...
首页> 外文期刊>Biological Trace Element Research >Role of Oxidative Stress, Apoptosis, and Intracellular Homeostasis in Primary Cultures of Rat Proximal Tubular Cells Exposed to Cadmium
【24h】

Role of Oxidative Stress, Apoptosis, and Intracellular Homeostasis in Primary Cultures of Rat Proximal Tubular Cells Exposed to Cadmium

机译:氧化应激,细胞凋亡和细胞内稳态在镉暴露大鼠近端肾小管细胞原代培养中的作用

获取原文
获取原文并翻译 | 示例
           

摘要

Cadmium (Cd) is a known nephrotoxic element. In this study, the primary cultures of rat proximal tubular (rPT) cells were treated with low doses of cadmium acetate (2.5 and 5 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, were seen in the experiment. Simultaneously, elevation of intracellular [Ca2+]i and reactive oxygen species (ROS) levels, significant depletion of mitochondrial membrane potential(Δ Ψ) and cellular glutathione (GSH), intracellular acidification, and inhibition of Na+, K+-ATPase and Ca2+-ATPase activities were revealed in a dose-dependent manner during the exposure, while the cellular death and the apoptosis could be markedly reversed by N-acetyl-l-cysteine (NAC). Also, the calcium overload and GSH depletion were significantly affected by NAC. In conclusion, exposure of rPT cells to low-dose cadmium led to cellular death, mediated by an apoptotic and a necrotic mechanism. The apoptotic death might be the chief mechanism, which may be mediated by oxidative stress. Also, a disorder of intracellular homeostasis induced by oxidative stress and mitochondrial dysfunction is a trigger of apoptosis in rPT cells.
机译:镉(Cd)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低剂量的乙酸镉(2.5和5μM)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步丧失,以及凋亡和坏死细胞数量的显着增加。同时,细胞内[Ca2 + ] i和活性氧(ROS)水平升高,线粒体膜电位(ΔΨ)和细胞谷胱甘肽(GSH)显着耗竭,细胞内酸化和Na +抑制,在暴露期间K + -ATPase和Ca2 + -ATPase活性呈剂量依赖性,而N-乙酰基-1-半胱氨酸(NAC)可以明显逆转细胞死亡和凋亡。 )。而且,NAC显着影响钙超载和GSH消耗。总之,rPT细胞暴露于低剂量镉会导致细胞死亡,这是由凋亡和坏死机制介导的。细胞凋亡的死亡可能是主要的机制,可能是由氧化应激介导的。同样,由氧化应激和线粒体功能障碍引起的细胞内稳态紊乱是rPT细胞凋亡的触发因素。

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