ABSTRACT
In stroke syndromes, the brain appears to be particularly sensitive to iron-mediated oxidative damage because of its high levels of polyunsaturated lipids which are vital for neural transmission, its acidic environment during ischemia, its high metabolic rate. Increasing evidence that reduced O2 metabolites participate in ischemic cerebrovascular disease is available in number of experimental models. Despite the theoretical importance of iron in oxidative brain injury, very little direct evidence exists to implicate iron in stroke. In unilateral hemispheric ischemia-reperfusion, therefore, brain iron and XO-derived oxidants appear to have a mechanistic link with development of cerebral edema. The importance of iron in stroke syndromes and the cooperative effects of iron and oxygen metabolites in precipitating oxidative injury to ischemic brain have only recently been appreciated. However, it is clear that iron must be tightly regulated within the brain parenchyma, and that the interaction between iron and free radicals has broad ranging impact on a variety of central nervous system diseases.
