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Notably, the acetylation-defective P53 mutant (P53 3KR) can indirectly inhibit the uptake of cysteine, decrease GSH production, and induce lipid ROS accumulation, leading to ferroptosis [67, 74]

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This innovative approach effectively halts the enzymatic activity of GPx, allowing for accurate quantification of residual H 2 O 2 through the formation of a stable ferri-Tiron complex