Home | | Introduction to Human Nutrition | Molybdenum: Toxicity, Genetic diseases, Requirements, dietary sources, Micronutrient interactions

Chapter: Introduction to Human Nutrition: Minerals and Trace Elements

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Molybdenum: Toxicity, Genetic diseases, Requirements, dietary sources, Micronutrient interactions

Molybdenum does not exist naturally in the pure metallic state but rather in association with other ele-ments, or predominantly in solution as the molybdate anion.

Molybdenum

 

Molybdenum does not exist naturally in the pure metallic state but rather in association with other ele-ments, or predominantly in solution as the molybdate anion. Insoluble molybdenum compounds include molybdenum dioxide and molybdenum disulfide. The metal has five oxidation states (2–6), of which +4 and +6 are the predominant species. Major molybdenum-containing ores are molybdenum sulfites and ferric molybdenum ores, usually produced as by-products of copper mining operations, while other molybdenum salts are by-products of uranium mining. Molybdenum is used mostly in metallurgical applications such as stainless steel and cast iron alloys, and in metal–ceramic composites. Molyb-denum compounds have anticorrosive and lubricant properties and can act as chemical catalysts.

 

Molybdenum uptake into plants and hence into the food chain occurs mostly from alkaline or neutral soils. Water usually contains little molybdenum except near major mining operations.

 


Toxicity

 

In 2001, the US Food and Nutrition Board set the tol-erable UL for molybdenum at 2 mg/day for adults (aged 19 years and older). Impaired reproduction and growth in animals were selected as the critical adverse effects on which to base their UL for molybdenum.

 

Genetic diseases

 

A rare unborn error of metabolism, resulting in the absence of the molybdenum pterin cofactor, may give some clue to the essentiality of molybdenum. These patients have severe neurological dysfunction, dislocated ocular lenses, mental retardation, and biochemical abnormalities, including increased urinary excretion of xanthine and sulfite and decreased urinary excretion of uric acid and sulfate.

 

Assessing status

 

Determining the body status of molybdenum is dif-ficult. Homeostatic control of molybdenum ensures that plasma concentrations are not elevated, except after extremely high dietary intakes. Decreased urinary concentrations of sulfite, hypoxanthine, zorithine, and other sulfur metabolites, however, are generally indicative of impaired activities of the molybdoenzymes. Adult requirements for molybde-num have been estimated at about 45 μg/day (Institute of Medicine, USA, 2001). Average intakes tend to be considerably above this value. Milk, beans, bread, and cereals (especially the germ) are good sources of molybdenum, and water also contributes small amounts to the total dietary intakes.

 

Micronutrient interactions

 

The major micronutrient interactions with molybde-num are those involving tungsten and copper. Molybdenum supplementation depletes body levels of the essential trace element, copper, and has been used as a chelating agent for conditions such as Wilson’s disease, which cause elevated concentrations of copper in the body.

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