Aluminum, present in our drinking water as hydroxide or sulfate, is limited by solubility to 2.5 mg/liter at pH 7.0. This study was carried out to determine if aluminum at doses typically found in drinking water would accumulate in rat tissues if a ligand such as citrate at neutral or acid pH is coadministered, or in the absence of citrate at acid pH. Al(OH)3 or AlCl3 was given ad libitum in drinking water to male Sprague-Dawley rats at 0, 0.1, 2.0, or 100 mg/liter, in 4 mm acetate, pH 3.2 (A), 4 mm citrate, pH 2.6 (C), 4 mm citrate, pH 7.0 (7C), or distilled water, pH 7.0 (W). After 10 weeks, rats were killed and tissues were wet-ashed in nitric acid for determination of aluminum by flameless atomic absorption. Copper, iron, and zinc were determined by flame atomic absorption. Metal ion concentrations in tibia, brain, liver, blood, and kidney did not differ significantly between treatment groups. Aluminum accumulated in intestinal cells of all 100 mg Al/liter rats, with the C group accumulating more aluminum than the A or W groups. In the C group, intestinal aluminum content increased significantly in a dose-dependent manner. Intestinal iron was decreased significantly in all the 100 mg Al/liter groups. Intestinal copper was decreased in the W group at 100 mg Al/liter, with a trend toward a decrease in A and C groups. We conclude that at these low levels studied, aluminum accumulates in intestinal tissue, and that this accumulation is enhanced by citrate ligand. At 100 mg Al/liter, intestinal iron accumulation is decreased, and copper accumulation is marginally decreased.
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