...
首页> 外文期刊>Colloids and Surfaces, B. Biointerfaces >Cellular interactions of zinc oxide nanoparticles with human embryonic kidney (HEK 293) cells
【24h】

Cellular interactions of zinc oxide nanoparticles with human embryonic kidney (HEK 293) cells

机译:氧化锌纳米粒子与人胚胎肾(HEK 293)细胞的细胞相互作用

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

Zinc oxide nanoparticles (ZnO NPs) have potential biomedical, industrial and commercial applications. So they constantly come into contact with the body parts during applications. Safety concerns about ZnO NPs are increasing today and yet only few reports are available about their toxicity in kidney cells. It is very essential to analyze the toxicity on kidney because kidney.plays a decisive role in nanoparticles excretion. Therefore, the present study focuses on the interaction of ZnO NPs with human embryonic kidney 293 (HEK 293) cells in vitro. The results showed that the cellular viability was much affected by ZnO NPs in a dose and time dependent manner. Oxidative stress increased the formation of reactive oxygen species (ROS), was found to be the prime mechanism of cytotoxicity. Formation of ROS eventually induced loss of mitochondrial membrane potential, lysosomal activity and nuclear condensation, which ultimately leads to apoptosis. (C) 2017 Elsevier B.V. All rights reserved.
机译:氧化锌纳米粒子(ZnO NPS)具有潜在的生物医学,工业和商业应用。 因此,它们在应用期间不断接触身体部位。 关于ZnO NPS的安全问题今天正在增加,但只有很少的报告可以在肾细胞中进行毒性。 为肾脏分析肾脏上的毒性是至关重要的.plays在纳米粒子排泄中的作用是一种决定性的作用。 因此,本研究侧重于ZnO NP与体外人胚胎肾293(HEK 293)细胞的相互作用。 结果表明,ZnO NP以剂量和时间依赖性方式影响细胞活力很大。 氧化应激增加了活性氧(ROS)的形成,发现是细胞毒性的主要机制。 ROS的形成最终诱导线粒体膜势,溶酶体活性和核凝结的丧失,最终导致细胞凋亡。 (c)2017 Elsevier B.v.保留所有权利。

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