BACKGROUND: Developments in accelerator mass spectrometry (AMS) now permit
the determination of femtogram amounts of 26Al in blood and in various
tissues with good precision and free of external contamination. METHODS: In
the present study we used trace quantities of 26Al 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 26Al were administered to six animals in each group
and, subsequently, 24-h post-load 26Al was analysed in serum, urine, bone,
liver, and spleen by means of AMS. RESULTS: Serum concentrations of 26Al
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 26Al in
uraemia. The target tissues of cellular transferrin-mediated 26Al uptake,
liver and spleen, 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, 26Al concentrations were more
elevated in uraemia (1.22 +/- 0.59 pg/g vs C: 0.68 +/- 0.30 pg/g).
Estimated total 26Al 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 26Al 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 26Al
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.
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