Oral Aluminum Administration to Uremic, Hyperparathyroid, or Vitamin D-Supplemented Rats

Abstract

In the present study, the role of factors was investigated that could possibly lead to changes in plasma and tissue aluminum (A1) concentrations following oral Al exposure. In chronically uremic rats that received an oral A1 supplementation of 150 μmol/g diet during 4 weeks, a significant increase in mean ( ± SEM) liver Al content was observed when compared to sham-operated, pair-fed control rats (9.9 ± 2.0 versus 4.8 ± 0.65 nmol/g wet weight, p < 0.02). No such difference was found in non-A1-supplemented rats. Plasma A1 and the A1 content of other organs studied except muscle were not increased in uremic as compared to control animals. In rats with hyperparathyroidism secondary to a calcium-poor diet, mean liver and bone A1 content was significantly decreased when not A1-exposed (2.5 ± 0.13 and 62 ± 5.5 nmol/g, respectively) and normal when A1-supplemented (4.7 ± 0.59 and 120 ± 23 nmol/g, respectively) as compared to normal control rats without A1 supplementation (5.1 ± 1.5 and 170 ± 17 nmol/g, respectively). However, in the hyperparathyroid rats, mean plasma A1 concentration was higher than in control, euparathyroid rats. In rats with exogenous hyperparathyroidism (parathyroid extract) a significant increase in liver A1 content was observed when compared to control rats (8.1 ± 0.95 versus 5.3 ± 0.53 nmol/g, p < 0.05). In A1-supplemented normal rats treated with 1,25(OH)₂ vitamin D₃ during 4 weeks, liver A1 content was significantly lower than in control rats receiving vehicle solution only (2.9 ± 0.76 versus 5.7 ± 0.59 nmol/g, p < 0.02). In conclusion, chronic renal failure favored liver Al accumulation in orally A1-exposed rats. Endogenous hyperparathyroidism was associated with a decrease but exogenous hyperparathyroidism with an increase in liver and bone A1 content. 1,25(OH)₂ vitamin D₃ administration led to a decrease in hepatic Al accumulation of orally A1-exposed rats.