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Zinc metabolism

Molecular classification
Other (metabolic pathway/process), Transporters: Zinc transporter (ZnT) family, Transporters: ZIP family, Storage proteins: Metallothioneins (MTs), Enzymes: Carbonic anhydrase, Enzymes: Carboxypeptidase, Enzymes: Superoxide dismutase (SOD), Receptor: Zinc-sensing receptor (ZnR/GPR39)
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Overview

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.

Other names
Zinc homeostasisZinc metabolic pathwayCellular zinc metabolism
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Mechanism of action

Supplementation increases zinc availability for enzymes, transporters, and transcription factors Chelation decreases intracellular zinc and alters signal transduction and metabolism

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Biological functions

Homeostasis of zinc levelsRegulation of cellular metabolismSignal transductionAntioxidant defenseImmune response modulationProtein and nucleic acid synthesisCell proliferation and apoptosisSynaptic plasticity and neuronal function
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Disease associations

CancerMetabolic syndromeNeurodegenerative diseaseImmune dysfunctionAcrodermatitis enteropathica
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Safety considerations

Zinc deficiency leads to impaired immune function, growth retardation, and neurocognitive deficitsExcess zinc causes toxicity, including gastrointestinal symptoms, interference with copper absorption, and possible neurotoxicityChelators may induce deficiency and related symptoms
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Interacting drugs

Zinc supplements (zinc sulfate, zinc acetate, etc.)

1 more in the full profile.

07

Biomarkers

Serum/plasma zinc concentrationExpression or mutation of zinc transporters (e.g., ZIP4 mutations in acrodermatitis enteropathica)Metallothionein levels

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