Optimal Result: 0.013 - 0.13 mEq/g creat.

Molybdenum is an essential activator of some important enzymes in the body: sulfite oxidase (catalyzes formation of sulfate from sulfite), xanthine oxidase (formation of uric acid and superoxide ion from xanthine), and aldehyde oxidase (processes aldehydes). Over 50% of absorbed Mo is normally excreted in urine; the remainder is excreted via bile to the feces or is excreted in sweat.

The level of molybdenum in urine may be a transient finding and may not reflect body tissue or liver levels. In copper deficiency, retention of molybdenum is increased (tissue levels could be normal or high), while urine levels might be subnormal. In renal insufficiency, molybdenum (and other elements) can be low in urine. Creatinine clearance and blood metabolite levels should be measured if a renal transport disorder is suspected.


- Carson B.L. et al., Toxicology and Biological Monitoring of Metals in Humans, Lewis Publishers, Chelsea, MI, pp 157-61, 1987.

- Nielson F.H., Chapter 14 in Modern Nutrition in Health and Disease vol 1, 8th ed., Shils, Olson and Shike eds., Lea & Febiger, Phildelphia PA, pp 277-79, 1994.

- Tsalev D.L. and Z.K. Zaprianov, Atomic Absorption Spectrometry in Occupational and Environmental Health Practice, vol. 1, CRC Press, Boca Raton FL, pp 169-73, 1983.

- Smith B.S.W. and H. Wright, ”Effect of Dietary Molybdenum on Copper Metabolism” Clin. Chem. Acta. 62, pp 55-63, 1975.

- Cohen J.J. et al., ”Molecular Basis of the Biological Function of Molybdenum” Proc. Nat. Acad. Sci. 70 no. 2 (Part I), pp 3655-59, 1973.

What does it mean if your Molybdenum result is too low?

Individuals receiving prolonged total parenteral nutrition (”TPN”) may have low body tissue and urine levels of molybdenum because it is occasionally omitted from TPN formulations.

Molybdenum in foods is mostly in soluble complexes, and only a small amount is required daily (100 to 200 micrograms, adults). Therefore, frank molybdenum deficiency is uncommon. However, GI dysfunctions, poor-quality diet, and stressors can combine to produce inadequate molybdenum. Tungsten is a powerful antagonist of molybdenum retention, copper less so. Episodic exposures to high levels of either may result in periods of low Mo excretion that follow prior periods of high Mo excretion. Sulfites, aldehydes and high amounts of purines in the diet may increase need for and retention of molybdenum. Prolonged use of dithiol chelators (DMPS, DMSA) or MSM can result in poor molybdenum status as indicated by low levels in red blood cells.

A multielement hair analysis plus analyses for serum and urine uric acid can be used to confirm or rule out molybdenum insufficiency.

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