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.
Sheng
H
H
Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710, USA.
Brady
T C
TC
Pearlstein
R D
RD
Crapo
J D
JD
Warner
D S
DS
D000818:Animals; D002544:Cerebral Infarction / Q000201:enzymology / Q000235:genetics / Q000503:physiopathology; D004195:Disease Models, Animal; D005109:Extracellular Matrix / Q000201:enzymology*; D002546:Ischemic Attack, Transient / Q000201:enzymology* / Q000235:genetics / Q000503:physiopathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D013482:Superoxide Dismutase / Q000172:deficiency* / Q000235:genetics*
D013482:Superoxide Dismutase