Abstract
Copper is an essential trace metal for all living organisms because this metal serves as a cofactor for activating numerous enzymes critical for homeostasis. However, when copper exceeds the cellular needs, it is toxic through the production of highly reactive hydroxyl radicals that have deleterious effects on cellular components, including destabilization of plasma membranes and lysosomal membranes, disturbance of mitochondrial respiration, depletion of glutathione reserves, and damage of nucleic acids (1). To prevent the accumulation of copper to the toxic level, cells are provided regulatory mechanisms that maintain the balance of intracellular copper.
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