| First Author | Sheng H | Year | 1999 |
| Journal | Neurosci Lett | Volume | 267 |
| Issue | 1 | Pages | 13-6 |
| PubMed ID | 10400237 | Mgi Jnum | J:107981 |
| Mgi Id | MGI:3622616 | Doi | 10.1016/s0304-3940(99)00316-x |
| Citation | Sheng H, et al. (1999) Extracellular superoxide dismutase deficiency worsens outcome from focal cerebral ischemia in the mouse. Neurosci Lett 267(1):13-6 |
| abstractText | 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. |
