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Lack of change in MnSOD during ischemia/reperfusion of isolated rat heart
R Subramanian1, A Volovsek, Y S Ho
1Department of Pathology, University of Wisconsin, Madison.
Abstract:
Decreased endogenous superoxide dismutase (SOD) activity has been implicated in free radical-mediated reperfusion injury of the ischemic myocardium. Antioxidant enzymes have been added to the modalities of reperfusion therapy of acute myocardial infarction based on this observation. We measured the content of MnSOD specific protein, activity of Mn and Cu, ZnSODs, and MnSOD mRNA in the working isolated rat heart subjected to various durations of ischemia and reperfusion. Recovery of mechanical function was monitored and lactate and lactic dehydrogenase released in the coronary effluent before and after ischemia were measured. In this model with reversible or irreversible myocardial injury, we noted no change in the myocardial MnSOD specific protein content and, contrary to some previous observations, no change in the activity levels of Mn or Cu,ZnSODs. Our results suggest that free radical-mediated damage in the heart during ischemia and reperfusion is probably not due to impaired activity or degradation of native SODs.
Insights
This study found that superoxide dismutase (SOD) activity and protein levels remain unchanged in the heart during ischemia and reperfusion. Therefore, free radical damage is unlikely due to impaired SOD function.
Area of Science:
- Cardiology
- Biochemistry
- Molecular Biology
Background:
- Decreased endogenous superoxide dismutase (SOD) activity is linked to reperfusion injury in ischemic myocardium.
- Antioxidant enzymes are used in reperfusion therapy for acute myocardial infarction.
Purpose of the Study:
- To investigate changes in MnSOD protein, Mn and Cu,ZnSOD activities, and MnSOD mRNA during myocardial ischemia and reperfusion.
- To determine if impaired SOD function contributes to free radical-mediated damage in the heart.
Main Methods:
- Working isolated rat heart model subjected to varying ischemia and reperfusion durations.
- Measurement of MnSOD specific protein content, Mn and Cu,ZnSOD activities, and MnSOD mRNA.
- Monitoring of mechanical function recovery and release of lactate and lactic dehydrogenase.
Main Results:
- No significant changes were observed in myocardial MnSOD specific protein content.
- Contrary to previous findings, Mn and Cu,ZnSOD activities did not change.
- Lactate and lactic dehydrogenase release indicated varying degrees of myocardial injury.
Conclusions:
- Free radical-mediated damage in the heart during ischemia and reperfusion is unlikely caused by impaired activity or degradation of native SODs.
- The role of SODs in myocardial reperfusion injury warrants further investigation.