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|
| Proper name |
Molybdenum |
| Category |
Trace
Mineral |
| Functions |
Molybdenum is a cofactor in the following three enzymes; xanthine oxidase,
aldehyde oxidase, and sulfite oxidase. Xanthine oxidase metabolizes xanthine
to uric acid for urinary excretion. Uric acid, while problematic in excess,
is a powerful antioxidant that neutralizes singlet oxygen and hydroxyl free
radicals. Aldehyde oxidase catalyses the conversion of aldehydes to acids.
Sulfite oxidase catalyzes the conversion of sulfite (which is toxic to the
nervous system) into sulfate for urinary excretion. |
| RDA |
75 to 250 mcg per day for adults. |
| Therapeutic
dose |
Doses of100 to 1,000 mcg per day have been reported in the scientific literature. |
| Deficiency symptoms |
Deficiency is extremely rare. Deficiency can occur in persons receiving
prolonged total parenteral nutrition (TPN) or in some individuals suffering
a rare molybdenum cofactor deficiency genetic disorder. Excessive intake
of sulfate or copper can cause increased excretion of molybdenum. Symptoms
include tachycardia, headache, mental disturbances and coma. Symptoms of
the genetic disorder include seizures and developmental delays in neonates. |
| Toxicity |
Toxicity is very rare however, molybdenum intake in excess of 10-15 mg per
day can cause gout-like symptoms due to elevated production of uric acid. |
| Best
forms
|
Not known. |
| Food
sources |
Legumes,
whole grains, milk, leafy vegetables and organ meats. |
| Lab
tests |
Hair mineral analysis. |
| Drug
interactions |
None
known |
| Nutrient interactions |
Molybdenum competes with iron, copper and sulfate for intestinal absorption. |
| Metabolism |
Molybdenum is very
rare, yet is found in all human tissues. The amount of molybdenum normally
found is less than 0.1 part per million. Molybdenum-dependent enzymes
are useful in liver detoxification.
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