Characterization of the cellular response during apoptosis induction in cadmium-treated Hep G2 human hepatoma cells
Characterization of the cellular response during apoptosis induction in cadmium-treated Hep G2 human hepatoma cells
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DOI：
10.1385/bter:95:2:139
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发表时间：
2003-11-01
影响因子：
3.9
通讯作者：
Batur, Y
中科院分区：
文献类型：
--
作者：
Aydin, HH;Celik, HA;Batur, Y
镉是一种有毒的过渡金属，对基因表达和细胞信号转导途径的调节具有广泛的不利影响，持续的职业和环境问题。镉对细胞的损伤会导致一系列复杂的事件，最终导致细胞死亡。已有研究表明镉可诱导多种细胞凋亡。然而，形态学特征导致细胞凋亡或随后的再生暴露于镉还没有澄清。我们评估是否人肝癌细胞在培养中保持暴露于镉时发生凋亡。用3-[4，5-二甲基噻唑-2-基]-2，5-二苯基四氮唑溴化物测定镉对Hep G2细胞的细胞毒性活性。通过电泳进行DNA梯状条带测定。通过流式细胞术定量细胞周期分析。用碘化丙啶和Hoechst 33342染色后，通过荧光显微镜研究核形态。用透射电镜观察CdCl_2处理培养肝细胞的形态学变化，结果表明，CdCl_2对HepG_2细胞的损伤主要是通过细胞凋亡来消除的，细胞凋亡先于细胞坏死。
Cadmium is a toxic transition heavy metal of continuing occupational and environmental concern, with a wide variety of adverse effects on regulation of gene expression and cellular signal transduction pathways. Injury to cells by cadmium leads to a complex series of events that can culminate in the death of the cell. It has been reported that cadmium induces apoptosis in many cell lines. However, the morphological characteristics leading to apoptosis or subsequent regeneration in cells exposed to cadmium have not been clarified.We evaluated whether human hepatoma cells maintained in culture undergo apoptosis when exposed to cadmium. Cytotoxic activity of cadmium on Hep G2 cells determined using 3-[4,5-dimethylthiazol-2-yl]-2,5diphenyltetrazolium bromide assay. A DNA ladder assay was performed by electrophoresis. Cell cycle analysis was quantified by flow cytometry. Nuclear morphology was studied by fluorescence microscopy after staining with propidium iodide and Hoechst 33342. Morphologic alterations in culture hepatocytes treated with CdCl2 were observed by transmission electron microscopy.We have demonstrated that apoptosis is a major mode of elimination of damaged HepG2 cells in cadmium toxicity and it precedes necrosis.