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Within cells, GSH primarily exists in a reduced state, along with two interchangeable oxidized forms: the disulfide form (GSSG) and a mixed disulfide with protein thiols (GSSR)

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This is attributable to a lag in mitochondrial ATP production brought about by a lag in PDC activity which results in an insufficient acetyl-CoA supply to match the demands of the TCA cycle (Krebs cycle energy producing)

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Maintaining the optimal balance between reduced and oxidized GSH within cell compartments is essential for preserving cellular redox homeostasis 45