The influence of molybdenum and lead intoxication on the mineral content of the femur, blood calcium level and its excretion with the urine in rats with hypo- and hypercalcaemia was studied. It is shown that metal intragastric administration in experimental hypoparathyroidism contributes to less pronounced changes in calcium metabolism. Calcitonin hypocalcaemia and experimental hypervitaminosis D in combination with intragastric metal receipt increase its bone accumulation and induce decalcification, markedly affect the calcium excretion and blood calcium content. For parenteral metal intake in rats with hypocalcaemia calcium metabolism is disturbed to a greater extent. Experimental hypercalcaemia has a protective effect on the development of symptoms of molybdenum and lead intoxication
