Biokinetics of Aluminum in Blood

The biochemistry of aluminum is, to a large extent, determined by its valency, ion size, and redox chemistry. The effective ionic radius of Al3+ is 54 pm. This is sufficiently similar to that of Fe3+ (65 pm) for it to follow some of its metabolic pathways.

However, its progress through these is halted at stages where iron is transformed to its divalent, Fe2+ state. Aluminum is also sufficiently similar to calcium to codeposit in the skeleton. In addition, aluminum binds particularly strongly to phosfates, giving it the potential to bind with DNA, ATP, and many other biomolecules.

Within the blood, transferrin, the iron-transport protein, binds aluminum most avidly. However, compared to Fe3+ ions, the strength of this affinity is low. Consequently, aluminum will not displace iron from transferrin. Aluminum also binds with low-molecular-weight proteins and citrate. Aluminum complexes with low-molecular-weight species may leak from blood vessels into surrounding tissue fluids. The extent of binding to low-molecular-weight molecules is uncertain, but studies indicate that 50% or less of blood aluminum may be bound to them. It has also been suggested that silicic acid in blood may also bind aluminum to form aluminosili-cate colloidal particles, which would then deposit within reticuloendothelial organs.

Aluminum is initially rapidly lost from the blood to other body fluids and to excretion, reflecting the weakness/kinetics of the binding of the Al3+ ion to proteins. Subsequently, the rate of loss slows. Volunteer studies showed that more than half of the ion had left the blood by 15 minutes postadministration, and that by 1 h an average of 68% had been lost. At 1 day, approximately 2% remained in the blood and by 5 days only 0.4% remained. These variations make the interpretation of isolated blood and serum aluminum levels particularly difficult. At 1 h after uptake, little or no aluminum in the blood is associated with red blood cells. However, at 880 days after intake 14% is associated with these cells. Unlike those in plasma, aluminum deposits in red blood cells are cleared with a long half-life and they may provide a basis for an aluminum assay.

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