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Reactive oxygen species (ROS) is not a promotor of taxol-induced cytoplasmic vacuolization

机译:活性氧(ROS)不是紫杉醇诱导的胞质空泡化的促进剂

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We have previously reported that taxol, a potent anticancer agent, induces caspase-independent cell death and cytoplasmic vacuolization in human lung adenocarcinoma (ASTC-a-1) cells. However, the mechanisms of taxol-induced cytoplasmic vacuolization are poorly understood. Reactive oxygen species (ROS) has been reported to be involved in the taxol-induced cell death. Here, we employed confocal fluorescence microscopy imaging to explore the role of ROS in taxol-induced cytoplasmic vacuolization. We found that ROS inhibition by addition of N-acetycysteine (NAC), a total ROS scavenger, did not suppress these vacuolization but instead increased vacuolization. Take together, our results showed that ROS is not a promotor of the taxol-induced cytoplasmic vacuolization.
机译:我们以前曾报道过,紫杉醇是一种有效的抗癌剂,可在人肺腺癌(ASTC-a-1)细胞中诱导caspase依赖性细胞死亡和胞浆空泡形成。但是,对紫杉醇诱导的细胞质空泡化的机制了解甚少。据报道活性氧(ROS)参与紫杉醇诱导的细胞死亡。在这里,我们采用共聚焦荧光显微镜成像来探索ROS在紫杉醇诱导的细胞质空泡中的作用。我们发现通过添加N-乙酰半胱氨酸(NAC)(一种总的ROS清除剂)来抑制ROS并不能抑制这些空泡,而可以增加空泡。两者合计,我们的结果表明,ROS并不是紫杉醇诱导的细胞质空泡的促进剂。

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