Extracellular superoxide dismutase deficiency worsens outcome from focal cerebral ischemia in the mouse
Copyright policy )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.
- Duke University United States
- National Center for Jewish Film United States
- Duke University Hospital United States
- Duke University Health System United States
- Duke Medical Center United States
Male, Mice, Inbred C57BL, Mice, Knockout, Disease Models, Animal, Mice, Ischemic Attack, Transient, Superoxide Dismutase, Animals, Cerebral Infarction, Extracellular Matrix
Male, Mice, Inbred C57BL, Mice, Knockout, Disease Models, Animal, Mice, Ischemic Attack, Transient, Superoxide Dismutase, Animals, Cerebral Infarction, Extracellular Matrix
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