Extracellular superoxide dismutase deficiency worsens outcome from focal cerebral ischemia in the mouse.
The role of endogenous extracellular superoxide dismutase (EC-SOD) was examined in a murine model of transient focal cerebral ischemia. Homozygous EC-SOD deficient (EC-SOD-/-; n = 18) and wild type (EC-SOD+/+; n = 19) littermates were anesthetized with halothane and subjected to 50 min of intraluminal middle cerebral artery occlusion with pericranial temperature maintained at 37.0 degrees C. After 24 h of reperfusion, resultant hemiparesis and cerebral infarct size were measured. Total infarct volume was 81% greater (P = 0.03) and hemiparesis was more severe (P = 0.01) in EC-SOD-/- versus EC-SOD+/+ mice. The worsened ischemic outcome observed in EC-SOD-/- mice is consistent with prior work which found transgenic EC-SOD overexpressing mice to exhibit enhanced tolerance to focal ischemia. The results suggest that endogenous antioxidant activity in the extracellular compartment plays an important role in the histologic/neurologic response to focal cerebral ischemia.
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Related Subject Headings
- Superoxide Dismutase
- Mice, Knockout
- Mice, Inbred C57BL
- Mice
- Male
- Ischemic Attack, Transient
- Extracellular Matrix
- Disease Models, Animal
- Cerebral Infarction
- Animals
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Superoxide Dismutase
- Mice, Knockout
- Mice, Inbred C57BL
- Mice
- Male
- Ischemic Attack, Transient
- Extracellular Matrix
- Disease Models, Animal
- Cerebral Infarction
- Animals