中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
首页 机构 成果 学者
  
  1. CAS IR Grid
  2. 近代物理研究所
  3. 中国科学院近代物理研究所
Carbon Ion Beams Induce Hepatoma Cell Death by NADPH Oxidase-Mediated Mitochondrial Damage

文献类型：期刊论文

作者Sun, Chao1,2,3,4; Wang, Zhenhua5; Liu, Yang1,2,3; Liu, Yuanyuan1,2,3; Li, Hongyan1,2,3,4; Di, Cuixia1,2,3; Wu, Zhenhua1,2,3; Gan, Lu1,2,3; Zhang, Hong1,2,3
刊名JOURNAL OF CELLULAR PHYSIOLOGY
出版日期2014
卷号229页码:100-107
ISSN号0021-9541
DOI10.1002/jcp.24424
文献子类Article
英文摘要Mitochondria are a major source of reactive oxygen species (ROS) and are also the target of cellular ROS. ROS damage to mitochondria leads to dysfunction that further enhances the production of mitochondrial ROS. This feed-forward vicious cycle between mitochondria and ROS induces cell death. Within a few minutes of radiation exposure, NADPH oxidase is activated to elevate the ROS level. Activated NADPH oxidase might induce the feed-forward cycle of mitochondria and this is a possible mechanism for cancer cell death induced by heavy ion irradiation. We found that after 4Gy of C-12(6+) ion radiation of HepG2 cells, the NADPH oxidase membrane subunit gp91(phox) was not involved in enzyme activation through increased expression; however, the subunit p47(phox) was involved in activation by being translocated to the membrane. C-12(6+) ion radiation clearly decreased the m of HepG2 cells, increasing mitochondrial DNA damage and inducing cell death. Pretreatment with apocynin (APO, an NADPH oxidase inhibitor) effectively prevented the m decrease, mitochondrial DNA damage, and cell death induced by radiation. However, these protective effects were not observed with APO treatment after irradiation exposure. These data demonstrated that NADPH oxidase activation was an initiator in mitochondrial damage. Once mitochondria entered the feed-forward cycle, cell fate was no longer controlled by NADPH oxidase. Only antioxidants that targeted mitochondria such as MitoQ could break the cycle and release cells from death. J. Cell. Physiol. 229: 100-107, 2014. (c) 2013 Wiley Periodicals, Inc.
WOS关键词OXIDATIVE STRESS ; DNA DAMAGE ; DYSFUNCTION ; NANOPARTICLES ; MECHANISMS ; GENERATION ; CANCER ; SKIN
资助项目Scientific Technology Research Projects of Gansu Province[0702NKDA045] ; Scientific Technology Research Projects of Gansu Province[0806RJYA020]
WOS研究方向Cell Biology ; Physiology
语种英语
WOS记录号WOS:000327883100014
出版者WILEY-BLACKWELL
源URL[http://119.78.100.186/handle/113462/49157]  
专题中国科学院近代物理研究所
通讯作者Zhang, Hong
作者单位1.Chinese Acad Sci, Inst Modern Phys, Dept Heavy Ion Radiat Med, Lanzhou 730000, Peoples R China
2.Chinese Acad Sci, Key Lab Heavy Ion Radiat Med, Lanzhou 730000, Peoples R China
3.Key Lab Heavy Ion Radiat Med Gansu Prov, Lanzhou, Peoples R China
4.Chinese Acad Sci, Grad Univ, Beijing, Peoples R China
5.Yantai Univ, Coll Life Sci, Yantai, Peoples R China
推荐引用方式
GB/T 7714		 Sun, Chao,Wang, Zhenhua,Liu, Yang,et al. Carbon Ion Beams Induce Hepatoma Cell Death by NADPH Oxidase-Mediated Mitochondrial Damage[J]. JOURNAL OF CELLULAR PHYSIOLOGY,2014,229:100-107.
APA Sun, Chao.,Wang, Zhenhua.,Liu, Yang.,Liu, Yuanyuan.,Li, Hongyan.,...&Zhang, Hong.(2014).Carbon Ion Beams Induce Hepatoma Cell Death by NADPH Oxidase-Mediated Mitochondrial Damage.JOURNAL OF CELLULAR PHYSIOLOGY,229,100-107.
MLA Sun, Chao,et al."Carbon Ion Beams Induce Hepatoma Cell Death by NADPH Oxidase-Mediated Mitochondrial Damage".JOURNAL OF CELLULAR PHYSIOLOGY 229(2014):100-107.

入库方式： OAI收割

来源：近代物理研究所

浏览0
下载0
收藏0
其他版本

除非特别说明，本系统中所有内容都受版权保护，并保留所有权利。