Molybdenum is an essential trace element in humans and
is required for enzyme activity as a cofactor.
Molybdenum is a transition element that can exist in multiple oxidation states and facilitate electron transfer in oxidation-reduction reactions.
Molybdenum in foods and as soluble complexes is readily absorbed. Copper can inhibit absorption in humans.
Under normal dietary conditions, molybdenum content of human tissue is quite low (0.1 to 1.0 mcg per gram wet weight). Liver, kidney, adrenal glands and bone contain the highest amounts of molybdenum.
After absorption, molybdenum is rapidly excreted through the kidney (90%) and smaller amounts are excreted in bile (10%).
In addition to the molybdenum cofactor, the other important form of molybdenum is molybdate. Evidence suggests that the molbydenum found in blood and urine exists mainly as the molybdate ion (MoO42).
Males 9 to 13 years 14 to 18 years 19+ years Females 9 to 13 years 14 to 18 years 19+ years
34 43 45
34 43 45
1100 1700 2000
1100 1700 2000
Pregnancy <= 18 years 19 to 50
years
250 50
1700 2000
Lactation <= 18 years 19 to 50
years
50 50
1700 2000
Values are Adequate Intakes (AI). ND= Tolerable Upper Intake Levels (UL) are not determinable
due to lack of data of adverse effects in this age group and concern with regard
to lack of ability to handle excess amounts.
Molybdenum deficiency is rare, unless the diet
contains high amounts of the antagonistic substances such as, sulfate, copper
or tungstate.
Signs of molybdenum deficiency are mouth and gum disorders, hypouricemia, hyperoxypurinemia, mental disturbance, and coma, as seen in patients with 'acquired molybdenum deficiency' resulting from parenteral methionine therapy.
Symptoms such as gout (inflammation of the joints due
to accumulation of uric acid) are possible due to high blood uric acid
concentrations and accumulation of uric acid around the joints. This occurs
especially when molybdenum intakes exceed 10 to 15 mg daily.
Gout affects primarily males over the age of 40 and occasionally, postmenopausal women. One aspect of gout related to molybdenum is decreased uric acid excretion caused by molybdenum and sulfur binding to copper in the kidneys.
Milk, milk products, legumes, organ meats, and cereals are good dietary sources of molybdenum. A diet high in processed foods
may lead to a deficiency in molybdenum.
There has been one recorded case of an apparent molybdenum deficiency occurring in a subject receiving total parenteral
nutrition (TPN) for 18 months due to Crohn’s disease. 3
Caution with pregnancy or nursing, consult physician before using.
Information on the relationship between substances and disease is provided for general information, in order to convey a balanced review of the scientific literature. In many cases the relationship between a substance and a disease is tentative and additional research is needed to confirm such a relationship.
Arthritis: Some
earlier research in the Utano National Hospital in Japan was conducted on 60
patients undergoing long-term hemodialysis. Although serum molybdenum
concentrations decreased significantly after hemodialysis, 9 patients with
dialysis related arthritis had elevated serum molybdenum concentrations.
Abnormal molybdenum accumulation may contribute to dialysis-related arthritis.
7
The dietary supplement information contained on this site has been compiled from published sources thought to be reliable, but it cannot be guaranteed. Efforts have been made to assure this information is accurate and current. However, some of this information may be purported or outdated due to ongoing research or discoveries. The authors, editors and publishers cannot accept responsibility for errors or omissions or for any consequences from applications of the information in this site and make no warranty, expressed or implied, with respect to the contents herein.
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