Background. Developments in accelerator mass spectrometry (AMS) now permit the determination of femtogram amounts of Al-26 in blood and in various tissues with good precision and free of external contamination. Methods. In the present study we used trace quantities of Al-26 to investigate the intestinal absorption and compartmentalization of aluminium in rats with renal failure (Nx, 5/6 nephrectomy) and in pair-fed controls (C). Single oral doses of 20 ng Al-26 were administered to six animals in each group and, subsequently, 24-h post-load Al-26 was analysed in serum, urine, bone, liver, and spleen by means of AMS. Results. Serum concentrations of Al-26 were significantly lower in uraemic rats compared to controls, whereas urinary excretion was comparable (Nx, 7.11 +/- 5.78 pg/day vs C, 9.46 +/- 6.10 pg/day), suggesting a higher fraction of ultrafiltrable serum Al-26 in uraemia. The target tissues of cellular transferrin-mediated Al-26 uptake, liver and sleen, tended to show a larger degree of aluminium accumulation in controls (0.26 +/- 0.31 pg/g vs Nx, 0.14 +/- 0.10 pg/g and 0.37 +/- 0.27 pg/g vs Nx, 0.25+/- 0.27 pg/g respectively). In contrast, in bone, a site of extracellular aluminium deposition, Al-26 concentrations were more elevated in uraemia (1.22 +/- 0.59 pg/g vs C: 0.68 +/- 0.30 pg/g). Estimated total Al-26 accumulation in all measured target tissues was significantly higher in uraemic rats (28.15 +/- 9.90 pg vs C: 17.03 +/- 7.03 pg) and total recovery of Al-26 from tissue and urine was 26.58 +/- 6.74 pg in controls and 35.75 +/- 7.03 pg in uraemic animals, suggesting a fractional absorption of 0.133% and 0.175% respectively. Conclusions. Our data suggest that fractional absorption from a dietary level dose of Al-26 is about 0.13%. Compartmentalization occurs in transferrin-dependent target tissues such as liver and spleen; however, in quantitative terms extracellular deposition in bone is more important. Uraemia has a significant effect on the intestinal absorption and compartmentalization of aluminium. It enhances fractional absorption and increases subsequent extracellular deposition of aluminium in bone. However, at the same time uraemia does not increase transferrin-dependent cellular accumulation of aluminium in liver and spleen.
