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High-affinity transport of glutathione is part of a multicomponent system essential for mitochondrial function

Regular glutathione and SOD are degraded and lost through digestion, making oral delivery ineffective

Based on these findings, it is reasonable to infer that decreased GPX-3 expression and production may increase vascular activity and damage owing to a diminished effect in suppressing the transcription of inflammatory mediators

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In this case, the glutathione anion with a charge of -2 transfers an electron to the methylcobalamin structure at the very beginning of the CASSCF(14,13) geometry optimization, breaking the Co-C bond, similarly to the interaction of methylcob(II)alamin with the dissociated homocysteine anion [2, 96, 97]