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Extracellular thiols and thiol/disulfide redox in metabolism

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In addition, our results suggest a novel mechanism involving low GSH-associated AMPK activation that prevents alcohol-induced steatosis, which challenges the existing knowledge on the role of low GSH in alcoholic liver disease

Richards HL, Ray DW, Kirby B, et al

22 Therefore, to determine whether the metabolite induces proteotoxicity in part through UPS inhibition, we reduced proteasome function with a range of MG132 concentrations and identified that (at concentrations above 5 M) MG132 induces neurodegeneration in the presence of -synuclein and that this neurotoxicity epistatically regulates metabolite-induced neurotoxicity (Supplementary Figure S4a)

This finding suggests that GSH administered intravenously degraded immediately into the three amino acids