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2015, Neurochemistry InternationalCitation Excerpt :The brain is highly susceptible to oxidative damage due to factors such as its high oxygen utilization rate, high iron content, presence of excess unsaturated fatty acids and decreased activities of detoxifying enzymes (Clarke and Sokoloff, 1999; Dringen, 2000; Gerlach et al., 1994; Halliwell, 2012). As mentioned above, a variety of cellular processes including excitotoxicity, metabolic unbalance, and inflammation, all involving the generation of ROS, would contribute to an increased neuronal death during the cerebral ischemic process (Liu et al., 1989; Kinouchi et al., 1991; Cao and Phillis, 1994). Therapeutic strategies to control the ischemic process have focused on one or another of these factors, and although experimental neuroprotective effects have been observed after, e.g. the utilization of NMDA receptor blockers or calcium channel blockers (Aoki et al., 2001; Williams et al., 2000), this therapeutic approach of one target therapy at a time has largely failed.
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