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Copper-Molybdenum Antagonism

High levels of molybdenum can interfere with the body's uptake of copper, producing copper deficiency. Molybdenum prevents plasma proteins from binding to copper, and it also increases the amount of copper that is excreted in urine. Ruminants that consume high amounts of molybdenum develop symptoms including diarrhea, stunted growth, anemia and achromotrichia (loss of hair pigment). These symptoms can be alleviated by the administration of more copper into the system, both in dietary form and by injection. The condition, as an effective copper deficiency, can be aggravated by excess sulfur.

Copper reduction or deficiency can also be deliberately induced for therapeutic purposes by the compound ammonium tetrathiomolybdate, in which the bright red anion tetrathiomolybdate is the copper-chelating agent. Tetrathiomolybdate was first used therapeutically in the treatment of copper toxicosis in animals. It was then introduced as a treatment in Wilson's disease, a hereditary copper metabolism disorder in humans; it acts both by competing with copper absorption in the bowel and by increasing excretion. It has also been found to have an inhibitory effect on angiogenesis, potentially via the inhibition of copper ion dependent membrane translocation process involving a non-classical secretion pathway.[81] This makes it an interesting investigatory treatment for cancer, age-related macular degeneration, and other diseases featuring excessive blood vessel deposition.

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