Oxygen radicals in focal cerebral ischemia

Brain Pathol. 1994 Jan;4(1):59-65. doi: 10.1111/j.1750-3639.1994.tb00811.x.

Abstract

Oxygen free radicals have been widely implicated in the pathogenesis of brain injury due to ischemia followed by reperfusion. The success of making transgenic animals overexpressing human CuZn-superoxide dismutase (CuZn-SOD) in brain cells allows researchers to discern the specific role of superoxide radicals in reperfusion injury after focal ischemia. It has been shown that increased brain levels of CuZn-SOD in transgenic mice protect neurons from ischemia/reperfusion injury. However, overexpression of CuZn-SOD does not provide neuronal protection in permanent focal ischemia in mice, when compared with non-transgenic mouse littermates. It is proposed that molecular genetic approaches of modifying antioxidant levels in the brain offer a unique tool for studying oxidative mechanisms in focal cerebral ischemia.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Antioxidants / metabolism
  • Brain / metabolism
  • Brain Ischemia / metabolism*
  • Humans
  • Lipid Peroxidation
  • Mice
  • Mice, Transgenic
  • Reactive Oxygen Species / metabolism*
  • Reperfusion Injury / metabolism*
  • Reperfusion Injury / prevention & control
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase / physiology*

Substances

  • Antioxidants
  • Reactive Oxygen Species
  • Superoxide Dismutase