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This Article Full Text Full Text (PDF) All Versions of this Article: 288/6/H2986    most recent 01144.2004v2 01144.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Jin, Z.-Q. Articles by Karliner, J. S. Search for Related Content PubMed PubMed Citation Articles by Jin, Z.-Q. Articles by Karliner, J. S.

MnSOD in mouse heart: acute responses to ischemic preconditioning and ischemia-reperfusion injury

¹Cardiology Section and ²Molecular Biology Section, Veterans Affairs Medical Center, San Francisco; and Departments of ³Medicine and ⁴Biochemistry and Biophysics, University of California, San Francisco, California

Submitted 15 November 2004 ; accepted in final form 20 January 2005

Manganese superoxide dismutase (MnSOD) is one of the main antioxidant enzymes that protects the heart against ischemia-reperfusion (I/R) injury. Ischemic preconditioning (IPC) is a short period of ischemia-reperfusion that reduces subsequent prolonged I/R injury. Although MnSOD localizes in mitochondria, the immediate subcellular distribution of MnSOD in heart after IPC and I/R has not been studied. In a Langendorff mouse heart model, IPC significantly improved cardiac function and reduced the infarction size induced by I/R. Immunoblotting and double immunostaining in fresh preparations revealed that I/R resulted in an increase in cytosolic MnSOD content accompanied by the release of cytochrome c. In contrast, IPC increased mitochondrial MnSOD and reduced cytosolic MnSOD and cytochrome c release induced by I/R. We found that compared with freshly prepared fractions, the freeze-thaw approach results in mitochondrial integrity disruption and release of large amounts of MnSOD into the cytosol along with mitochondrial markers even in the absence of I/R. In contrast, fresh preparations exhibit early MnSOD release into the cytosol after I/R that is prevented by IPC and cyclosporin A administration.

manganese superoxide dismutase; reactive oxygen species; myocardial infarction; mitochondria; cytosol; permeability transition pore

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