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Characterization of the cell death induced by cadmium in HaCaT and C6 cell lines

机译:HaCaT和C6细胞系中镉诱导的细胞死亡的表征

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Cell death resulting from cadmium (Cd) intoxication has been confirmed to induce both necrosis and apoptosis. The ratio between both types of cell death is dose- and cell-type-dependent. This study used the human keratinocytes HaCaT expressing a mutated p53 and the rat glial cells C6 expressing a wild p53 as models to characterize Cd-induced apoptosis, using sub-lethal and lethal doses. At these concentrations, features of apoptosis were observed 24 h after C6 cell treatment: apoptotic DNA fragmentation and caspase-9 activation, whereas Cd did not induce caspase-3. In HaCaT, Cd did not induce apoptotic DNA fragmentation or caspase-9 and -3 activation. The results also showed that the inhibition of p53 led to a resistance of the C6 cells to 20 mu M Cd, decreased the apoptosis and increased the metallothioneins in these cells. p53 restoration increased the sensitivity of HaCaT cells to Cd but did not affect the MT expression. The results suggest that Cd induced apoptosis in C6 cells but a non-apoptotic cellular death in HaCaT cells.
机译:镉(Cd)中毒导致的细胞死亡已被证实可诱导坏死和凋亡。两种类型的细胞死亡之间的比率是剂量依赖性和细胞类型依赖性的。这项研究使用亚致死剂量和致死剂量,将表达突变的p53的人类角质形成细胞HaCaT和表达野生的p53的大鼠神经胶质细胞C6作为表征Cd诱导凋亡的模型。在这些浓度下,在C6细胞处理24小时后观察到凋亡特征:凋亡DNA片段化和caspase-9激活,而Cd不诱导caspase-3。在HaCaT中,Cd不会诱导凋亡性DNA片段化或caspase-9和-3激活。结果还表明,p53的抑制导致C6细胞对20μMCd的抗性,减少了这些细胞中的细胞凋亡并增加了金属硫蛋白。 p53还原增加了HaCaT细胞对Cd的敏感性,但不影响MT表达。结果表明,Cd诱导了C6细胞凋亡,但HaCaT细胞非凋亡性细胞死亡。

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