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Aluminium is a non-essential trivalent metal cation that lacks a known physiological role in the human body but is ubiquitous in the environment and medical products (Exley, 2011). It is commonly encountered in clinical practice as an active component of antacids, a phosphate binder in renal failure, and an adjuvant in various vaccines to stimulate the immune system (Moraes et al., 2011). Despite its utility, aluminium is a potent neurotoxin and bone toxin, particularly in individuals with compromised renal function who cannot effectively excrete the metal (Yokel, 2002). It interferes with essential biological processes by mimicking other metal ions like iron and calcium, leading to oxidative stress, disrupted enzyme activity, and the formation of amyloid-like aggregates (Walton, 2014). Chronic exposure has been linked to dialysis encephalopathy, osteomalacia, and is a suspected factor in the pathogenesis of Alzheimer's disease (Kawahara & Kato-Negishi, 2011). Therapeutic intervention for aluminium overload typically involves chelation therapy with agents such as deferoxamine, which bind the metal to facilitate its elimination (Yokel, 2002).
The primary mechanism for drugs targeting aluminium is chelation, where agents like deferoxamine bind to trivalent aluminium ions (Al3+) to form stable, water-soluble complexes that are subsequently excreted by the kidneys or bile (Yokel, 2002).
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