Molybdenum is an essential constituent of
two enzymes found in humans: xanthine oxidase, which is involved in uric acid
formation, and aldehyde oxidase, which catalyzes the chemical oxidation of
Molybdenum is concentrated primarily in
the liver, kidney, bone, and skin. There is estimated to be approximately nine
milligrams of molybdenum in the adult human body.
Molybdenum is an antagonist to copper
absorption, as is copper to molybdenum absorption. Excess molybdenum intake can
induce copper deficiencies with the subsequent symptoms.
Molybdenum is an important constituent of
aldehyde oxidase and xanthine oxidase. Aldehyde oxidase catalyzes the oxidation
of an aldehyde functional group to the corresponding carboxylic acid. Xanthine
oxidase catalyzes the oxidation of xanthine to uric acid for excretion.
Xanthine is a product formed in the chemical degradation of purine nucleotides
found in DNA and RNA.
Molybdenum, in the presence of inorganic
sulfate, tends to reduce copper absorption and retention. Several theories for
why this antagonistic relationship occurs have been postulated. There is
evidence that copper and molybdenum form an insoluble complex called
lingrenite, which cannot be absorbed easily. Other theories include the
postulated interference of ceruplasm synthesis: ceruplasm is a protein
necessary for copper transport into blood.
Molybdenum absorption occurs readily in
gastrointestinal tract, and excretion occurs primarily via the urine.
Molybdenum has been implicated as a
possible contributor to decreased incidence of dental carries, a reduced
incidence of cancer, and a bringing into balance of female hormones for the
control of premenstrual syndrome.
Molybdenum deficiencies in humans have not
been conclusively linked to any specific set of symptoms; however, one source
indicates that a high incidence of cancer of the esophagus may be the result of
low molybdenum intake.
Symptoms of molybdenum toxicity include
diarrhea, depressed growth rate, and anemia. Gout-like symptoms may result from
High levels of molybdenum intake can
induce a high rate of copper excretion (due to the antagonistic effect the two
minerals have on each other), which could possibly result in a copper
A high intake of molybdenum can alter the
activity of alkaline phosphatase, resulting in certain bone abnormalities.
Alkaline phosphatase enzymatically releases phosphate groups from the molecule
glucose 1-phosphate, thereby producing high levels of inorganic phosphate;
phosphate is necessary to produce hydroxyapatite crystals in bone.
The RDA for adults is from 0.15 to 0.5 mg.
The RDA for children is not yet established, but is a relatively small
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