Molybdenum

  • Molybdenum (Mo) is an essential trace mineral in animal and human nutrition. Exerts its biological activity as a cofactor that forms the active site of all Mo enzymes, except nitrogenase. The Mo cofactor consists of the metal covalently bound to one or two dithiolates attached to a tricyclic pterin moiety referred to as molybdopterin (1). A defect in Mo cofactor synthesis results in the pleiotropic loss of all Mo-dependent enzyme activities. Mo enzymes catalyze redox reactions in purine catabolism (xanthine dehydrogenase), intermediate metabolism (aldehyde oxidase) and detoxification reactions (sulfite oxidase). Mo is also required for a class of hydroxylases that unlike the former three catalyze the hydroxylation of carbon centers using oxygen derived from water (2).
  • It is now well established that Mo cofactor deficiency is a hereditary metabolic disorder characterized by severe neurodegeneration caused by anomalies in the functioning of xanthine dehydrogenase, aldehyde oxidase and sulfite oxidase. This disorder usually results in early childhood death. Characteristic biochemical defects in affected infants include hypouricemia, augmented urine sulfate and S-sulfocysteine (3).
  • Exerts an insulin-like action as demonstrated by the improvement of carbohydrate and lipid metabolism in streptozotocin-diabetic rats (4). As cell culture experiments have shown, Mo salts treatment has also a positive effect on insulin secretion and function of pancreatic beta cells (5). In alloxan-induced diabetic rats it was found that sodium molybdate supplementation significantly reduced lipid peroxidation and increased the activity of antioxidant enzymes superoxide dismutase, catalase and GSH peroxidase (6).
  • Interactions: Increased molybdenum intake leads to higher levels of urinary excretion of copper.
  • Health benefits: Several pathological cases in animals and one in humans have been clearly attributed to Mo deficiency (7). The need for Mo supplementation in human nutrition appears to be supported by existing data suggesting that this ultratrace element as well as several others (Se, Mn, Cr, B and I) should be given essential element status and RDA values (8). On the other hand, experiments with animal models have shown that sodium molybdate can aleviate diabetes mellitus symptoms (6) and tetrathiomolybdate inhibits cytokines in lung inflammation and fibrosis (9). The latter effect may prove useful in cases of pulmonary inflammation/fibrosis often associated with bleomycin (an antitumor antibiotic) cancer therapy.
  • Best food sources: Legumes, brewer's yeast, whole grains.


References
1. Schwarz, G. et al. (2005) Cell Mol. Life Sci. 62(23) 2792-2810. Molybdenum cofactor biosynthesis and
    deficiency.
2. Hille, R. (2005) Arch.Biochem.Biophys. 433(1) 107-116. Molybdenum-containing hydroxylases.
3. Arnold, G.L. et al. (1993) J.Pediatr. 123(4) 595-598. Molybdenum cofactor deficiency.
4. Ozcelikay, A.T. et al. (1996) Am.J.Physiol. 270(2 Pt.1) E344-352. Improvement of glucose and lipid
    metabolism in diabetic rats treated with molybdate.
5. Liu, H.K. et al. (2004) Pancreas 28(4) 364-368. Long-term beneficial effects of vanadate, tungstate and
    molybdate on insulin secretion and function of cultured beta cells.
6. Panneerselvam, S.R. & Govindasamy, S. (2004) Clin.Chim.Acta 345(1-2) 93-98. Effect of sodium
    molybdate on the status of lipids, lipid peroxidation and antioxidant systems in alloxan-induced
    diabetic rats.
7. Neve, J. (1991) J.Pharm.Belg. 46(3) 189-196. The nutritional importance and physiopathology of
    molybdenum in man.
8. Nielsen, F.H. (1996) J.Nutr. 126(9 Suppl.) 2377S-2385S. How should dietary guidance be given for
    mineral elements with beneficial actions or suspected of being essential?
9. Brewer, G.J. et al. (2004) J.Inorg.Biochem. 98(12) 2160-2167. Inhibition of key cytokines by
    tetrathiomolybdate in the bleomycin model of pulmonary fibrosis.