Molybdenum is an essential trace element for virtually all life forms. It functions as a cofactor for a number of enzymes that catalyze important chemical transformations in the global carbon, nitrogen, and sulfur cycles. Thus, molybdenum-dependent enzymes are not only required for the health of the Earth's people, but for the health of its ecosystems as well. Food is the major source of molybdenum for most people. Common sources of molybdenum include legumes (beans, peas, and lentils), grains, leafy vegetables, liver, and nuts. However, the amount of molybdenum in plants varies with how much is in the soil. Humans require very small amounts. Molybdenum deficiency appears to happen only under the most unusual circumstances; for example, a person fed entirely through the veins for a very long time, or a person with a genetic problem in which the body can't use the molybdenum that is eaten in foods.
The biological form of molybdenum present in almost all molybdenum-containing enzymes (molybdoenzymes) is an organic molecule known as the molybdenum cofactor. In humans, molybdenum is known to function as a cofactor for three enzymes. Sulfite oxidase catalyzes the transformation of sulfite to sulfate, a reaction that is necessary for the metabolism of sulfur-containing amino acids, such as cysteine. Xanthine oxidase and aldehyde oxidase catalyze hydroxylation reactions involving a number of different molecules with similar structures. Xanthine oxidase catalyzes the breakdown of nucleotides (precursors to DNA and RNA) to form uric acid, which contributes to the antioxidant capacity of the blood. Xanthine oxidase and aldehyde oxidase also play a role in the metabolism of drugs and toxins. Of these three enzymes, only sulfite oxidase is known to be crucial for human health.
Copper: Excess dietary molybdenum has been found to result in copper deficiency in grazing animals (ruminants). In ruminants, the formation of compounds containing sulfur and molybdenum, known as thiomolybdates, appears to prevent the absorption of copper. This interaction between thiomolybdates and copper does not occur to a significant degree in humans. One early study reported that molybdenum intakes of 500 and 1,500 mcg/day from sorghum increased urinary copper excretion. However, the results of a more recent and well-controlled study of molybdenum intake and copper metabolism in eight healthy young men indicated that very high dietary molybdenum intakes (up to 1,500 mcg/day) did not adversely affect copper nutritional status.
Dietary molybdenum deficiency has never been observed in healthy people. The only documented case of acquired molybdenum deficiency occurred in a patient with Crohn's disease on long-term total parenteral nutrition (TPN) without molybdenum added to the TPN solution. The patient developed rapid heart and respiratory rates, headache, night blindness, and ultimately became comatose. He also demonstrated biochemical signs of molybdenum deficiency, including low plasma uric acid levels, decreased urinary excretion of uric acid and sulfate, and increased urinary excretion of sulfite. The symptoms disappeared when the administration of amino acid solutions was discontinued. Molybdenum supplementation (160 mcg/day) reversed the amino acid intolerance and improved his clinical condition.
Current understanding of the essentiality of molybdenum in humans is based largely on the study of individuals with very rare inborn errors of metabolism that result in a deficiency of the molybdoenzyme, sulfite oxidase. Two forms of sulfite oxidase deficiency have been identified: 1) isolated sulfite oxidase deficiency, in which only sulfite oxidase activity is affected and 2) molybdenum cofactor deficiency, in which the activity of all three molybdoenzymes is affected. Because molybdenum functions only in the form of the molybdenum cofactor in humans, any disturbance of molybdenum cofactor metabolism can disrupt the function of all molybdoenzymes. Together, molybdenum cofactor deficiency and isolated sulfite oxidase deficiency have been diagnosed in more than 100 individuals worldwide. Both disorders result from recessive traits, meaning that only individuals who inherit two copies of the abnormal gene (one from each parent) develop the disease.
Individuals who inherit only one copy of the abnormal gene are known as carriers of the trait but do not exhibit any symptoms. The symptoms of isolated sulfite oxidase deficiency and molybdenum cofactor deficiency are identical and usually include severe brain damage, which appears to be due to the loss of sulfite oxidase activity. At present, it is not clear whether the neurologic effects are a result of the accumulation of a toxic metabolite, such as sulfite, or inadequate sulfate production. Isolated sulfite oxidase deficiency and molybdenum cofactor deficiency can be diagnosed relatively early in pregnancy (10-14 weeks of gestation) through chorionic villus sampling, and in some cases, carriers of molybdenum cofactor deficiency can be identified through genetic testing. No cure is presently available for either disorder, although anti-seizure medications and dietary restriction of sulfur-containing amino acids may be beneficial in some cases.
Gastroesophageal cancer: Linxian is a small region in northern China where the incidence of cancer of the esophagus and stomach is very high (10 times higher than the average in China and 100 times higher than the average in the U.S. The soil in this region is low in molybdenum and other mineral elements, so dietary molybdenum is also low. Increased intake of nitrosamines, which are known carcinogens, may be one of a number of dietary and environmental factors that contributes to the development of gastroesophageal cancer in this population. Plants require molybdenum to synthesize nitrate reductase, a molybdoenzyme necessary for converting nitrates from the soil to amino acids. When soil molybdenum content is low, plant conversion of nitrates to nitrosamines increases, resulting in increased nitrosamine exposure for those who consume the plants. Adding molybdenum to the soil in the form of ammonium molybdenate may help decrease the risk of gastroesophageal cancer by limiting nitrosamine exposure. It is not clear whether dietary molybdenum supplementation is beneficial in decreasing the risk of gastroesophageal cancer. In a large intervention trial, dietary supplementation of molybdenum (30 mcg/day) and vitamin C (120 mg/day) did not decrease the incidence of gastroesophageal cancer or other cancers in residents of Linxian over a five-year period.
Importance of Diet
For good health, it is important that you eat a balanced and varied diet. Follow carefully any diet program your health care professional may recommend. For your specific dietary vitamin and/or mineral needs, ask your health care professional for a list of appropriate foods. If you think that you are not getting enough vitamins and/or minerals in your diet, you may choose to take a dietary supplement. The amount of molybdenum in foods depends on the soil in which the food is grown. Some soils have more molybdenum than others. Peas, beans, cereal products, leafy vegetables, and low- fat milk are good sources of molybdenum.
Uses for Molybdenum
Preliminary evidence indicates that molybdenum, through its involvement in detoxifying sulfites, might reduce the risk of sulfite-reactive asthma attacks. However, a physician should be involved in the evaluation and use with sulfite sensitivity. Molybdenum is indicated in cases of molybdenum deficiency due to prolonged use of total parenteral nutrition. Despite some epidemiological evidence showing a higher incidence of esophageal carcinoma in those who live in areas where the soil is low in molybdenum, there is as not currently any indication for the use of supplemental molybdenum in the prevention of cancer. Claims that molybdenum may help prevent anemia, dental cavities, and help in cases of sexual impotence have no credible support.