It has been well documented that free radicals (e.g., ROS and RNS) contribute to hy-poxic-ischemic neuronal death. Pharmacological or genetic intervention of ROS and RNS has been neuroprotective against hypoxic-ischemic injury as discussed above. However, neither tirilazad mesylate, a lipid peroxidation inhibitor, nor ebselen, a se-leno-organic compound with antioxidant activity, showed therapeutic efficacy in primary outcome measure of stroke patients. This lack of efficacy may be attributed to inappropriate administration of drugs that is insufficient to block ROS production following hypoxic ischemia. In addition, blockade of ROS neurotoxicity may result in appearance of the other death pathways, excitotoxicity, and apoptosis.
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