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Once inside the mitochondrial matrix, Cu 2+ is reduced to the more reactive Cu + by ferredoxin-1 (FDX1) ( + binds to the lipoyl-lysine residues of DLAT, promoting its oligomerization and functional disruption, which impairs the pyruvate dehydrogenase complex and compromises TCA cycle activity, leading to proteotoxic stress and mitochondrial dysfunction (47)