Effect of Parathyroid Hormone on the Uptake of Orally Administered Cadmium

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Abstract
The uptake of Cd and thus its toxic effects are enhanced when the level of Ca in the diet is low. An increase in intestinal Ca-binding protein (CaBP) activity, due to Ca restriction is apparently responsible for this increased Cd absorption. Male thyroparathyroidectomized (TPX) rats were fed purified diets with low (0.1%) Ca and deionized water ad lib. Each rat received 8.4 mg Ca (as calcium gluconate, s.c.) every 12 h. After 48 h, 11 TPX rats received 20 units of PTH (s.c.) every 12 h instead of the Ca injections. After another 48 h each rat received 3 .mu.Ci 115mCd Cl2 (carrier free) by stomach tube and were killed 24 h later. The liver and kidneys were dry ashed and the 115mCd content determined by liquid scintillation counting. Those rats that received PTH exhibited a 2-fold increase (P < 0.01) in 115mCd uptake in both liver and kidney. PTH did not elevate the serum Ca concentration. It is not likely that the PTH effect involves Cd reabsorption by the kidney since virtually no radioactivity is detected in the urine of rats given oral 109Cd. The enhanced Cd accumulation in tissue in animals fed a low Ca diet is the result of enhanced Cd absorption by the intestine. The signal that activates this metabolic response appears to involve PTH which supports an involvement of CaBP in Cd uptake during dietary Ca restriction.

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