Molybdenum Deficiency and Tungstate Inhibition Studies

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Abstract
Rats maintained on a purified diet containing approximately 20 µg Mo/kg grew at a normal rate, reproduced, accumulated xanthine oxidase (XO) in tissues other than the intestine, and oxidized xanthine normally. Second and third generation rats had very low levels of tissue XO at weaning, but these increased to relatively normal values on the diet. Feeding a low-molybdenum protein-free diet to adult rats for two to three weeks had little or no effect on the molybdenum content of colon, spleen, lung or skin, but removed one-fourth of the molybdenum normally present in stomach, intestine and kidney, one-half of the molybdenum in muscle and brain, and two-thirds of molybdenum in liver. One-fourth of the molybdenum in normal liver and one-third of the molybdenum remaining after protein depletion was present in the supernatant fraction. Dietary Na2WO4 equivalent to a W:Mo ratio of 100:1 completely inhibited the deposition of intestinal XO and markedly reduced the XO and molybdenum in rat liver. Rats fed Na2WO4 in a 1000 or 2000:1 ratio of W:Mo grew normally and oxidized xanthine to uric acid and allantoin as well as the controls in spite of the fact that all tissues were depleted of molybdenum and XO; the tissue changes were deversed by additional dietary Na2MoO4. Chicks fed synthetic diet containing approximately 20 µg Mo/kg developed normally, but the addition of Na2WO4 at a level equivalent to a W:Mo ratio of 1000 or 2000:1 produced an apparent molybdenum deficiency. Growth rates were depressed somewhat, and mortality was approximately 25% in 5 weeks. All tissue xanthine dehydrogenase and molybdenum concentrations were markedly depleted by the tungstate, and about one-half of the uric acid normally excreted by chicks was replaced by a mixture of xanthine and hypoxanthine. All of the effects of the 1000:1 tungstate level were completely reversed by adding an additional 2 mg molybdenum, as Na2MoO4, per kilogram of diet. The molybdenum removed from the tissues by protein deficiency or tungstate feeding appeared in the urine as a sharp spike in molybdenum excretion; neither diet interfered with the absorption of molybdenum from rat intestine. Neither Na2SO4 nor Na2CrO4 affected the metabolism of molybdenum.