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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/24172
Title: Mitochondrial and nuclear p53 localization in cardiomyocytes: Redox modulation by doxorubicin (Adriamycin)?
Authors: Ramaneeya Nithipongvanitch
Wanida Ittarat
Marsha P. Cole
Jitbanjong Tangpong
Daret K. St. Clair
Terry D. Oberley
University of Wisconsin School of Medicine and Public Health
Mahidol University
University of Kentucky
VA Medical Center
Keywords: Biochemistry, Genetics and Molecular Biology
Issue Date: 1-Jul-2007
Citation: Antioxidants and Redox Signaling. Vol.9, No.7 (2007), 1001-1008
Abstract: 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). © Mary Ann Liebert, Inc.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=34250375254&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/24172
ISSN: 15230864
Appears in Collections:Scopus 2006-2010

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