Oxygen radicals in focal cerebral ischemia

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.