Although molybdenum is an essential mineral, no known deficiencies have been reported in humans at the time of writing. However, molybdenum cofactor deficiency has been identified in a large number of patients. A diet low in sulfur amino acids can be therapeutic. Molybdenum cofactor deficiency results in the loss of 2 molybdenum-dependent enzymes, namely sulfate oxidase and xanthine dehydrogenase.
The exact mechanism by which molybdenum prevents copper toxicity is poorly understood. However, it is known that an insoluble complex of copper and molybdenum can be formed in the gastrointestinal tract thus reducing copper absorption. This theory is substantiated by the fact that increasing dietary copper is an effective treatment of molybdenum toxicity.
Xanthine oxidase, the enzyme that immediately produces uric acid, uses molybdenum as a cofactor. Molybdenum is known to raise uric acid levels, which is why people with gout (a condition of elevated high uric acid levels) are told to avoid molybdenum supplements.
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