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Mitochondrion-targeted selenium nanoparticles enhance reactive oxygen species-mediated cell death.
Nanoscale ( IF 6.7 ) Pub Date : 2020-01-08 , DOI: 10.1039/c9nr09039h
Yuan Zhuang 1 , Longjie Li , Liandong Feng , Shuangshuang Wang , Huimin Su , Haijuan Liu , Hongmei Liu , Yuzhou Wu
Affiliation  

Selenium nanoparticles (SeNPs) can induce reactive oxygen species (ROS)-mediated cell death when accumulated in cancer cells, while rendering anti-oxidation and cancer prevention in healthy tissues at low doses. Although they are promising anticancer agents with fewer side effects, their application is limited by their relative low toxicity to cancer cells. Therefore, we propose a mitochondrion-targeting strategy to improve their cancer cell killing efficiency. Such mitochondrion-targeted SeNPs could efficiently increase ROS production and mitochondrion damage in cancer cells; however, only a slightly increased toxicity to normal cells was observed, indicating a potentially better therapeutic window for anticancer treatments.

中文翻译:

线粒体靶向的硒纳米颗粒增强了活性氧介导的细胞死亡。

硒纳米颗粒(SeNPs)积聚在癌细胞中时,可诱导活性氧(ROS)介导的细胞死亡,同时在低剂量下可在健康组织中提供抗氧化作用和预防癌症。尽管它们是有希望的副作用较少的抗癌药,但它们的应用受到其对癌细胞相对较低的毒性的限制。因此,我们提出了线粒体靶向策略,以提高其癌细胞杀伤效率。这种靶向线粒体的SeNPs可以有效地增加癌细胞中ROS的产生和线粒体的损​​伤。然而,仅观察到对正常细胞的毒性略有增加,这表明抗癌治疗可能具有更好的治疗窗口。
更新日期:2020-01-08
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