鉛中毒ラット肝におけるカルシウム蓄積の機構について

概要

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This experiment was attempted to determine whether the increased liver calcium accumulation induced by lead administration is caused by thyrocalcitonin. Lead acetate solution of 20 mg Pb/100 g body weight was administered intraperitoneally 2 hr after thyroparathyroidectomy. After 36 hr, thyrocalcitonin of 80 MRC mU/100 g was administered subcutaneously 5 times at 3 hr intervals, and 2.0 mg calcium/100 g were administered intraperitoneally 4 times at 4 hr intervals. Rats were sacrificed 1 hr after the last injection. Control injections consisted of sterile distilled water and calcium. The calcium concentration in tha serum and liver was determined by atomic absorption spectrophotometry. In lead-treated intact rats, thyrocalcitonin significantly increased liver calcium concentration, while serum calcium decreased significantly. Thyroparathyroidectomy markedly reduced the rise in liver calcium concentration induced by lead. Calcium injection to thyroparathyroidectomized and lead-treated rats did not significantly increase liver calcium compared to that of noninjected rats. However, after an additional thyrocalcitonin injection, liver calcium concentration became 70% of that of lead-treated intact rats. These results demonstrate that liver calcium accumulation induced by lead administration is caused by the endogenous thyrocalcitonin.
公益社団法人日本薬学会の論文
1975-04-30