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Therefore, depletion of NADPH stores in G6PD-d has the potential to both limit the production of ROS by NOX family enzymes, while simultaneously expediting the accumulation of ROS from non-NADPH-dependent sources, such as the mitochondrial electron transport chain, peroxisomal -oxidation, oxidative protein folding, and other cytoplasmic enzymes (xanthine oxidase, cyclooxygenase, lipoxygenase) 95,96

Our experimental data demonstrate that selenocystine supplementation significantly increases GPX4 protein levels under various conditions, including with or without cystine and RSL3 treatment (Fig