Zinc-induced hypocalcemia and bone resorption in rats.
The changes of calcium levels in serum and in the femur were examined in rats administered oral doses of zinc sulfate (0.1, 1.0, and 10 mg Zn/100 g body weight) for 3 days. All doses of zinc caused significant decreases in calcium levels in serum and in the femoral diaphysis and epiphysis. The decrease in these femoral calcium levels was seen 1 day after administration of zinc (10 mg/100 g). Furthermore, time course studies of the effect of zinc administration showed that, at 1 hr after zinc administration, calcium levels in serum and in femoral epiphysis but not in diaphysis were significantly decreased. In thyroparathyroidectomized rats, however, no significant decrease of the epiphyseal calcium was observed by administration of zinc (10 mg Zn/100 g), but the serum calcium level was significantly lowered. Zinc administration to intact rats caused a significant increase in acid phosphatase activity in the femoral epiphysis but not in the diaphysis. This increase was clearly prevented by thyroparathyroidectomy. Accumulations of zinc in the femoral epiphysis and diaphysis after zinc administration was not significantly altered by thyroparathyroidectomy. These results suggest that zinc-induced hypocalcemia may cause bone resorption which is primarily mediated by the action of the parathyroid hormone and it is related to calcium homeostasis in rats.