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However, when the physiological demand for antioxidants surpasses their bioavailability, the brain enters a state of REDOX imbalance in which ROS accumulate, leading to neuronal damage [6, 7]
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For example, in the case of Bumetanide, the induction of diuresis, concomitant risk for hypokalemic alkalosis and potential ototoxicity clearly limits the application of bumetanide for chronic treatment of CNS disorders (Sica, 2004
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