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Here, we show in hepatocytes and other metabolically active cells that decreasing the availability of substrate for the tricarboxylic acid (TCA) cycle diminished NADPH production, elevated glutathione oxidation, led to altered oxidative maturation of ER client proteins, and attenuated ER stress

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These studies demonstrate a previously undiscovered mechanism by which increasing glutathione (GSH) status positively influences the bioavailability of 25(OH)VD