Molybdenum is an essential trace element for virtually all life forms. It functions as a cofactor for a number of enzymes that catalyze important chemical transformations in the global carbon, nitrogen, and sulfur cycles. Thus, molybdenum-dependent enzymes are not only required for human health, but also for the health of our ecosystem.


The biological form of molybdenum, present in almost all molybdenum-containing enzymes (molybdoenzymes), is an organic molecule known as the molybdenum cofactor. In humans, molybdenum is known to function as a cofactor for three enzymes:

* Sulfite oxidase catalyzes the transformation of sulfite to sulfate, a reaction that is necessary for the metabolism of sulfur-containing amino acids (methionine and cysteine).

* Xanthine oxidase catalyzes the breakdown of nucleotides (precursors to DNA and RNA) to form uric acid, which contributes to the plasma antioxidant capacity of the blood.

* Aldehyde oxidase and xanthine oxidase catalyze hydroxylation reactions that involve a number of different molecules with similar chemical structures. Xanthine oxidase and aldehyde oxidase also play a role in the metabolism of drugs and toxins.

Of these three enzymes, only sulfite oxidase is known to be crucial for human health.

Nutrient Interactions


Excess dietary molybdenum has been found to result in copper deficiency in grazing animals (ruminants). In ruminants, the formation of compounds containing sulfur and molybdenum, known as thiomolybdates, appears to prevent the absorption of copper. This interaction between thiomolybdates and copper does not occur to a significant degree in humans. One early study reported that molybdenum intakes of 500 mcg/day and 1,500 mcg/day from sorghum increased urinary copper excretion. However, the results of a more recent, well-controlled study indicated that very high dietary molybdenum intakes (up to 1,500 mcg/day) did not adversely affect copper nutritional status in eight, healthy young men.


Dietary molybdenum deficiency has never been observed in healthy people. The only documented case of acquired molybdenum deficiency occurred in a patient with Crohn's disease on long-term total parenteral nutrition (TPN) without molybdenum added to the TPN solution. The patient developed rapid heart and respiratory rates, headache, night blindness, and ultimately became comatose. He also demonstrated biochemical signs of molybdenum deficiency, including low plasma uric acid levels, decreased urinary excretion of uric acid and sulfate, and increased urinary excretion of sulfite. Thus, the patient was diagnosed with defects in uric acid production and sulfur amino acid metabolism. The patient's clinical condition improved and the amino acid intolerance disappeared when the TPN solution was discontinued and instead supplemented with molybdenum (160 mcg/day).

Current understanding of the essentiality of molybdenum in humans is based largely on the study of individuals with very rare inborn errors of metabolism that result in a deficiency of the molybdoenzyme, sulfite oxidase. Two forms of sulfite oxidase deficiency have been identified:

* Isolated sulfite oxidase deficiency: only sulfite oxidase activity is affected.
* Molybdenum cofactor deficiency: the activities of all three molybdoenzymes are affected.

Because molybdenum functions only in the form of the molybdenum cofactor in humans, any disturbance of molybdenum cofactor metabolism can disrupt the function of all molybdoenzymes. Together, molybdenum cofactor deficiency and isolated sulfite oxidase deficiency have been diagnosed in more than 100 individuals worldwide. Both disorders result from recessive traits, meaning that only individuals who inherit two copies of the abnormal gene (one from each parent) develop the disease. Individuals who inherit only one copy of the abnormal gene are known as carriers of the trait but do not exhibit any symptoms. The symptoms of isolated sulfite oxidase deficiency and molybdenum cofactor deficiency are identical and usually include severe brain damage, which appears to be due to the loss of sulfite oxidase activity. At present, it is not clear whether the neurologic effects are a result of the accumulation of a toxic metabolite, such as sulfite, or inadequate sulfate production. Isolated sulfite oxidase deficiency and molybdenum cofactor deficiency can be diagnosed relatively early in pregnancy (10-14 weeks' of gestation) through chorionic villus sampling, and in some cases, carriers of molybdenum cofactor deficiency can be identified through genetic testing. No cure is presently available for either disorder, although anti-seizure medications and dietary restriction of sulfur-containing amino acids may be beneficial in some cases.

The Recommended Dietary Allowance (RDA)

The recommended dietary allowance (RDA) for molybdenum was most recently revised in January 2001. It was based on the results of nutritional balance studies conducted in eight, healthy young men under controlled laboratory conditions. The RDA values for molybdenum are listed in the table below in micrograms (mcg)/day by age and gender. Adequate intake (AI) levels were set for infants based on mean molybdenum intake from human milk, exclusively.

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