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The impact of changed redoxin function on ferroptosis could also be based on secondary effects, e.g., the increase in superoxide formation upon loss of mitochondrial redoxins [90,91] or activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway [92,93] , a major regulator of transcription of antioxidant and anti-ferroptotic enzymes [65]

capsule forms of glutathione are destroyed in the gut

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see Role of the Mercapturate Pathway and Cysteine S-Conjugate -Lyases in the Bioactivation of Toxic Halogenated Alkenes section)

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