Inhibition by Magnesium and Calcium Acetates of Lead Subacetate- and Nickel Acetate-induced Lung Tumors in Strain A Mice1

The ability of the physiologically essential divalent metals calcium and magnesium to inhibit the tumorigenic activities of lead and nickel towards the lungs of strain A mice was investi gated. The tumorigenic salts lead(ll) subacetate and nickel(ll) acetate were injected i.p. at their maximal tolerated doses (0.04 mmol/kg/injection of each metal) for a total of 24 injections, whenever possible. Calcium(ll) acetate and magnesium(ll) ace tate were administered in the same preparation along with the lead and nickel salts at molar doses of approximately 1,3, 10, and 30 times the maximal tolerated dose of the tumorigen. The animals were sacrificed 30 weeks after the first injection, and the lung tumors were counted. The lead and nickel salts, admin istered alone, each produced a significant increase in the ob served number of lung adenomas per mouse. When administered with any of the doses of calcium acetate or magnesium acetate tested, neither lead subacetate nor nickel acetate showed any significant tumorigenic activity. Calcium acetate alone (total dose, 11 mmol/kg of body weight) appeared to yield a significant rise in lung adenomas observed. The results indicate an antagonism between magnesium and calcium and the tumorigenic metals nickel and lead.