Molybdenum is a very tough white-silver metal, but softer and denser than tungsten. Molybdenum has one of the highest melting points of all pure elements.
Molybdenum is a valuable alloying agent, as it contributes to hardness and improves the strength of steel at high temperatures. Molybdenum is used in alloys, electrodes and catalysts. Molybdenum is used in electrodes and glassware, in nuclear power applications and in rocket and aircraft parts, and as a catalyst in refining oil. It still has applications as a material in electronic and electrical devices. Molybdenum is an essential trace element in plant nutrition. Some arid soils may lack this element.
Molybdenum in the environment
Molybdenum differs from other soil micronutrients in that it is less soluble in acidic and more soluble in alkaline soils, so its availability to plants is dependent upon soil pH and drainage conditions. Some plants can absorb up to 500 ppm of molybdenum when grown in alkaline soils.
Impact of molybdenum on human health
Based on animal experiments, molybdenum and its compounds appear to be extremely toxic. In chronic exposure to molybdenum, evidence of liver dysfunction with hyperbilirubinemia has been reported, also arthritis with knee, hand and foot pain, with arthritic deformities, erythema and edema.
Molybdenum is essential for all types of organisms. Although, as with other trace elements, small quantities are essential, high doses can be extremely toxic. Animal experiments have shown that excessive intake of molybdenum causes fetal deformities, diarrhea, growth retardation, infertility, low birth weight and gout. It can also affect the lungs, kidneys and liver. Tungsten is a competitive molybdenum Inhibitor. Dietary intake of tungsten reduces the concentration of molybdenum in the tissues.
The average daily intake of molybdenum varies between 0.12 and 0.24 mg, depending on its content in foods. Dietary sources of molybdenum include beans, peas, red meats, eggs, sunflower seeds, wheat flour, lentils, cucumbers and whole grains. It is a trace element important in the oxidation systems of xanthine, aldehydes and sulfites (metabolism of sulfur-containing amino acids). Molybdenum also participates in the mitochondrial enzyme amidoxime reductase. Xanthine oxidase catalyzes the oxidative hydroxylation of purines and pyrimidines to uric acid, aldehyde oxidase oxidizes purines, pyrimidines and pteridines and participates in the metabolism of nicotinic acid. The activity of xanthine oxidase is directly proportional to the amount of molybdenum in the body. However, the very high concentration of molybdenum reverses the trend and can act as an inhibitor of both the purine catabolism and other processes. Molybdenum concentration also affects protein synthesis, metabolism and growth. Deficiency or absence of sulfur oxidase results in neurological symptoms and premature death. People with severe molybdenum deficiency and malfunction of the sulfur oxidase enzyme are prone to toxic reactions to sulfites found in many foods. Reduced intake of molybdenum through food can lead to decreased urinary molybdenum excretion, low serum uric acid and excess urinary xanthine excretion. Molybdenum deficiency has been reported in genetic metabolism defects and in patients receiving total parenteral nutrition. Although most consider molybdenum deficiency to be uncommon, an Austrian study of 1750 patients found that 41.5% had molybdenum deficiency.
The human body contains about 0.07 mg molybdenum per kilogram of body weight, with higher concentrations in the liver and kidneys and lower concetrations in the vertebrae. Molybdenum is present in tooth enamel and can help prevent it from being worn. Molybdenum dietary deficiency is associated with increased rates of esophageal cancer.
Molybdenum deficiency has also been reported as a consequence of total parenteral nutrition (complete intravenous feeding) for long periods of time resulting in high levels of sulfur and the congenital lack of molybdenum cofactor.However, the neurological consequences are not as significant as in cases of congenital deficiency of the cofactor.
High levels of molybdenum in the body interfere with copper intake, ultimately leading to copper deficiency. Molybdenum also interferes with the binding of copper to plasma proteins and increases the amount of copper excreted in the urine.
How can one determine if one has been exposed to molybdenum?
The organism's ability to molybdenum is best evaluated by measuring it in whole blood. We can measure molybdenum levels in blood and most biological materials.
Determination of metals is done by ICP-MS (Inductively Coupled Plasma Mass Spectrometry, Inductively Coupled Argon Plasma Mass Spectrometry), a method that enables the simultaneous detection of many metals. Its sensitivity and accuracy are significantly better than conventional atomic absorption, with the ability to measure metals at concentrations up to 1 in 1015 (1 in 1 quadrillion, ppq)!
Laboratory test results are the most important parameter for the diagnosis and monitoring of all pathological conditions. 70%-80% of diagnostic decisions are based on laboratory tests. Correct interpretation of laboratory results allows a doctor to distinguish "healthy" from "diseased".
Laboratory test results should not be interpreted from the numerical result of a single analysis. Test results should be interpreted in relation to each individual case and family history, clinical findings and the results of other laboratory tests and information. Your personal physician should explain the importance of your test results.
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