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Aluminum ions (Al3+) are non-essential trivalent cations that lack a known physiological role in human biology but represent a significant toxicological target, particularly in individuals with impaired renal function [21, 22]. In the gastrointestinal tract, aluminum absorption is typically low but can be significantly increased by the presence of citrates, which disrupt tight junctions and facilitate paracellular transport [14, 23]. Once in the systemic circulation, aluminum ions primarily bind to transferrin, allowing them to mimic iron and distribute to various tissues, most notably the bone matrix and the central nervous system [4, 19]. Chronic accumulation of aluminum leads to severe clinical manifestations, including dialysis encephalopathy, vitamin D-resistant osteomalacia, and microcytic anemia [6, 11, 12]. Therapeutic management of aluminum overload focuses on the use of chelating agents, such as deferoxamine, which bind the ions to form stable, water-soluble complexes that can be subsequently removed through the kidneys or via dialysis [5, 13, 24]. Monitoring of aluminum levels is critical in high-risk populations, such as those on long-term hemodialysis or receiving parenteral nutrition, to prevent irreversible organ damage [1, 11]. Furthermore, aluminum's interference with essential metal homeostasis and its pro-oxidant activity contribute to its systemic toxicity [4, 21].
Chelation of trivalent aluminum ions to form stable, water-soluble complexes (e.g., aluminoxamine) that are excreted renally or removed via dialysis.
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