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Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry
Published on: October 4, 2024
Melatonin attenuates I/R-induced mitochondrial dysfunction in skeletal muscle
Wei Z Wang1, Xin-Hua Fang, Linda L Stephenson
1Department of Surgery, Division of Plastic Surgery, University of Nevada School of Medicine, Las Vegas, Nevada 89102, USA. wwang@medicine.nevada.edu
The Journal of Surgical Research
|April 28, 2010
Summary
Melatonin protects skeletal muscle cells from ischemia/reperfusion injury by preserving mitochondrial function. This study shows melatonin prevents mitochondrial membrane potential loss and cytochrome c release, crucial for cell survival.
Area of Science:
- Biomedical Science
- Cell Biology
- Physiology
Background:
- Ischemia/reperfusion (I/R) causes significant cell death in skeletal muscle.
- Melatonin has previously shown protective effects against I/R-induced damage.
- Mitochondria are vital for cell survival and regulating cell death pathways.
Purpose of the Study:
- To investigate the protective effects of melatonin on ischemia/reperfusion-induced mitochondrial dysfunction in skeletal muscle in vivo.
- To assess melatonin's impact on mitochondrial membrane potential and cytochrome c release.
Main Methods:
- A rat gracilis muscle model was subjected to 4 hours of ischemia and 24 hours of reperfusion.
- Mitochondrial and cytosolic fractions were isolated to assess mitochondrial dysfunction.
- Mitochondrial membrane potential and cytochrome c release were measured in sham, I/R with vehicle, and I/R with melatonin groups.
Main Results:
- Melatonin treatment (I/R-Mel) significantly improved mitochondrial membrane potential compared to vehicle (I/R-V).
- Melatonin administration inhibited the release of cytochrome c from mitochondria into the cytoplasm.
Conclusions:
- Melatonin effectively attenuates ischemia/reperfusion-induced mitochondrial dysfunction in skeletal muscle.
- Melatonin preserves mitochondrial membrane potential and prevents the release of pro-apoptotic cytochrome c.
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