Molybdenum is an essential element required to form molybdopterin, a cofactor essential to the function of the human enzymes xanthine oxidase, sulphite oxidase and aldehyde oxidase. The dietary requirement to prevent deficiency is so small that symptoms associated with inadequate intake have not been described except in experimental studies with animals. A situation of possible deficiency in a patient receiving total parenteral nutrition has been noted.
Veterinary and agricultural interest in molybdenum has existed for many years. A tetrathiomolybdate is formed in the rumen of grazing animals, which interferes with the absorption of copper and can lead to deficiency of this latter element in areas where the forage has a high molybdenum content.
Molybdenum is a valuable component of steels and high strength alloys including the materials used for joint prostheses. Compounds of molybdenum are used in lubricants, catalysts and pigments. Increased exposure is mainly from occupational activity but there can be release of molybdenum (and other metals) from implants and artificial joints. Few symptoms have been reported but an increased incidence of gout has been recorded in one group of factory workers and in the inhabitants of molybdenum-rich areas of Armenia.
Laboratory Indices of Exposure
Normal concentrations in serum and urine are very low, and deficiency of molybdenum is difficult to determine from measurements of the element in these fluids. Deficiency can be indicated by increased urinary excretion of xanthine and sulphite which is reversed by administration of molybdate.
Increased exposures are shown by high levels of molybdenum in urine and blood and by hyperuricaemia with elevated caeruloplasmin concentrations.
The rare condition of molybdenum cofactor deficiency, inherited as an autosomal recessive trait, results in severe neurological abnormalities, mental retardation, lens dislocation and xanthinuria in affected children. Liver specimens from these patients are deficient in the molybdenum – containing cofactor and have reduced enzyme activities. Plasma concentrations of molybdenum are normal, and dietary supplementation effects no clinical improvement.
References:
Stokinger HE Chapter 29 – Metals, in Patty’s Industrial Hygiene and Toxicology, 3rd Revised Edition, Volume 2A. Eds Clayton GD and Clayton FE. Wiley Interscience, 1981.
Johnson JL, Rajagopalan KV, Lanman JT, Schutgens RBH, van Gennip AH, Sorensen P, Applegarth DA. Prenatal diagnosis of molybdenum cofactor deficiency by assay of sulfite oxidase activity in chorionic villus samples. J Inher Metab Dis 1991; 14: 932-7