Molybdenum (Mo) is a transition metal that forms oxides and is a component of a pterin coenzyme essential for the activity of xanthine oxidase, sulfite oxidase, and aldehyde oxidase. Genetically conditioned sulfite oxidase deficiency was described in 1967 in a child with mental retardation, convulsions, opisthotonus, and lens dislocation. This disorder was due to the child’s inability to form the molybdenum coenzyme despite the presence of adequate molybdenum.
Sulfite toxicity due to molybdenum deficiency was noted in a patient on long-term TPN who developed tachycardia, tachypnea, headache, nausea, vomiting, and coma. A metabolic study showed high levels of sulfite and xanthine and low levels of sulfate and uric acid in his blood and urine, which led to the diagnosis. Giving ammonium molybdate 300 µg/day IV led to a dramatic recovery. Both genetically conditioned and nutritional deficiencies of molybdenum are rare. The intake of molybdenum varies from 100 to 500 µg/day and is derived principally from organ meats, whole-grain cereals, and legumes.
The Food and Nutrition Board of the NAS/NRC states that a safe, adequate intake of molybdenum is 75 to 250 µg/day for adults and 25 to 75 µg/day for children aged 1 to 6 yr.