Publication: Mitochondrial and nuclear p53 localization in cardiomyocytes: Redox modulation by doxorubicin (Adriamycin)?
1
Issued Date
2007-07-01
Resource Type
ISSN
15230864
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2-s2.0-34250375254
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Mahidol University
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SCOPUS
Bibliographic Citation
Antioxidants and Redox Signaling. Vol.9, No.7 (2007), 1001-1008
Suggested Citation
Ramaneeya Nithipongvanitch, Wanida Ittarat, Marsha P. Cole, Jitbanjong Tangpong, Daret K. St. Clair, Terry D. Oberley Mitochondrial and nuclear p53 localization in cardiomyocytes: Redox modulation by doxorubicin (Adriamycin)?. Antioxidants and Redox Signaling. Vol.9, No.7 (2007), 1001-1008. doi:10.1089/ars.2007.1632 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/24172
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Title
Mitochondrial and nuclear p53 localization in cardiomyocytes: Redox modulation by doxorubicin (Adriamycin)?
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.