Know Your Nutrients: Molybdenum

Molybdenum is an essential trace element required by the human body for daily function. Discovered in 1778 by Swedish chemist Karl Scheele in a mineral known as molybdenite, which was mistakenly believed to be a lead compound, it was later isolated by another Swedish chemist, Peter Jacob Hjelm, in 1781.1,2 Later, in the 1950s, molybdenum necessity for life was established with the discovery of the first molybdenum-containing enzymes.2 

Sources and Requirements

A variety of foods contain molybdenum. Legumes are considered to be the richest source, followed by whole grains, nuts, and beef liver.3,4 Leafy vegetables, bananas, dairy products, and chicken also contain some amount of molybdenum.3,4 Varying but typically low amounts of molybdenum may also be found in drinking water.3

According to the United States (US) National Institutes of Health (NIH) Office of Dietary Supplements, the recommended daily amount of molybdenum for Americans varies according to age from 2μg in those six months of age or younger to 45μg in those 19 years of age or older.4 Pregnant and breastfeeding women require 50μg/day.4 The daily upper limit varies similarly from 300μg in children 1 to 3 years of age to 2,000μg in adults (no daily upper limit has been established for those ≤1 year of age).4 

Molybdenum is also available in supplement form, and research has shown that purified molybdenum is roughly 16-percent more absorbable than molybdenum sources from food.5 

In the Body

A total of four enzymes that require molybdenum for their function have been identified in humans to date. First is the mitochondrial enzyme sulfite oxidase, which catalyzes the oxidation of sulfite to sulfate.6 Sulfite is generated endogenously during the metabolism of sulfur-containing amino acids, such as methionine and cysteine; present as a pollutant in the atmosphere; and used a preservative in some drinks, foods, and medications.6 Another molybdenum-containing enzyme, xanthine oxidase, catalyzes the oxidation of hypoxanthine to xanthine (both of which are produced during the degradation of purines, which are present in varying amounts in different foods) and, further, that of xanthine to uric acid, which is excreted by the kidneys as a waste product in urine.7 The third known molybdenum-containing enzyme, aldehyde oxidase, catalyzes the oxidation of aldehydes into carboxylic acid and the hydroxylation of some heterocycles;8 it thus assists in the metabolism of drug compounds containing aldehydes and nitrogen-containing heterocyclic fragments; foods that naturally contain aldehydes, such as vegetables, spices, and nuts; and foods that yield aldehydes as byproducts, such as alcoholic beverages and fruit juices.8,9 Finally, mitochondrial amidoxime-reducing component, which is the most recently discovered molybdenum-containing enzyme, catalyzes the reduction of nitrogen-hydroxylated structures (e.g., amidoxime prodrugs) in the body.10

Molybdenum is absorbed primarily into the circulation from the gastrointestinal tract.11 It is conserved in the body at low intake levels but is rapidly excreted in the urine when intake is high.12 

In Disease

According to the US NIH Office of Dietary Supplements, molybdenum deficiency is rare in Americans.4 However, individuals may present with molybdenum cofactor deficiency (MoCD), a genetic condition characterized by the body’s inability to process molybdenum. The characteristics of affected individuals vary according to MoCD type. Infants with early-onset or severe MoCD experience seizures, developmental delays, and microcephaly as a result of progressive brain degeneration, often dying during the neonatal period.13 In contrast, late-onset or mild MoCD may be identified only years later (e.g., by an acute neurologic decompensation in the setting of an infection, which may improve after infection or progress during the lifetime).13 Exposure (e.g., occupational) to high levels of molybdenum can lead to aching joints, gout-like symptoms, and high levels of uric acid in the blood.14,15 

Molybdenum plays a role in preventing disease by supporting proper actions of its enzymes. For example, xanthine oxidase, by catalyzing the oxidation of products of purine degradation, helps to prevent a buildup of purines in the body, which can cause gout if retained at high levels.9 Dietary molybdenum has been shown to treat iron-deficiency anemia and may help manage joint pain in arthritis.16 Researchers are also exploring the use of molybdenum compounds for the treatment of other health conditions, such as cancer.17

Editor’s note: Please consult with your primary care practitioner to determine what kind of molybdenum intake is right for you. 

