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Disruption of mitochondrial repositioning and function elevates ROS levels and triggers early apoptosis

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Other relevant repair/oxidative stress protection mechanisms of NAC may also be relevant and worth exploring [33], including mechanisms by which NAC scavenges free radicals [34], induces neurogenesis [35], reduces mitochondrial apoptosis [36], reduces glutamatergic neurotransmission [29], and chelates metals as a form of oxidative stress protection [37]