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1 Cardiology, VA Medical Center, San Francisco, CA, USA
2 Cardiology, VA Medical Center, San Francisco, CA, USA; Medicine, UCSF, San Francisco, CA, USA
3 Molecular Biology, VA Medical Center, San Francisco, CA, USA; Biochemistry and Biophysics, UCSF, San Francisco, CA, USA
4 Medicine, UCSF, San Francisco, CA, USA
* To whom correspondence should be addressed. E-mail: joel.karliner{at}med.va.gov.
Manganese superoxide dismutase (MnSOD) is one of the main antioxidant enzymes that protects the heart against ischemia/reperfusion (IR) injury. Ischemic preconditioning (IPC) is a short period of ischemia/reperfusion which reduces subsequent prolonged IR injury. Although MnSOD localizes in the mitochondria, the immediate subcellular distribution of MnSOD in heart following IPC and IR has not been studied. In a Langendorff mouse heart model, IPC significantly improved cardiac function and reduced infarction size induced by IR. Immunoblotting and double immunostaining in fresh preparations revealed that IR 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 IR. 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 IR. In contrast, fresh preparations exhibit early MnSOD release into the cytosol after IR that is prevented by IPC and cyclosporine A.
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