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All use is restricted to in-vitro and preclinical research settings

However, under defined pathophysiological stresses, including inflammatory cues, metal overload, cysteine deprivation, or drug exposure, GSH oxidation and thiol chemistry may become coupled to metal redox cycling and mitochondrial damage amplification, thereby increasing susceptibility to forms of regulated cell death such as ferroptosis and cuproptosis

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10.1073/pnas.0911516107 Proc

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