Mitochondrial and nuclear p53 localization in cardiomyocytes: Redox modulation by doxorubicin (Adriamycin)?

Ramaneeya Nithipongvanitch, Wanida Ittarat, Marsha P. Cole, Jitbanjong Tangpong, Daret K. St. Clair, Terry D. Oberley

Research output: Contribution to journalReview articlepeer-review

62 Scopus citations

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).

Original languageEnglish
Pages (from-to)1001-1008
Number of pages8
JournalAntioxidants and Redox Signaling
Volume9
Issue number7
DOIs
StatePublished - Jul 2007

Funding

FundersFunder number
National Childhood Cancer Registry – National Cancer InstituteR01CA094853

    ASJC Scopus subject areas

    • Physiology
    • Biochemistry
    • Molecular Biology
    • Clinical Biochemistry
    • Cell Biology

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