Molybdenum Deficiency

Molybdenum is an important trace elements for almost all life forms. It serves as a cofactor for numerous enzymes that catalyze essential chemical transformations in the global nitrogen, carbon, and sulfur cycles. Therefore, enzymes that are molybdenum-dependent are needed for both the health of our ecosystem and human health.

The term molybdenum came from the Greek word “molybdae” which was given by a Greek doctor and pharmacist Dioscurides. Carl Wilhelm Scheele isolated white oxide, known as molybdenum trioxide, and subjected molybdenite, molybdenum disulfide (molybdenum glance), which had until then mostly mistaken for graphite, to repeated doses of diluted nitric acid. Scheele distilled off the acid and gave the name “molybdic ocher” (terra molybdaenae) and observed that the oxide’s characteristic is acidic in nature and is blue in color when influenced by reducing agents.

Molybdenum, as part of certain enzymes such as sulfite oxidase and xanthine oxidase, plays a major role in metabolism. The xanthine oxidase is responsible in converting the formation of purines into uric acid during food metabolism in order for them to be eliminated out of the body through the kidneys. Recent tests indicate that molybdenum has an inhibitive effect on certain diseases such as breast cancer, anterior stomach cancer, cancer of the esophagus, and other types of cancer. Other studies suggest that molybdenum promotes fluoride intake in teeth and bone enamel that aids in preventing tooth decay as well as bone decomposition.

Dietary Molybdenum Deficiency

Dietary deficit of molybdenum has never been observed in healthy people. Molybdenum deficiency cases are only documented in patients who have acquired Crohn’s disease on long-term total parenteral nutrition (TPN) wherein molybdenum is not added to the TPN solution. The observed patient developed headache, rapid heart and respiratory rates, night blindness, and ultimately became comatose. Biochemical signs of molybdenum deficiency are also demonstrated by the patient that include decreased urinary excretion of sulfate and uric acid, low plasma uric acid levels, and increased urinary excretion of sulfite. The patient was then diagnosed with defects in sulfur amino acid metabolism and uric acid production. When the TPN solution was discontinued, an improved condition was manifested in the patient with the disappearance of the amino acid intolerance. The patient was supplemented with molybdenum instead of the TPN solution.

Molybdenum cofactor deficiency

Due to the fact that the function of molybdenum is only in the form of molybdenum cofactor in humans, certain forms of molybdenum cofactor metabolism disturbance can disturb the task of all molybdoenzymes. Isolated sulfite oxidase deficiency and molybdenum cofactor deficiency are both diagnosed in more than 100 individuals worldwide. These disorders resulted from recessive traits, meaning that those individuals who inherit two copies of abnormal gene from each parent are more likely to develop the disease. A person who had inherited a single copy of the abnormal gene will not exhibit any molybdenum deficiency symptoms but will serve as a carrier of the trait.

The molybdenum cofactor deficiency and isolated sulfite oxidase deficiency symptoms are almost the same that normally include severe brain damage, because of the sulfite oxidase activity loss. It is still not clear as to whether or not the neurologic effects are due to the accumulation of sulfite or any toxic metabolite; or because of inadequate sulfate production.

Molybdenum Deficiency References and Further Reading

New York University; LPI; USDA; Lawrence Berkeley Lab.