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In contrast, the buildup of lipid ROS and the consequent onset of ferroptosis can be hindered through intervention with iron-chelating agents (e.g., deferoxamine) and lipophilic antioxidants (e.g., ferrostatin-1 and liproxstatin-1) [77]

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This H₂O₂, though less reactive, is still potentially harmful and is further detoxified by CAT and GSH-Px, which break it down into water and oxygen, reducing its potential for cellular damage