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


  • eng

Conference Location

  • Ireland