Related Experiment Videos
Hydrogen peroxide release by mitochondria from normal and hypoxic lungs
1Birmingham VA Medical Center, Alabama.
The American Journal of the Medical Sciences
|October 1, 1994
Summary
Lung collapse due to hypoxia/hypoperfusion did not alter mitochondrial hydrogen peroxide (H2O2) release. This suggests other sources contribute to lung oxidant injury during reperfusion.
Area of Science:
- Biochemistry
- Cell Biology
- Pulmonary Medicine
Background:
- Ischemia/reperfusion injury is implicated in lung transplantation and pulmonary embolism.
- Hypoxia and substrate deprivation occur when lung ventilation and perfusion are interrupted.
- Mitochondria are potential sources of reactive oxygen species during reperfusion.
Purpose of the Study:
- To investigate if lung hypoxia/hypoperfusion from collapse alters mitochondrial hydrogen peroxide (H2O2) release.
- To determine the role of mitochondria in oxidant injury following lung collapse.
Main Methods:
- Mitochondria were isolated from collapsed and control rabbit lungs.
- Mitochondrial H2O2 release was measured fluorometrically.
- Succinate dehydrogenase activity assessed mitochondrial recovery and content.
Main Results:
- Lung collapse and hypoxia did not change mitochondrial number or H2O2 release capacity in vitro.
- Mitochondrial recovery and lung succinate dehydrogenase activity were comparable across groups.
- Mitochondria released H2O2 in a dose-dependent manner with cyanide and NAD+.
Conclusions:
- Mitochondria do not appear to be the primary source of oxidant injury in this lung collapse model.
- Other reactive oxygen metabolite sources, such as xanthine oxidase and neutrophils, likely contribute to injury.