It is an extremely important enzymatic component, very widespread in bacteria and indispensable in the cellular metabolism of higher eukaryotes.
Molybdenum cannot be synthesized independently by the human body and, for this reason, it is considered an essential nutrient.
The primary nutritional sources are muscle meat, liver and some seeds. The recommended rations are lower than the average dietary molybdenum intake.
Deficiency is rare, but leads to identifiable metabolic imbalances related to compromised enzymes; excess is also unlikely.
(more numerous), plants and animals.In most types of enzymes, molybdenum is present in the completely oxidized Mo (VI) form, bound in the so-called molybdenum protein, giving rise to the molybdenum cofactor.
The only exception is nitrogenase enzymes, which contain Mo (III) or Mo (IV) and also iron, in a cofactor called iron-molybdenum (FeMoco) - formula Fe7MoS9C.
Nitrogenases are involved in the nitrogen fixing of bacteria and cyanobacteria, intervening in the breaking of the chemical bond of atmospheric molecular nitrogen.
The magnitude of the reactions catalyzed by the enzymes containing molybdenum make it an essential element for all higher eukaryotic organisms, including man.
and carbon.Four molybdenum-dependent enzymes are known in mammals, all of which harbor a pterin-based cofactor (Moco) in the active site: sulfite oxidase, xanthine oxidoreductase, aldehyde oxidase and mitochondrial amidoxime reductase.
In some animals and in man, a typical example of a molybdoenzymatic function is the so-called oxidation of xanthine to uric acid, a process of purine catabolism mediated by xanthine oxidase.
The activity of xanthine oxidase is directly proportional to the amount of molybdenum in the body, which also affects protein synthesis, metabolism and growth.
The "average" human body contains about 0.07 mg of molybdenum per kilogram of body weight (mg / kg), with higher concentrations in the liver and kidneys, and lower in the vertebrae of the spine. It is also present in the enamel of human teeth and can help prevent tooth decay.
However, an extremely high concentration of molybdenum can reverse this trend and act as an inhibitor in both purine catabolism and other processes.
with food, but also with "accumulation of xanthine and urates, their precipitation in the urine e increased possibility of kidney stones.As anticipated, however, the activity of xanthine oxidase, protein synthesis, other metabolic reactions and growth in general can be negatively influenced by the low presence of molybdenum.
Molybdenum deficiency in parenteral nutrition
Molybdenum deficiency is reported as a consequence of "unintegrated" total parenteral nutrition over long periods of time - as well as, for example, chromium deficiency.
Pure molybdenum deficiency results in elevated blood levels of sulfites and urates, in much the same way as molybdenum cofactor deficiency.
Presumably due to the increased interest in the adult population, the neurological consequences are not as marked as in cases of congenital cofactor deficiency.
Soil Molybdenum Deficiency and Esophageal Cancer Risk
A low soil concentration of molybdenum in a geographic range from Northern China to Iran has resulted in a general food shortage of molybdenum and is associated with increased rates of esophageal cancer.
Compared to the United States and Europe, which have a greater availability of molybdenum in the soil, people living in those areas have an approximately 16 times greater risk of esophageal squamous cell carcinoma.
) which reaches 180 mg / kg.Although the data on its toxicity in the human organism are unknown, other studies performed on animals have shown that chronic ingestion> 10 mg / day of molybdenum could cause diarrhea, growth retardation, infertility, low birth weight and gout; other effects affected lungs, kidneys and liver.
Sodium tungstate is a competitive inhibitor of molybdenum and food-grade tungsten reduces the molybdenum concentration in tissues.
