Cellular copper pools

Cellular copper pools represent the compartmentalized and protein-bound fractions of copper within a cell, which are strictly regulated to prevent oxidative damage while ensuring availability for essential cuproenzymes (Tsvetkov et al., 2022). Copper serves as a critical cofactor for enzymes involved in energy production (cytochrome c oxidase), antioxidant defense (superoxide dismutase), and neurotransmitter synthesis (Ge et al., 2022). Dysregulation of these pools leads to severe pathologies: copper overload causes Wilson's disease and can trigger a unique form of regulated cell death known as cuproptosis, while copper deficiency characterizes Menkes disease (NIH, 2023). In oncology, drugs like elesclomol act as copper ionophores to overload mitochondrial copper pools, inducing proteotoxic stress and cell death in malignant cells (PubChem). Conversely, chelating agents like trientine are used to deplete toxic copper accumulations in metabolic disorders (FDA). Maintaining the balance of these pools is crucial, as both deficiency and excess are linked to severe metabolic and neurodegenerative conditions.

Other names

Intracellular copper poolsLabile copper poolBioavailable copperCytosolic copper poolMitochondrial copper pool

Copper chelation, Copper ionophore-mediated transport, Induction of cuproptosis, Inhibition of intestinal copper absorption