-stimulating group and 39% and 55% in LPS-stimulating group, respectively. CdCl(2) could also induce apoptosis of splenic cells at concentrations of 12.50 to 50.00 micromol/L. RESULTS: of FACS analysis showed 30% - 60% of cell apoptosis. Higher concentration of CdCl(2) could also cause reduction of cell survival. Effect of Cd-induced apoptosis was earlier and at a lower concentration of CdCl(2) than that of Cd-induced inhibition of lymphocyte transformation. CONCLUSION: CdCl(2) could induce cell apoptosis in vitro, which was one of the mechanisms of its suppression of lymphocyte function.