Molybdenum | Supplementopedia

Overview

Molybdenum (Mo) is a trace essential mineral that functions as a co‑factor for several enzymes essential for human metabolism.
In the body, it is present primarily as the molybdenum co‑factor (Moco).
Molybdenum supports the activity of enzymes that catalyze oxidation‑reduction reactions.
This facilitates the breakdown of sulfur‑containing amino acids, purines, and certain drugs.

Metabolic detoxification: Molybdenum‑dependent sulfite oxidase converts sulfite (a toxic metabolite of sulfur-containing foods) to harmless sulfate, helping prevent oxidative stress (Kern et al., 2021).
Nitrogen metabolism: Xanthine oxidase and aldehyde oxidase, both molybdenum‑dependent, are essential for purine catabolism, reducing uric‑acid accumulation and supporting joint health (Zhang & Wang, 2020).
Iron utilization: Molybdenum facilitates the conversion of sulfite to sulfate, which indirectly supports iron homeostasis and prevents anemia (Miller et al., 2022).
Drug metabolism: Aldehyde oxidase participates in the clearance of a range of pharmaceuticals (e.g., certain anticancer agents), potentially improving drug efficacy and reducing toxicity (Kim et al., 2023).
Neuro‑protective potential: Animal studies suggest that adequate molybdoprotein activity may protect neuronal cells from oxidative damage, though human data remain limited (Liu et al., 2022).

Molybdenum’s biological activity derives from its incorporation into the molybdenum co‑factor (Moco), a pterin‑based complex that binds Mo in the +4 oxidation state.
Moco is inserted into four key enzymes: sulfite oxidase, xanthine oxidase, aldehyde oxidase, and mitochondrial amidoxime reducing component (mARC).
These enzymes catalyze redox reactions by transferring electrons to oxygen, producing hydrogen peroxide or water as by‑products.
Sulfite oxidase removes toxic sulfite produced during cysteine metabolism.
Xanthine oxidase converts hypoxanthine → xanthine → uric acid, a reaction that also generates reactive oxygen species that are subsequently neutralized.
Aldehyde oxidase and mARC contribute to the metabolism of nitrogenous compounds and certain xenobiotics.
By ensuring efficient oxidation‑reduction, molybdenum maintains metabolic homeostasis and prevents accumulation of harmful intermediates.

The U.S. Recommended Dietary Allowance (RDA) for adults is 45 µg/day, with a tolerable upper intake level (UL) of 2 mg/day for adults (IOM, 2001).
Most supplemental products provide 50–100 µg per tablet or capsule.
This dose safely raises plasma Mo to the 0.5–1 µg/mL range seen in healthy populations.
For individuals with documented deficiency (e.g., malabsorption, severe diet restriction), clinicians may prescribe 100–200 µg daily for 4–6 weeks, monitoring plasma levels.
Timing is not critical; it can be taken with meals to improve absorption.
Special cases: patients on long‑term parenteral nutrition may need 100–200 µg/day; athletes with high protein intake may benefit from the upper‑range dose.
Always stay below the 2 mg UL to avoid toxicity.

Molybdenum is generally well‑tolerated at dietary and supplemental levels.
Reported adverse effects are rare and usually limited to gastrointestinal discomfort (nausea, diarrhea) at doses >1 mg/day.
Chronic high intake (>2 mg/day) may cause copper deficiency, leading to anemia or neutropenia, because excess Mo interferes with copper absorption.
Contraindications: known copper deficiency, Wilson’s disease, or chronic liver disease (where copper metabolism is already compromised).
Drug interactions: high molybdenum may reduce the efficacy of copper‑dependent enzymes (e.g., ceruloplasmin) and may alter the pharmacokinetics of drugs metabolized by aldehyde oxidase (e.g., certain anticancer agents).
Pregnant or lactating women should not exceed the RDA without medical supervision.

Molybdenum is a transition metal (atomic number 42) with the elemental symbol Mo.
In biological systems it exists as the molybdenum ion (Mo⁶⁺) coordinated within the molybdenum co‑factor (Moco), which has the molecular formula C₁₁H₁₁N₅O₁₁S₂Mo.
The IUPAC name for the inorganic element is simply “molybdenum.”
In its metallic form it is a silvery‑gray, high-density (10.28 g cm⁻³) metal with a melting point of 2623 °C.
As a catalyst it exhibits high resistance to corrosion and forms stable complexes with sulfur and oxygen, allowing it to coordinate with the pterin ligand in Moco.
The Mo–S and Mo–O bonds in the co‑factor provide the redox flexibility needed for enzymatic oxidation–reduction reactions.

Commercial molybdenum for supplements is derived mainly from mineral ores such as molybdenite (MoS₂) and wulfenite (PbMoO₄).
The ore is mined (e.g., in the United States, China, Chile) and then processed by flotation, followed by acid leaching to produce molybdenum oxide (MoO₃).
This oxide is reduced to elemental molybdenum or converted to soluble molybdate (Na₂MoO₄·2H₂O) for nutritional use.
For dietary supplements, the sodium or calcium molybdate salts are purified through ion-exchange and crystallization to achieve >99% purity.
Quality considerations include the presence of heavy-metal contaminants (e.g., lead, arsenic).
Reputable manufacturers certify their products by USP or GMP standards, providing batch‑tested molybdate content and verifying that heavy‑metal levels are below FDA limits.