Literature regarding the biochemistry of aluminum and eight similar ions is reviewed. Close and hitherto unknown similarities were found. A hypothetical model is presented for the metabolism, based on documented direct observations of Al3+ and analogies from other ions. Main characteristics are low intestinal absorption, rapid urinary excretion, and slow tissue uptake, mostly in skeleton and reticuloendothelial cells. Intracellular Al3+ is probably first confined in the lysosomes but then slowly accumulates in the cell nucleus and chromatin. Large, long-lived cells, e.g., neurons, may be the most liable to this accumulation. In heterochromatin, Al3+ levels can be found comparable to those used in leather tannage. It is proposed that an accumulation may take place at a subcellular level without any significant increase in the corresponding tissue concentration. The possible effects of this accumulation are discussed. As Al3+ is neurotoxic, the brain metabolism is most interesting. The normal and the lethally toxic brain levels of Al3+ are well documented and differ only by a factor of 3-10. The normal brain uptake of Al3+ is estimated from data on intestinal uptake of Al3+ and brain uptake of radionuclides of similar ions administered intravenously. The uptake is very slow, 1 mg in 36 years, and is consistent with an assumption that Al3+ taken up by the brain cannot be eliminated and is therefore accumulated. The possibility that Al3+ may cause or contribute to some specific diseases, most of them related to aging, is discussed with the proposed metabolic picture in mind.

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The serum concentration of α2-macroglobulin and that of haptoglobin, the two main components of the electrophoretic α2fraction, and of α1-antitrypsin were studied in a series of outpatients with diabetes mellitus. In all age groups a significant increase of α2-macroglobulin was noted. In adults the increase showed a significant positive correlation with the duration of the disease and was accentuated in the presence of nephropathy with proteinuria. No further increase was noted in the occurrence of other vascular complications. In adult diabetics haptoglobin and α1-antitrypsin were significantly increased. No correlation was found between the duration of the disease and the concentration of haptoglobin or α1-antitrypsin. Neither haptoglobin nor α1-antitrypsin were increased in diabetic children. It is proposed that the concentration of α2-macroglobulin is more related to diabetes mellitus per se than that of haptoglobin or α1-antitrypsin, which are increased most in response to complications with inflammatory reaction.