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.
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