Abstract
1. Plasma, urinary, liver and kidney cell aluminium (Al) levels were monitored in the rat, 1h after intravenous administration of 29630 nmol (800 micrograms) Al as either Al chloride or as Al citrate (Al chloride plus excess sodium citrate). Al levels were measured in plasma, urine and liver by atomic absorption spectroscopy (AAS). Liver and kidney Al content was measured at the cellular and subcellular level by electron probe X-ray microanalysis (EPXMA). 2. Urinary excretion of Al was significantly higher (P < 0.01), when Al was given as the citrate than as the chloride. After 1h, plasma Al levels were significantly lower in the Al citrate group than the Al chloride group (59 +/- 3.7 vs 877 +/- 214 nmol ml-1, respectively; P < 0.01). 3. Al concentrations were significantly higher in the livers of rats receiving Al chloride (818 +/- 252 nmol g-1 wet weight; P < 0.05), than in either control or Al citrate groups (122 +/- 41 and 107 +/- 26 nmol g-1 wet weight, respectively). Al concentrations derived from EPXMA measurements were in agreement with AAS values for the three groups, with significantly higher Al concentrations in the Al chloride group (1.7 +/- 0.4 nmol mg-1 dry weight; P < 0.05) than in the control or Al citrate groups, where Al was not detectable. EPXMA analysis showed that Al was distributed in all liver organelles analysed (cytoplasm, mitochondria, nucleus, ER) and was not preferentially taken up by any one organelle in Al chloride treated rats. 4. Significant amounts of Al were found in cytoplasm and mitochondria of proximal tubule cells of rats given Al citrate (0.64 +/- 0.15 and 0.80 +/- 0.11 nmol mg-1 dry weight, respectively), but not in nuclei or lysosomes of these cells. Al levels were not detectable in control kidneys, in proximal tubule cells after Al chloride administration or distal tubule cells after either Al treatment.
Published Version
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