- Overview of Minerals
- Chromium Deficiency
- Chromium Toxicity
- Copper Deficiency
- Copper Toxicity
- Wilson Disease
- Fluorine Deficiency
- Fluorine Toxicity
- Iodine Deficiency
- Iodine Toxicity
- Iron Deficiency
- Iron Toxicity
- Manganese Deficiency
- Manganese Toxicity
- Molybdenum Deficiency
- Molybdenum Toxicity
- Selenium Deficiency
- Selenium Toxicity
- Zinc Deficiency
- Zinc Toxicity
Molybdenum (Mo) is a component of coenzymes necessary for the activity of xanthine oxidase, sulfite oxidase, and aldehyde oxidase.
Genetic and nutritional deficiencies of molybdenum have been reported but are rare. Genetic sulfite oxidase deficiency was described in 1967 in a child. It resulted from the inability to form the molybdenum coenzyme despite the presence of adequate molybdenum. The deficiency caused intellectual disability, seizures, opisthotonus, and lens dislocation.
Molybdenum deficiency resulting in decreased activity of sulfite oxidase and sulfite toxicity occurred in a patient receiving long-term total parenteral nutrition. Symptoms were tachycardia, tachypnea, headache, nausea, vomiting, and coma. Laboratory tests showed high levels of sulfite and xanthine and low levels of sulfate and uric acid in the blood and urine. Ammonium molybdate 300 mcg/day IV caused dramatic recovery.
(See also Overview of Mineral Deficiency and Toxicity.)
