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首页> 外文期刊>Cell biology international. >2,4-Dinitrophenol induces apoptosis in As4.1 juxtaglomerular cells through rapid depletion of GSH.
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2,4-Dinitrophenol induces apoptosis in As4.1 juxtaglomerular cells through rapid depletion of GSH.

机译：2,4-二硝基苯酚通过快速消耗GSH诱导As4.1肾小球细胞凋亡。

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摘要

2,4-Dinitrophenol (DNP) is an uncoupler of oxidative phosphorylation in mitochondria. Here, we investigated the in vitro effect of DNP on apoptosis and the involvement of reactive oxygen species (ROS) in As4.1 juxtaglomerular cell death. Dose- and time-dependent induction of apoptosis was evidenced by flow cytometric detection of sub-G1 DNA content and annexin V binding assay. The intracellular H(2)O(2) and O(2)(-) levels were markedly increased in DNP-treated cells. However, the reduction of intracellular H(2)O(2) level by Tiron and catalase did not prevent apoptosis induced by DNP. Moreover, DNP rapidly reduced intracellular GSH content in As4.1 cells. Taken together, apoptosis in DNP-treated As4.1 cells is correlated with the rapid change of intracellular GSH levels rather than ROS levels.
机译：2,4-二硝基苯酚（DNP）是线粒体中氧化磷酸化的解偶联剂。在这里，我们调查了DNP对As4.1肾小球细胞死亡的凋亡和活性氧（ROS）的体外影响。流式细胞术检测亚G1 DNA含量和膜联蛋白V结合试验证明了剂量依赖性和时间依赖性诱导凋亡。在DNP处理的细胞内细胞内H（2）O（2）和O（2）（-）水平显着增加。但是，通过Tiron和过氧化氢酶降低细胞内H（2）O（2）的水平并不能防止DNP诱导的细胞凋亡。此外，DNP迅速降低了As4.1细胞中的细胞内GSH含量。两者合计，经DNP处理的As4.1细胞的凋亡与细胞内GSH水平而非ROS水平的快速变化相关。

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