The role of NADPH oxidase in brain ischemia


Oxygen free radicals or oxidants that arise from molecular oxygen by successive single-electron reduction reactions, include the superoxide anion (O2-), the hydrogen peroxide (H2O2), and hydroxyl radicals (·OH) (Chan 1996). Physiological levels of free radicals are needed for redox sensitive signal pathways, cell development and cell apoptosis (Chan 2001). During brain ischemia/reperfusion (I/R), oxygen is not well used; and robust oxygen radicals are generated in the brain. Excessive free radicals cause the cellular macromolecular damages of lipids, proteins, and nucleotide acids; thus, they play a crucial role in ischemic/reperfusion brain damage. NADPH oxidase (NOX) is a pro-oxidant enzyme that is expressed in various brain regions and its level is regulated by ischemia. This review is focused on the role of NOX in brain ischemia. Results from both in vivo and in vitro studies suggested that NOX plays a role in ischemic brain damage through producing oxygen radicals, contributing to excitotoxicity, and exacerbating post-ischemic inflammation process.