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The reduction of the mixed-disulfides between Ec CnoX and its substrates after stress depends on glutathione (Goemans et al., 2018b), an abundant tripeptide that functions as a redox buffer and is mostly present in its reduced form (GSH) under normal conditions (Chesney et al., 1996)

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Through these mechanisms, GPX4 establishes the redox threshold that separates cell survival from lipid peroxidation-induced death, functioning as the master regulator of ferroptosis