Mitochondrial and nuclear p53 localization in cardiomyocytes: Redox modulation by doxorubicin (adriamycin)?
Mitochondrial and nuclear p53 localization in cardiomyocytes: Redox modulation by doxorubicin (adriamycin)?
复制标题
DOI：
10.1089/ars.2007.1632
复制
发表时间：
2007-07-01
影响因子：
6.6
通讯作者：
Oberley, Terry D.
中科院分区：
文献类型：
--
作者：
Nithipongvanitch, Ramaneeya;Ittarat, Wanida;Oberley, Terry D.
Reactive oxygen (ROS) and nitrogen species (RNS) generation have been proposed to be an important mechanism of doxorubicin (Adriamycin; ADR)-induced cardiotoxicity and cardiomyocyte apoptosis, processes that may be mediated by p53 protein. We note that ADR treatment resulted in increased levels of p53 protein in cardiomyocyte mitochondria and nuclei. Modulation of the cardiomyocyte redox state in genetically engineered mice by modulation of enzymes involved in metabolism of ROS/RNS, manganese superoxide dismutase (MnSOD), or inducible nitric oxide synthase (iNOS), or a combination of these, regulated levels of mitochondrial/nuclear p53 in cardiomyocytes after ADR administration. These observations led to the hypothesis that mitochondrial/ nuclear p53 localization and function in the cardiomyocyte response to ADR may be regulated through redox-dependent mechanism(s).
