Both copper and molybdenum influence the internal transport and release of iron. There is evidence that copper, as a component of ceruloplasmin, increases the rate of oxidation of ferrous to ferric iron for transport by plasma transferrin; and that molybdenum, as a component of xanthine oxidase, participates in the reduction of cellular ferric to ferrous ferritin.
An excess of either copper or molybdenum, by giving rise to a relatively undissociable Cu-Mo-S complex, may produce a deficit of the metal in marginal supply. As dietary excess of copper is known to be common in the United States, and preliminary data suggest that molybdenum intake may not be optimal, it is possible that a conditioned deficit of molybdenum may contribute to abnormalities of iron metabolism and utilization.
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