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Inflammatory cytokines including tumor necrosis factor alpha (TNF), interferon gamma (IFN), and interleukin-1 beta (IL-1), cause beta-cell dysfunction by impairing ATP production, inducing DNA damage, and promoting apoptosis ( Figure 3 ) (84, 85)

Our mechanistic investigations revealed that intracellular GSSG elevation sensitizes hepatocytes to TNF killing by inducing IKK--SSG formation, leading to suppressed NF-B activation

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N-acetyl-L-cysteine (NAC), a well-characterized thiol antioxidant and precursor of reduced glutathione (GSH), not only scavenges intracellular ROS directly but also replenishes depleted GSH stores in erythrocytes, thereby inhibiting ROS-mediated Ca 2+ influx and PS externalization induced by eryptosis triggers such as desipramine or uremic toxins