Abstract
Many previous studies have shown that reactive oxygen radicals play important roles in the pathophysiology of various neurological disorders (8, 56, 81). Experimental ischemia and reperfusion models, such as transient focal / global ischemia model in rodents, have been well studied and the accumulated evidence suggest the involvement of oxygen radicals in the pathogenesis of their ischemic lesion. In these models, cerebral blood flow (CBF) is reduced in brain regions that are supplied with oxygen by the occluded vessels. Reoxygenation during reperfusion provides oxygen as a substrate for numerous enzymatic oxidation reactions. In this review, the mechanisms of formation / clearance and intracellular signalling pathways of oxygen radicals after cerebral ischemia / reperfusion will be discussed.
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