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These findings suggest that although GSH-dependent reductive metabolism supports cellular survival under physiological conditions, sustained mitochondrial activity enabled by GSH can become deleterious under stress (Fig

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when this process is compromised, Fe + activates lipid peroxidases, producing reactive oxygen species (50), which oxidize membrane polyunsaturated fatty acids (PUFAs) to PUFA-OOHs, resulting in irreversible membrane damage and cellular apoptosis ( Figure 4 )

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