Persistent aluminum accumulation after prolonged systemic aluminum exposure.

To determine the distribution of aluminum (A1) following systemic exposure, female New Zealand white rabbits were given 20 subcutaneous injections, over 4 weeks, of 0, 25, 50, 100, 200, or 400 μmol A1/kg/injection, as the lactate salt. They were sacrificed 5 weeks after completion of injections and selected tissues removed for graphite furnace atomic absorption analysis of tissue A1 content. Rabbits not receiving A1 injections had mean tissue A1 concentrations ranging from 1.5-7.4 μg/g. Bone was higher, 18.7 μg/g. All tissues, except for muscle, demonstrated an increase in A1 concentration correlating with the A1 exposure. After 400 μmol A1/kg/injection for 20 injections, tissue A1 concentrations were: bone 90, heart 12, kidney-cortex 1290, kidney-medulla 245, liver 246, lung 19, and spleen 465 μg A1/g. The average of the 5 central nervous system regions sampled (frontal grey, white, hippocampus, cerebellum, and spinal cord) rose 53% over controls. Determination of A1 in kidney, liver, or bone may be useful in diagnosis of A1 overload conditions in humans (dialysis encepthalopathy, dialysis osteomalacia, and parenteral nutrition-associated osteomalacia). The rabbit appears to be a useful model to further study A1 intoxication syndromes.