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Detection of drug-induced apoptosis and necrosis in human cervical carcinoma cells using (1)H NMR spectroscopy.

机译:使用(1)H NMR光谱检测人宫颈癌细胞中药物诱导的凋亡和坏死。

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Apoptosis and necrosis need to be differentiated in order to distinguish drug-induced cell death from spontaneous cell death due to hypoxia. The ability to differentiate between these two modes of cell death, especially at an early stage in the process, could have a significant impact on accessing the outcome of anticancer drug therapy in the clinic. Nuclear magnetic resonance spectroscopy was used to distinguish apoptosis from necrosis in human cervical carcinoma (HeLa) cells. Apoptosis was induced by treatment with the topoisomerase II inhibitor etoposide, whereas necrosis was induced by the use of ethacrynic acid or cytochalasin B. We found that the intensity of the methylene resonance increases significantly as early as 6 h after the onset of apoptosis, but that no such changes occur during necrosis. The spectral intensity ratio of the methylene to methyl resonances also shows a high correlation with the percentage of apoptotic cells in the sample (r(2)=0.965, P<0.003).
机译:为了区分药物引起的细胞死亡与由于缺氧引起的自发性细胞死亡,需要区分凋亡和坏死。区分这两种细胞死亡模式的能力,尤其是在该过程的早期阶段,可能会对在临床上获得抗癌药物治疗的结果产生重大影响。核磁共振波谱用于区分人类宫颈癌(HeLa)细胞的凋亡和坏死。拓扑异构酶II抑制剂依托泊苷治疗可诱导细胞凋亡,而乙炔酸或细胞松弛素B则可诱导坏死。我们发现亚甲基共振的强度早在细胞凋亡开始后6小时就显着增加,但是坏死期间不会发生此类变化。亚甲基与甲基共振的光谱强度比也显示出与样品中凋亡细胞的百分比高度相关(r(2)= 0.965,P <0.003)。

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