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Indeed, oxidation damage is highly dependent on the inherited or acquired defects in enzymes involved in the redox-mediated signaling pathways
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8 Characterization of dHTC1 and SR-1114 activity
This ensures sustained homocysteine flux, which is critically converted to cysteine for GSH biosynthesis when the canonical cystine/glutamate antiporter (system xc-) is inhibited, a common trigger for ferroptosis (Cao et al., 2020)