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molybdate

Also known as: Molybdate, sodium molybdate, molybdenum oxyanion, MoO4^2−

Overview

Molybdate is the bioavailable oxyanion form of molybdenum, an essential trace element vital for human health. It is naturally present in foods like legumes, grains, and leafy vegetables. Primarily, molybdate supplementation is used to prevent or treat molybdenum deficiency, a rare condition typically observed in individuals receiving total parenteral nutrition (TPN) or those with extremely low dietary molybdenum intake. Molybdenum acts as a crucial cofactor for several enzymes, including xanthine oxidase, aldehyde oxidase, sulfite oxidase, and mitochondrial amidoxime reducing component (mARC). These enzymes play significant roles in the metabolism of sulfur amino acids, purines, pyrimidines, and in detoxification processes. While its biochemical role is well-established, clinical research on molybdate supplementation is limited due to the rarity of deficiency, with most evidence stemming from biochemical studies and animal models.

Benefits

The primary benefit of molybdate supplementation is the correction of molybdenum deficiency, which can prevent severe metabolic disturbances caused by impaired enzyme function. This deficiency is exceedingly rare, with only one documented human case, typically occurring in patients on long-term total parenteral nutrition (TPN) or those with specific genetic disorders affecting molybdenum metabolism. For these specific populations, supplementation is clinically significant as it restores the function of critical molybdenum-dependent enzymes. While direct human clinical trials are scarce, the biochemical necessity of molybdenum for enzymes like sulfite oxidase, which detoxifies sulfites, underscores its importance. Animal studies, however, suggest that while essential, excess exposure to sodium molybdate can lead to metabolic disruption, indicating a narrow therapeutic window. The time course for benefits in deficiency correction would typically range from weeks to months, depending on the severity of the deficiency and the dosage administered.

How it works

Molybdate functions as an essential cofactor for several key enzymes in the human body. Once absorbed, it is incorporated into a molybdopterin cofactor, which is then integrated into molybdenum-dependent enzymes. These enzymes, including xanthine oxidase, aldehyde oxidase, sulfite oxidase, and mitochondrial amidoxime reducing component (mARC), catalyze crucial oxidation-reduction reactions. Specifically, sulfite oxidase is vital for the detoxification of sulfites, while xanthine oxidase is involved in purine metabolism. Molybdenum-dependent enzymes collectively regulate the metabolism of sulfur amino acids, purines, pyrimidines, and participate in various detoxification pathways. Molybdate is absorbed passively in the intestine with a high bioavailability ranging from 40% to 100% in adults, although the exact absorption site remains unknown.

Side effects

Molybdate is generally considered safe when consumed at recommended dietary levels. However, excessive intake can lead to adverse effects, though human data on toxicity are limited due to the rarity of high-dose exposure. Animal studies, particularly in mice, have shown that exposure to sodium molybdate at doses relevant to humans (0.01 and 1 mg/kg/day) can cause metabolic disorders, indicating a potential for toxicity at higher concentrations and a narrow safety margin for excess. Common side effects are not well-documented in humans at normal supplemental doses. Rare side effects from excessive intake could include symptoms related to metabolic disruption, but specific clinical manifestations are not clearly established. There are no clearly established contraindications, but caution is advised in patients with pre-existing metabolic disorders. While molybdenum-dependent enzymes metabolize some drugs, specific drug interactions with molybdate supplementation are not well characterized. Special populations, such as those on TPN or with malabsorption, may require careful monitoring and supplementation to prevent deficiency, but also to avoid potential overload.

Dosage

The minimum effective dose of molybdate to prevent deficiency in adults is approximately 20 micrograms per day. Typical optimal dosage ranges in supplements are between 20-40 micrograms daily. Higher doses may be administered under strict medical supervision for specific clinical conditions. The maximum safe dose, or Upper Intake Level (UL), for molybdenum has not been clearly defined for humans, but animal studies suggest that excessive intake can lead to metabolic disruption. Daily dosing is sufficient, and there are no specific timing considerations for supplementation. Sodium molybdate is a commonly used and well-absorbed form in supplements. Absorption can vary with dietary factors, but no specific cofactors are known to be required for its absorption.

FAQs

Is molybdate supplementation necessary for most people?

No, molybdenum deficiency is extremely rare in the general population, making routine supplementation unnecessary for most individuals.

Can molybdate be toxic?

Yes, excessive intake of molybdate can cause metabolic issues, as demonstrated in animal studies, indicating a potential for toxicity at high doses.

How quickly does supplementation work?

The time it takes for supplementation to show effects depends on the severity of the deficiency, but improvements typically occur over several weeks to months.

Are there interactions with medications?

Molybdenum-dependent enzymes metabolize some drugs, but clinical interactions with molybdate supplementation are not well-established or clearly understood.

Research Sources

https://www.mdpi.com/2305-6304/12/4/288 – This experimental study in mice investigated the metabolic effects of sodium molybdate exposure. It found that doses relevant to humans (0.01 and 1 mg/kg/day) caused metabolic disorders, suggesting potential toxicity at higher concentrations. The study highlights the need for caution regarding excessive molybdate intake, despite its limitations as an animal model.
https://archive.hshsl.umaryland.edu/server/api/core/bitstreams/7bee4beb-39fa-4211-9b2d-d866cd4f7d47/content – This comprehensive narrative review examined sodium molybdate and molybdenum deficiency, concluding that human deficiency is extremely rare, with only one documented case linked to TPN. It recommends a daily intake of 20 mcg to prevent deficiency, drawing on observational data and clinical guidelines due to the lack of RCTs.
https://www.science.org/doi/10.1126/sciadv.adq9686 – This molecular biology and infection model study focused on molybdate uptake in bacteria. It revealed that molybdate uptake via the ModA protein is crucial for bacterial growth and infection, underscoring molybdate's biological importance and its potential as a target for antibacterial strategies. The study's findings are specific to bacterial systems, not human supplementation.
https://ods.od.nih.gov/factsheets/Molybdenum-HealthProfessional/ – This source from the Office of Dietary Supplements provides general information on molybdenum for health professionals. It covers the essentiality of molybdenum, its role in enzyme function, dietary sources, and recommended intakes. It also touches upon deficiency and toxicity, serving as a foundational reference for understanding molybdenum's role in human health.