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Glutathione is a ubiquitous, thiol-containing tripeptide (γ-glutamyl-cysteinyl-glycine) serving as a critical intracellular antioxidant that regulates cellular redox status, detoxifies harmful reactive intermediates, and maintains mitochondrial and cellular functions. Its reduced form (GSH) donates electrons to neutralize reactive oxygen species (ROS)—which include superoxide, hydrogen peroxide, and hydroxyl radical—thereby preventing oxidative damage and modulating redox-sensitive signaling pathways. Glutathione and ROS are tightly linked: glutathione depletion allows ROS accumulation, promoting signaling or cell death; conversely, glutathione supplementation attenuates oxidative stress and apoptosis. Their interplay is central to numerous physiological and pathological processes, such as aging, cancer, neurodegeneration, and cardiovascular disease. Therapeutic approaches often target glutathione metabolism or ROS levels to influence cell fate.
Drugs that increase glutathione levels promote antioxidant defenses and inhibit apoptosis by scavenging ROS. Drugs that deplete glutathione sensitize cells to oxidative stress and promote cell death. Direct ROS scavengers neutralize reactive oxygen species to limit cell and tissue damage.
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