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Zinc metabolism refers to the coordinated molecular processes that maintain zinc homeostasis in cells and tissues. Zinc is a vital trace element required for the structural integrity and catalytic activity of hundreds of enzymes and for inter- and intracellular signaling. Key components include zinc transporters (ZIP and ZnT families), which regulate zinc import and export; metallothioneins (MTs), which store and buffer zinc; and a variety of zinc-dependent enzymes such as carbonic anhydrase and superoxide dismutase. Zinc metabolism is essential to cellular energetics, immune defense, synaptic plasticity, and regulation of apoptosis and proliferation. Disruption of zinc homeostasis is implicated in metabolic syndrome, cancer, neurodegeneration, and inherited disorders such as acrodermatitis enteropathica, which is caused by ZIP4 mutations. Unlike classical therapeutic targets (receptors, enzymes), "zinc metabolism" is not a discrete molecular target, but rather a systemic network of molecules and pathways.
Supplementation increases zinc availability for enzymes, transporters, and transcription factors Chelation decreases intracellular zinc and alters signal transduction and metabolism
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