Clinical Information

Molybdenum is an essential trace element found in the daily diet. It is a cofactor for some enzymes important in nitrogen metabolism (aldehyde dehydrogenase, xanthine oxidase, nicotinamide adenine dinucleotide dehydrogenase). Due to the wide distribution of molybdenum in the environment and particularly in plant materials, molybdenum deficiency is rare in adults with normal, diverse diets. Typical molybdenum intake in most geographic locations is between 45 and 90 mcg/day. Urine is the primary source of excretion, though excesses are sometimes excreted by the biliary route.

Molybdenum deficiency associated with parenteral nutrition is indicated by symptoms such as stunted growth, reduced appetite, tachycardia, tachypnea, blindness, and coma. These symptoms can be corrected by introducing molybdenum supplementation. Molybdenum cofactor disease is a severe genetic disorder that is due to defective variants in the MOCS1, MOCS2, and GEPH genes.

Molybdenum toxicity is rare and usually related to molybdenum mining exposure; however, it has been observed in cases of intake above 400 mcg/day. Molybdenum interferes with copper uptake; molybdenum toxicity is predominantly due to copper deficiency (hypochromic anemia and neutropenia) and inhibition of xanthine oxidase (uric acid accumulation).

Serum molybdenum concentrations are likely to be increased above the reference range in patients with metallic joint prosthesis. Prosthetic devices produced by Depuy Company, Dow Corning, Howmedica, LCS (low contact stress), PCA (porous-coated anatomic), Osteonics, Richards Company, Tricon, and Whiteside are typically made of chromium, cobalt, and molybdenum. This list of products is incomplete, and these products change occasionally; see prosthesis product information for each device for composition details.