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A mechanism for the unchanged tissue glutathione content in riboflavin deficiency could be the increased biosynthesis of glutathione from its precursor amino acids as a compensatory action ( Reference Kaplowitz, Aw and Ookhtens 30 )

Indeed, increased activities of ThDP-dependent dehydrogenases (assayed in vitro ) are known as a compensatory response to their in vivo inhibition (38, 150)

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