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Introduction Several studies have concluded that oxidative stress, due to increased production of reactive oxygen species (ROS), for instance, because of infection, can trigger inflammation, although the concept has been considered an oversimplification ( While in the context of oxidative stress GSH acts as an antioxidant ROS scavenger, in the context of redox regulation the couple GSH/GSSG (oxidized GSH) acts as a signaling molecule that regulates protein function via thioldisulfide exchange reactions including protein glutathionylation ( To investigate the role of endogenous GSH in inflammation, whether it acts as an antioxidant or a signaling molecule, we used the mouse macrophage RAW cell line stimulated with lipopolysaccharide (LPS) with and without pretreatment with the GSH synthesis inhibitor buthionine sulfoximine (BSO)

They also noticed a decrease in the markers of oxidative stress at 6 months, as shown by the improvement in the GSSG/GSH ratio

Elevated intracellular GSH (or precursors like NAC) in autoimmune conditions has been shown to downregulate the activity of NF-B which mediates pro-inflammatory gene transcription (Limongi et al., 2019)