Ando M, Shimizu M, Matsui S, Sayato Y, Takeda M
Toxicol Appl Pharmacol. 1987 Jun 30;89(2):158-64. doi: 10.1016/0041-008x(87)90036-6.
In order to obtain further information on the effects of cadmium (Cd) on the mechanism of activation of vitamin D3 in the kidney, the serum concentrations of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] and 24,25-dihydroxycholecalciferol [24,25(OH)2D3] were determined by radioimmunoassay techniques. The serum concentration of 1,25(OH)2D3 in Cd-exposed rats was always higher than that in control rats. The concentrations of serum 1,25(OH)2D3 in parathyroidectomized rats (PTX), both in the control and in the Cd-exposed groups, were markedly lower than those in non-PTX rats. On the other hand, the concentration of serum 24,25(OH)2D3 in Cd-exposed rats was less than that in control rats. In other words, the pathway from secretion of parathyroid hormone (PTH) to synthesis of 1,25(OH)2D3 or 24,25(OH)2D3 was normal, but the pathway from stimulation of PTH to secretion of PTH was abnormal. These results suggest that rats exposed to Cd for 90 days were in a state of either deficiency of 1,25(OH)2D3 or excess secretion of parathyroid hormone. Although hypophosphatemia occurred in the Cd-exposed rats, the 1,25(OH)2D3 serum level in rats was not increased by PTX. On the basis of these results, it is suggested that hypophosphatemia occurring after the exposure of rats to Cd is a secondary hypophosphatemia.