Balance and Tissue Distribution of Vanadium after Short-Term Ingestion of Vanadate

Forty-six female Sprague-Dawley rats (170–200 g) were randomly assigned to one of six treatment groups receiving 0.1, 5.0, or 25.0 ppm dietary vanadium with either normal (0.13 mEq/g) or high (1.82 mEq/g) dietary potassium. Supplemental vanadium was administered as sodium metavanadate. These diets were fed for 2 weeks, and all feces and urine collected. At the end of the treatment period, brain, liver, renal cortex and medulla, whole blood, and plasma were obtained and analyzed for vanadium by atomic absorption spectrophotometry, as were the urine and feces samples. Tissue vanadium concentrations increased significantly (P< 0.00001) with increasing food vanadium content, but were not affected by dietary potassium in spite of the polyuria induced in animals on the high potassium diets. The highest vanadium concentrations were found in the renal cortex and the lowest in the brain. Although urinary vanadium excretion was higher in animals fed the high potassium diets, a relatively small percentage of ingested vanadium was excreted in the urine. Rats fed diets containing no supplementa sodium metavanadate (0.1 ppm vanadium) were in negative vanadium balance, but their growth was not inhibited. Animals receiving 5.0 and 25.0 ppm vanadium diets retained 39.7 ± 18.5% of ingested vanadium and excreted 59.1 ± 18.8% of ingested vanadium in the feces. These values indicate greater absorption and retention of ingested vanadium than found in previously reported investigations.