Glucose deprivation induces mitochondrial dysfunction and oxidative stress in PC12 cell line
Glucose deprivation induces mitochondrial dysfunction and oxidative stress in PC12 cell line
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DOI：
10.1111/j.1582-4934.2003.tb00202.x
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发表时间：
2003-01-01
影响因子：
5.3
通讯作者：
Zuo, J
中科院分区：
文献类型：
--
作者：
Liu, Y;Song, DX;Zuo, J
葡萄糖代谢在许多生理和病理条件下发挥着关键作用。为了研究低血糖（通过葡萄糖剥夺获得）对 PC 12 细胞系的影响，我们分析了葡萄糖剥夺 (GD) 后的细胞活力、线粒体功能（通过 MTT 还原、细胞 ATP 水平、线粒体跨膜电位评估）和活性氧 (ROS) 水平。暴露于GD后，ROS水平立即升高，MTT减少立即降低，细胞内ATP水平在前3小时内升高，随后进行性降低直至GD处理结束，线粒体跨膜电位（DeltaPsi（m））在6小时后下降。 24小时后明显发生坏死和凋亡，这是通过碘化丙啶(PI)和Hoechst 33342的细胞核染色确定的。这些数据表明GD的细胞毒性主要是由于PC12细胞中ROS的积累和ATP的消耗。
Glucose metabolism plays a pivotal role in many physiological and pathological conditions. To investigate the effect of hypoglycemia (obtained by glucose deprivation) on PC 12 cell line, we analyzed the cell viability, mitochondrial function (assessed by MTT reduction, cellular ATP level, mitochondrial transmembrane potential), and the level of reactive oxygen species (ROS) after glucose deprivation (GD). Upon exposure to GD, ROS level increased and MTT reduction decreased immediately, intracellular ATP level increased in the first 3 hours, followed by progressive decrease till the end of GD treatment, and the mitochondrial transmembrane potential (DeltaPsi(m)) dropped after 6 hours. Both necrosis and apoptosis occurred apparently after 24 hours which was determined by nuclei staining with propidium iodide(PI) and Hoechst 33342. These data suggested that cytotoxity of GD is mainly due to ROS accumulation and ATP depletion in PC12 cells.