Abstract
An ischemic stroke is the sudden and permanent death of brain cells that occurs when the flow of blood to a part of the brain is blocked and oxygen cannot be delivered to the brain. Oxidative stress (OS) is a potential contributor to the pathophysiological consequences of stroke. On the basis of experimental models, there is ample evidence for enhanced free-radical production in the brain after stroke. Furthermore, reactive oxygen species (ROS) generation after stroke is a prolonged process. It is assumed that oxidative stress (OS) contributes to the initiation and development of stroke via different interrelated mechanisms: excitotoxicity resulting in cellular enzyme activation and ROS generation; mitochondrial dysfunction accompanied by excessive radical production; inflammation leading to leukocyte priming and activation; activation and oxidative damage of endothelium resulting in reduced bioavailability of nitric oxide; and lipid peroxidation of plasma and cellular components. Some studies demonstrate the protective role of natural and synthetic antioxidants in experimental stroke models—for example, the supplementation of vitamins C and E reduces the infarct size and severity of neurological damage after permanent ischemia/reperfusion in rats.
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