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In summary, our results suggest that DMP-mediated GSH elevation by a novel post-translational mechanism can inhibit neuronal hyperexcitability both in-vitro and in-vivo and a plausible link is the redox sensitive mTORC1 pathway

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This auto-oxidation process generates toxic reactive oxygen species (ROS), quinones, and free radicals that damage intracellular organelles, deplete cellular glutathione, and ultimately trigger apoptotic cell death (Lohr et al., 2014