The difference between the effects of both QIs on the cell viability ( Figure 2 ) and caspase 3 activation ( Figure 4 ) suggests that upon GSH depletion, the decrease in cell viability is not only apoptosis dependent but also most likely depends other cell death pathways, such as necrosis ( IC 50 values of QIs under GSH-depleted conditions were around 20 M ( Figure 2 ), which is higher than the plasma concentrations of AQ and DEAQ found in patients, normally in nanomolar to micromolar ranges ( in vivo may be lower, exposure continues for a prolonged period as the half-life of DEAQ is 10 to 12 days ( The relative contribution of GSTP1 to GSH-conjugation of both QIs was highest at GSH-depleted conditions, while in absolute quantities a higher GSTP1-dependent increase of GSH conjugate formation was seen without BSO pre-treatment ( Figure 5 )
The more interesting question is why it does so, and what those mechanisms might imply for human biology beyond the skin barrier
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In cases when patients are resistant to NSAIDs, intra-articular corticosteroid injections are contemplated
3.3.3 Intestinal barrier integrity and metabolic endotoxemia The intestinal barrier represents a selectively permeable barrier between the internal environment and intestinal luminal contents, comprising mechanical barriers (epithelial cells and tight junctions), chemical barriers (mucus layer and antimicrobial peptides), immune barriers, and biological barriers (commensal microbiota) (86)
