Molybdenum.pdfVIP

EXCERPTED FROM: Vitamin and Mineral Safety 3rd Edition (2013) Council for Responsible Nutrition (CRN) Molybdenum Introduction Molybdenum is present in food and water in the form of soluble molybdates. It is a component of and/or cofactor for various enzymes in plants and animal organisms (European Commission, Scientific Committee on Food [EC SCF] 2000). In humans, molybdenum acts as a cofactor for several enzymes, including aldehyde oxidase, sulfite oxidase, and xanthine oxidase (EC SCF 2000; Institute of Medicine [IOM] 2001). These and perhaps other functions make it a nutritionally essential element. Attempts to produce deficiency in experimental animals have succeeded only when the diet contained large amounts of tungsten, an antagonist of molybdenum metabolism (Nielsen 1994, 1996). Molybdenum deficiency in experimental animals inhibits growth and development, especially in prenatal and neonatal stages of development. Human deficiencies of molybdenum function have been linked not to simple dietary deficiency but rather to inborn errors of metabolism, specifically a genetic defect in the molybdenum cofactor that prevents the synthesis of sulfite oxidase, resulting in the accumulation of sulfite, severe neurological damage, and early death (Nielsen 1994, 1999; Johnson, 1997). Safety Considerations Most of the toxicity data pertaining to molybdenum in animals is in ruminants, which are susceptible to the adverse effects of molybdenum under conditions of copper deficiency and marginal sulfur amino acid intake (Underwood 1977). However, the basis for toxicity in ruminants is not considered to be of relevance to humans (IOM 2001). In monogastric laboratory animals, variable responses to excess molybdenum have been reported, including growth depression, renal effects, and skeletal abnormalities (EC SCF 2000; IOM 2001). Supplemental molybdenum intakes of 1.6 mg p