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The intracellular zinc pool, also known as the labile or mobile zinc pool, consists of zinc ions that are loosely bound to low-affinity ligands such as amino acids or organic acids, making them readily available for biological signaling (Maret, 2017). This pool is distinct from the structural zinc found tightly bound in metalloproteins and serves as a crucial second messenger that modulates various signal transduction pathways, including those involving protein kinases and phosphatases (Kambe et al., 2015). Maintaining the homeostasis of this pool is essential, as it influences gene expression, cell proliferation, and programmed cell death. In pathological states such as Alzheimer's disease, the redistribution of zinc from this pool can lead to the formation of amyloid plaques, while in certain cancers, a significant depletion of intracellular zinc is often observed (Adlard et al., 2008). Therapeutic strategies targeting the intracellular zinc pool utilize ionophores to facilitate zinc entry into cells or chelators to remove toxic excess ions, thereby restoring physiological balance and potentially treating neurodegenerative and metabolic disorders.
Modulation of intracellular zinc concentration through ionophoric transport, chelation, or redistribution to restore homeostasis or trigger zinc-dependent signaling pathways (Maret, 2017).
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