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Decrease in mitochondrial complex I activity in ischemic/reperfused rat heart: involvement of reactive oxygen species
Giuseppe Paradies1, Giuseppe Petrosillo, Marilva Pistolese
1Department of Biochemistry and Molecular Biology and CNR Institute of Biomembranes and Bioenergetics, University of Bari, Bari, Italy. g.paradies@biologia.uniba.it
Circulation Research
|December 6, 2003
Summary
Mitochondrial damage from reactive oxygen species (ROS) impairs heart function during reperfusion. Restoring cardiolipin levels can reverse this complex I defect, suggesting a key role in cardiac injury.
Area of Science:
- Biochemistry
- Cardiovascular Biology
- Mitochondrial Physiology
Background:
- Reactive oxygen species (ROS) contribute significantly to ischemia/reperfusion injury in cardiac myocytes.
- Mitochondrial respiration is a primary source of ROS, potentially exacerbating cardiac reperfusion injury.
Purpose of the Study:
- To investigate the impact of ischemia and reperfusion on mitochondrial function in rat hearts.
- To assess changes in complex I activity, oxygen consumption, ROS production, and cardiolipin content.
Main Methods:
- Isolation of mitochondria from ischemic and reperfused rat hearts.
- Measurement of complex I activity, state 3 respiration, and hydrogen peroxide (H2O2) production.
- Quantification of cardiolipin content and assessment of exogenous cardiolipin's effect on complex I activity.
Main Results:
- Complex I activity decreased by 25% (ischemia) and 48% (reperfusion).
- Mitochondrial H2O2 production increased upon reperfusion.
- Cardiolipin content decreased by 28% (ischemia) and 50% (reperfusion); exogenous cardiolipin restored complex I activity.
Conclusions:
- ROS-induced cardiolipin damage is proposed as the cause of impaired complex I activity in ischemic/reperfused hearts.
- These findings offer insights into the mechanisms underlying myocardial reperfusion injury.