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Mice lacking extracellular superoxide dismutase are more sensitive to hyperoxia
L M Carlsson1, J Jonsson, T Edlund
1Department of Clinical Chemistry, Umeå University Hospital, Sweden.
Summary
Extracellular superoxide dismutase (EC-SOD) is crucial for survival under high oxygen stress. While other antioxidant systems compensate normally, EC-SOD deficiency leads to reduced survival and lung edema when stressed.
Area of Science:
- Biochemistry
- Physiology
- Genetics
Background:
- Extracellular superoxide dismutase (EC-SOD) is a secreted enzyme containing copper and zinc.
- It is a tetrameric glycoprotein primarily bound to heparan sulfate proteoglycans in tissue interstitium.
- EC-SOD plays a role in antioxidant defense.
Purpose of the Study:
- To investigate the in vivo function of EC-SOD.
- To determine the physiological consequences of EC-SOD deficiency.
Main Methods:
- Generation of EC-SOD null mutant mice via gene targeting.
- Assessment of survival rates and lung edema under hyperoxic conditions (>99% oxygen).
- Analysis of compensatory changes in other SOD isoenzymes and antioxidant enzymes.
Main Results:
- EC-SOD null mutant mice developed normally and remained healthy up to 14 months of age.
- No compensatory induction of other antioxidant enzymes was observed.
- EC-SOD null mutant mice exhibited significantly reduced survival times and earlier onset of severe lung edema when exposed to hyperoxia compared to wild-type mice.
Conclusions:
- Under normal physiological conditions, other antioxidant systems can compensate for the absence of EC-SOD.
- However, these compensatory systems are insufficient to provide adequate protection during severe oxidative stress.
- EC-SOD is essential for maintaining survival and preventing lung injury under hyperoxic stress.