Aluminum Metabolism

Human exposure to Al is unavoidable through drinking water, pharmacological products, dust, cosmetics, etc., as may be seen in Figure 1.

The metabolism of aluminum is rather complex, though a more precise knowledge becomes possible following the relatively recent utilization of the radioactive isotope 26Al. In spite of its natural abundance, Al accumulates very poorly in living organisms (0.1%) due to the efficient protection of natural physiological barriers (Figure 1), i.e., the cutaneous, respiratory, GI, BBB, bone marrow, etc. barriers [55]. Use of the radiotracer 26Al has led to the basic feature of Al biokinetics/bioavailability being unraveled: Al is predominantly retained in the skeleton, with some deposited in the brain [56]. Following 26Al citrate injection, about 83% of the dose was found to be excreted in the urine and less than 2% in the feces during 13 days; it was noteworthy that the i1/2 of the retained 26Al was 7 years confirming the limited ability of systemic aluminum to be eliminated via the GI tract [57]. Yokel et al. [58] reported that 26Al concentrations in the rat brain were decreased only slightly from 1 to 35 days after systemic 26Al injection, either in the absence or in the presence of the aluminum chelator deferroxamine, suggesting prolonged brain Al retention.

The GI tract is a formidable, but not impervious barrier to the entry of Al, and the metal speciation is of paramount importance in Al uptake and excretion. Physiologically, the pH plays a central role in the solubility of Al compounds, and it is likely that absorption occurs in the acidic medium of the stomach and

Aluminium Metabolism
Figure 1. Metabolic pathways of the absorption and transport of aluminum from the external environment to various compartments (organs and tissues) of the body. The various biological barriers strongly protect from metal ion accumulation that could be detrimental in terms of toxicological impact.

proximal duodenum. Moreover, the combination of aluminum and citrate (which form a neutral complex at pH ~ 5 [15]) considerably enhances the GI absorption of Al [5]. Other factors that affect Al absorption are fluoride and silicon. The former forms stable complexes, apparently decreasing Al excretion; this aspect warrants further studies. Silicon has been proposed to form insoluble compounds with Al, thereby decreasing absorption [59-61], but the clinical evidence is not unambiguous. Feinroth et al. [62] proposed an energy-dependent process for Al absorption through use of an everted gut sac from the rat small intestine; however, whether the GI absorption of Al is related to a concentration gradient of ionized aluminum or to an active transport mechanism, is still rather unclear.

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