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Thus, as far as mitochondrial oxidative stress homeostasis is concerned, mGSH is a vital factor maintaining mitochondrial function, controlling cell survival/death, and its depletion causes cell damage and facilitates cell death [57, 59]

& Gonzalez-Aseguinolaza, G

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These compositional disruptions contribute to increased intestinal permeability and sustained peripheral inflammation, creating conditions conducive to -synuclein misfolding within the enteric nervous system and its subsequent propagation along gutbrain pathways [25]

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