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oral glutathione is hydrolysed to its constituent amino acids in the gut, and the trials showing raised body stores are inconsistent

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FIGURE 8 The aforementioned abnormalities at the molecular level (downregulation of the Nrf2/HO-1 axis and GPX4) and subcellular structural level (neuronal somata and mitochondrial impairment) were consistent with the GSH metabolism perturbations identified by multi-omics analyses, collectively reflecting oxidative stress-associated damage in the hippocampus during SAE