Generation of hypophosphatemia in rats by continuous oral administration of cadmium.
To obtain further information on the negative calcium balance caused by cadmium (Cd), the factors associated with serum calcium and phosphorus homeostasis other than inhibition of intestinal calcium absorption were studied by using parathyroid hormone (PTH) and 1 alpha-hydroxycholecalciferol (1 alpha-OH-D3). In rats exposed to Cd for 30 or 90 days, the concentrations of serum calcium after treatment with PTH, parathyroidectomy (PTX) or 1 alpha-OH-D3 showed almost the same patterns as those of control animals. It was considered that the mechanism of regulation of calcium in Cd-exposed rats was normal. The continuous oral administration of Cd generated hypophosphatemia in rats. On the other hand, in 30- and 90-day-treated rats, the low concentration of serum phosphorus caused by Cd was further decreased by administration of PTH, whereas it was increased by PTX. The hypophosphatemia found in rats exposed to Cd for 30 days, but not for 90 days, was reversed by treatment with 1 alpha-OH-D3. From these results, it was concluded that the hypophosphatemia caused by long term oral administration of Cd resulted from secondary hyperparathyroidism, due to inhibited calcium absorption from the intestine, as was demonstrated previously.
Ando
M
M
National Institute of Hygienic Sciences, Tokyo, Japan.
Matsui
S
S
Jinno
H
H
Sayato
Y
Y
Takeda
M
M
D000284:Administration, Oral; D000818:Animals; D002104:Cadmium / Q000008:administration & dosage / Q000633:toxicity*; D002118:Calcium / Q000097:blood*; D005260:Female; D006706:Homeostasis / Q000187:drug effects; D006887:Hydroxycholecalciferols / Q000494:pharmacology; D010280:Parathyroid Glands / Q000502:physiology; D010281:Parathyroid Hormone / Q000494:pharmacology; D010710:Phosphates / Q000097:blood*; D051381:Rats; D011919:Rats, Inbred Strains
D006887:Hydroxycholecalciferols; D010281:Parathyroid Hormone; D010710:Phosphates; D002104:Cadmium; D002118:Calcium; C008088:alfacalcidol