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Fe overload triggers direct mitochondrial membrane lipid peroxidation via Fenton reaction-derived hydroxyl radicals, while Cd impairs mitochondrial antioxidant defenses by suppressing glutathione peroxidase 4 (GPX4) activity

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Doubling the blend dose doubles cost and copper exposure while providing marginal or zero additional benefit

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The pathogenesis of these disorders is generally attributed to the direct toxicity of acetaminophen-derived reactive oxidation products