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 levels of molybdenum suffer from diarrhea, stunted growth, anemia, and achromotrichia (loss of fur pigment). These symptoms can be alleviated by copper supplements, either dietary or injection. The 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 by inhibiting the membrane translocation process that is dependent on copper ions. This is a promising avenue for investigation of treatments for cancer, age-related macular degeneration, and other diseases that involve a pathologic proliferation of blood vessels.
In some grazing livestock, most strongly in cattle, molybdenum excess in the soil of pasturage can produce scours (diarrhea) if the pH of the soil is neutral to alkaline; see teartness.