  1. Bhattacharya PT, Misra SR, Hussain M. Nutritional aspects of essential trace elements in oral health and disease: an extensive review. Scientifica (Cairo). 2016;2016:5464373.
  2. Novotny JA, Peterson CA. Molybdenum. Adv Nutr. 2018;9(3):272–273.
  3. United States National Institutes of Health Office of Dietary Supplements. Molybdenum. Fact sheet for health professionals. Accessed 23 Jul 2022.
  4. United States National Institutes of Health Office of Dietary Supplements. Molybdenum. Fact sheet for consumers. Accessed 23 Jul 2022.
  5. Novotny Dura J, Turnlund JR. Molybdenum disposition in humans during molybdenum depletion and repletion. J Nutr. 2006;136:953–957.
  6. Velayutham M, Hemann CF, Cardounel AJ, Zweier JL. Sulfite oxidase activity of cytochrome c: role of hydrogen peroxide. Biochem Biophys Rep. 2016;5:96–104.
  7. Aziz N, Jamil RT. Biochemistry, Xanthine oxidase. [Updated 2021 Aug 1]. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2022.
  8. Montefiori M, Jørgensen FS, Olsencorresponding L. Aldehyde oxidase: reaction mechanism and prediction of site of metabolism. ACS Omega. 2017;2(8):4237–4244.
  9. Sinharoy P, McAllister SL, Vasu M, Gross ER. Environmental aldehyde sources and the health implications of exposure. Adv Exp Med Biol. 2019;1193:35–52.
  10. Krompholz N, Krischkowski C, Reichmann D. The mitochondrial amidoxime reducing component (mARC) is involved in detoxification of N-hydroxylated base analogues. Chem Res Toxicol. 2012;25(11):2443–2450.
  11. Giussani A, Arogunjo AM, Cantone MC. Rates of intestinal absorption of molybdenum in humans. Appl Radiat Isot. 2006;64(6):639–644.
  12. Turnlund JR, Keyes WR, Peiffer GL. Molybdenum absorption, excretion, and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Am J Clin Nutr. 1995;62(4):790–796.
  13. Misko A, Mahtani K, Abbott J, et al. Molybdenum cofactor deficiency. In: Adam MP, Mirzaa GM, Pagon RA, et al., editors. GeneReviews® [Internet]. Seattle, WA: University of Washington, Seattle; 1993–2022. 
  14. Walravens PA, Moure-Eraso R, Solomons CC, et al. Biochemical abnormalities in workers exposed to molybdenum dust. Arch Environ Health. 1979;34(5):302–308.
  15. Seldén AI, Berg NP, Söderbergh A, Bergström BEO. Occupational molybdenum exposure and a gouty electrician. Occup Med (Lond). 2005;55(2):145–148.
  16. Department of Primary Industries and Regional Development, Government of Western Australia. Copper deficiency in sheep and cattle. Accessed 25 Jul 2022.
  17. Grech BJ. Mechanistic insights into the treatment of iron-deficiency anemia and arthritis in humans with dietary molybdenum. Eur J Clin Nutr. 2021;75(8):1170–1175.
  18. Odularu AT, Ajibade PA, Mbese JZ. Impact of molybdenum compounds as anticancer agents. Bioinorg Chem Appl. 2019;2019:6416198.
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Written by

ALIZA BECKER, BA, MPS—Ms. Becker is the managing editor of The Journal of Innovations in Cardiac Rhythm Management. She also works as a freelance editor and as a teaching assistant for the George Washington University’s Master of Professional Studies in Publishing program.   

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