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Another mechanism of GSH protection is reverse post-translational modifications of proteins by S-glutathionylation/deglutathionylation), which is common for the Krebs cycle and the electron transport chain proteins catalyzed by glutathione-S-transferase and glutaredoxins (Mar et al., 2020)

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Indeed, germ-free mice exhibit defects in the maturation of gut-associated lymphoid tissues and mesenteric lymph nodes, leading to attenuated production of secretory IgA (S-IgA) (17)