Bile is an important route of elimination of ingested aluminum by conscious male Sprague-Dawley rats.

We assessed the importance of bile as an excretory route for ingested aluminum (AI). Bile dusts in 30 male Sprague-Dawley rats were cannulated to allow both bile collection and reinfusion of bile acids. Five days after surgery, rats (average weight = 191 +/- 4 g) were given a single oral dose of aluminum (0, 0.2, 0.4, or 0.8 mmol) as aluminum lactate in 1 ml of 16% citrate by gavage. Bile was collected 1-7 h after dosing from unanesthetized rats. Biliary aluminum secretion was highest during the first hour of bile collection. All rats dosed with aluminum secreted significantly greater amounts of aluminum in bile than control rats. However, biliary aluminum secretion did not vary among animals given the different aluminum doses suggesting that biliary secretion of aluminum was saturated at these doses. Rats dosed with 0.8 mmol A1 retained significantly greater amounts of aluminum in soft tissues than those given 0.2 or 0.4 mmol A1. This result suggests that physiological were unable to prevent tissue aluminum accumulation in the rats given the highest dose.

Biliary manganese excretion in conscious rats is affected by acute and chronic manganese intake but not by dietary fat.

We hypothesized that biliary excretion of manganese would be sensitive to acute and chronic variations in manganese and fat intakes. In the acute study, we gavaged rats with solutions containing 54Mn with either 0, 0.2, 1 or 10 mg Mn as MnCl2. We collected bile from unanesthesized rats that were simultaneously reinfused with bile acids. Total manganese excretion (from 0.5 to 6.5 h after dosing) was proportional to the acute doses (approximately 3.4% of doses). In the chronic study, weanling rats were fed diets containing 5 or 20 g corn oil/g diet and 0.49 or 72 micrograms Mn/g diet for 8 wk and then deprived of food for 12 h before bile collection. Manganese-deficient animals excreted only 0.7% as much manganese in bile as manganese-replete animals, but this reduction was not sufficient to prevent 50-80% reduction of tissue manganese concentrations. Moreover, biliary manganese excretion (calculated for 24 h) by both manganese-deficient and manganese-replete rats (deprived of food for previous 12 h) accounted for only 1% of their manganese intake on the previous day. Dietary fat and manganese concentrations had few effects on excretion of total or individual bile acids. Ours is the first report of biliary excretion of orally administered manganese by conscious rats.

Tissue aluminium distribution in growing, mature and ageing rats: relationship to changes in gut, kidney and bone metabolism.

The purpose of this study was to determine whether accumulation and turnover of aluminium differed among growing (2 month old), mature (8 month old) and ageing (19 month old) rats and assess whether these differences could be ascribed to physiological changes with age. One day after a large oral dose (0.8 mmol Al in 0.75 M citrate) growing rats had the highest concentrations of aluminium in tibias, whereas ageing rats had the highest concentrations of aluminium in kidneys. The half-life of aluminium in tibias (38 v. 58 v. 173 days in growing, mature and ageing rats, respectively) and kidneys (9 v. 12 v. 16 days) lengthened with age. According to stepwise multiple regression analysis, 73% variation in tibia aluminium concentrations was explained by final body weight of rats, length of time after dosing, tibia weights, haematocrits, urinary hydroxyproline excretion, ulna calcium concentrations, and urinary creatinine excretion but 57% variation in kidney aluminium concentrations was explained by length of time after dosing and feed intake. Although age, per se, was a significant predictor of spleen and liver aluminium concentrations, the measured changes in gut, kidney, bone and mineral metabolism were less predictive of aluminium concentrations in livers and spleens than in bone.

Comparison of tissue retention of aluminum and Ga-67: effects of iron status in rats.

The purposes of this study were to separate the effect of iron status from the effect of acute iron intake on tissue retention of aluminum and Ga-67 and to evaluate Ga-67 as a marker for aluminum. Anemic and control rats were dosed by gavage with a citrate solution containing 20 microCi Ga-67 with no added aluminum and iron (Gavage Ga-67), with 0.8 mmol aluminum (Gavage Al), with 0.8 mmol iron (Gavage Fe), or with both 0.8 mmol aluminum and 0.8 mmol iron (Gavage Fe and Al). After 24 h, anemic rats in the Gavage Al treatment had lower concentrations of aluminum in their tibias, kidneys, and spleens than control rats in that treatment. In contrast, anemic rats dosed with only Ga-67 (Gavage Ga-67 treatment) had lower concentrations of Ga-67 in their tibias and kidneys, but greater concentrations of Ga-67 in their livers and spleens than control rats in that treatment. The single dose of iron had no effect on tissue aluminum concentrations but depressed tissue Ga-67 concentrations. All rats accumulated aluminum predominantly in bone and control rats accumulated Ga-67 predominantly in bone, but anemic rats accumulated Ga-67 predominantly in liver. A major limitation of Ga-67 as a marker for aluminum is its greater sensitivity than aluminum to iron intake and status.