Aluminum is a ubiquitous metal with significant toxic potential for humans. It is eliminated principally by the kidney, however the mechanisms involved remain obscure. The purpose of this study was to define and quantify the uptake process for aluminum by incubated slices of rabbit kidney cortex. Time-course experiments demonstrated that aluminum uptake was progressive and substantial, with a slice-to-medium ratio (S/M) exceeding 20 after four hours of incubation of slices in the presence of 0.01 mM aluminum (as the lactate). Concentration-dependent uptake studies suggested that the process was of limited capacity with maximal tissue uptake of approximately 24 micrograms/gm wet wt. Incubation of slices with aluminum in the presence of metabolic inhibitors (NaCN, 2,4-DNP) demonstrated that about 20-35% of the uptake could be attributed to an energy-dependent component. The calcium channel blockers verapamil, diltiazem and lanthanum decreased S/M aluminum by 65-73% compared to control, suggesting that a calcium dependent process plays a role in aluminum accumulation in renal cortex. Aluminum was not acutely toxic to the renal tubular cells even at a medium concentration of 1.0 mM.
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