Extracellular superoxide dismutase deficiency worsens outcome from focal cerebral ischemia in the mouse.
Journal Article
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.
Full Text
Duke Authors
Cited Authors
- Sheng, H; Brady, TC; Pearlstein, RD; Crapo, JD; Warner, DS
Published Date
- May 21, 1999
Published In
Volume / Issue
- 267 / 1
Start / End Page
- 13 - 16
PubMed ID
- 10400237
Pubmed Central ID
- 10400237
International Standard Serial Number (ISSN)
- 0304-3940
Digital Object Identifier (DOI)
- 10.1016/s0304-3940(99)00316-x
Language
- eng
Conference Location
- Ireland