首页> 外文期刊>Archives of Toxicology >Oxidative stress and apoptotic changes in primary cultures of rat proximal tubular cells exposed to lead
【24h】

Oxidative stress and apoptotic changes in primary cultures of rat proximal tubular cells exposed to lead

机译:暴露于铅的大鼠近端肾小管细胞原代培养物中的氧化应激和凋亡变化

获取原文
获取原文并翻译 | 示例
           

摘要

Lead is a known nephrotoxic element. In this study, primary cultures of rat proximal tubular (rPT) cells were treated with different concentrations of lead acetate (0.25, 0.5 and 1 μM) to investigate its cytotoxic mechanism. A progressive loss in cell viability together with a significant increase in the number of apoptotic and necrotic cells and lactate dehydrogenase release were seen in the experiment. Simultaneously, elevation of reactive oxygen species levels and intracellular [Ca2+]i, depletion of mitochondrial membrane potential and intracellular glutathione were revealed during the lead exposure. In addition, apoptotic morphological changes induced by lead exposure in rPT cells were demonstrated by Hoechst 33258 staining. The apoptosis was markedly prevented by N-acetyl-l-cysteine, while the necrosis was not affected. Moreover, catalase and superoxide dismutase activities in the living cells rose significantly. In conclusion, exposure of rPT cells to low-concentration lead led to cell death, mediated by an apoptotic and a necrotic mechanism. The apoptotic death induced by oxidative stress was the chief mechanism. Meanwhile, a group of cells survived lead action, mediated by their ability to activate antioxidant defense systems.
机译:铅是已知的肾毒性元素。在这项研究中,大鼠近端肾小管(rPT)细胞的原代培养物用不同浓度的乙酸铅(0.25、0.5和1μM)处理,以研究其细胞毒性机制。在实验中观察到细胞活力的逐渐丧失以及凋亡和坏死细胞数量的显着增加以及乳酸脱氢酶的释放。同时,在暴露于铅的过程中发现了活性氧水平的升高和细胞内[Ca 2 + ] i,线粒体膜电位的消耗和细胞内谷胱甘肽的升高。此外,通过Hoechst 33258染色证明了rPT细胞中铅暴露诱导的凋亡形态学变化。 N-乙酰基-1-半胱氨酸可明显阻止细胞凋亡,而坏死不受影响。此外,活细胞中的过氧化氢酶和超氧化物歧化酶活性显着上升。总之,rPT细胞暴露于低浓度会导致细胞死亡,这是由凋亡和坏死机制介导的。氧化应激诱导的细胞凋亡死亡是其主要机制。同时,一组细胞通过激活抗氧化防御系统的能力而幸免于铅的作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号