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Based on prior reports linking mitochondrial protein stability to a short fragment within the cyclic structural domain of SLC25A39 (amino acids 7286) that mediates glutathione (GSH) response and recruits SLC25A39 to AFG3L2 for proteolysis, we generated a deletion mutant lacking this fragment (aa72-86), confirmed by Sanger sequencing (Fig

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Chelation's ability to inhibit Fe 2 -mediated lipid peroxidation and other oxidative processes highlights its therapeutic and preservative potential in biomedical and food sciences