Molybdenum

Molybdenum (Mo) containing stainless steel was introduced due to its resistivity
towards reaction with organic compounds and biologic fluids.

From: Biomaterials and Bionanotechnology, 2019

Related terms:

Chromium, Manganese, Cobalt, Enzyme, Protein, Alloy, Tungsten, Toxicity, Xan-

thine Oxidase

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Molybdenum
Jeffery O. Hall, in Veterinary Toxicology (Third Edition), 2018

Abstract
Molybdenum is an essential nutrient in animals that functions as an oxygen transfer
reaction in some body enzymes. Because molybdenum is required at very min-
imal amounts in the diet; deficiency has not been reported under natural con-
ditions. Excessive molybdenum intake by way of high forage concentrations or
oversupplementation can result in molybdenosis. Molybdenum poisoning is directly
tied to dietary concentrations of molybdenum, copper and sulfur and the relative
concentration ratios of copper to molybdenum. Most but not all of the clinical
effects of molybdenosis are directly related to resultant overt or functional copper
deficiencies. These deficiencies are the result of molybdenum being converted to
thiomolybdates in the rumen by binding to sulfide and subsequently binding copper
(producing cupric thiomolybdate complexes) to render it nonbioactive. These cupric
thiomolybdate complexes can cause gastrointestinal and systemic loss of copper.
Treatment entails the balancing of the copper: molybdenum ratio and potentially
decreasing sulfur exposure.

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Molybdenum
Jeffery O. Hall, in Veterinary Toxicology (Second Edition), 2012

Introduction
Molybdenum (Mo) is an essential nutrient in plants and animals. Thorough reviews
on Mo have been published (Dick, 1956; Underwood, 1977; Ward, 1978; Friberg
and Lener, 1986; Mills and Davis, 1987; Rajagopalan, 1988; Nielsen, 1996; Johnson,
1997; NRC, 2006). In plants and microbes, reduction of nitrate to nitrite and nitrogen
fixation requires Mo (Williams and daSilva, 2002). Higher animals require Mo for
oxygen transfer reactions of aldehyde oxidase, sulfite oxidase and xanthine oxidase,
where Mo is bound to a pterin nucleus (Johnson et al., 1980). Although dietary clinical
deficiencies have not been reported under natural conditions (Mills and Davis, 1987),
deficiency has been produced in animals fed purified Mo deficient diets (Mills and
Bremner, 1980; Anke et al., 1985). Functional Mo deficiency has been caused by
genetic disorders in humans (Reiss, 2000) and competitive replacement of tungsten
for Mo in enzymes (Nell et al., 1980). And, iatrogenic Mo deficiency, resulting in
aberrant sulfur-containing amino acid metabolism, has been reported following
prolonged total parenteral nutrition (Abumrad et al., 1981).

Mo toxicity is intricately tied to interactions with copper and sulfur. Predominant

manifestations of Mo poisoning are associated with secondary copper deficiency,
but not all clinical symptoms are alleviated by copper supplementation. The cop-
per–sulfur–Mo interactions are complex and vary greatly in degree of severity among
species.

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Molybdenum
R.W. KappJr., in Encyclopedia of Toxicology (Third Edition), 2014

Exposure and Exposure Monitoring

Molybdenum is an essential trace element for both animals and plants; hence,
trace quantities of molybdenum are beneficial and perhaps essential for the normal
growth and development of plants and animals. In mammals, molybdenum is
a component of certain metalloflavoproteins, including xanthine oxidase, sulfite
oxidase, and aldehyde oxidase, and it protects against poisoning by copper, mercury,
and other metals, and may have anticarcinogenic properties. In plants, it is necessary
for fixing of atmospheric nitrogen by bacteria at the start of protein synthesis. For
all organisms, the interpretation of molybdenum residues depends on knowledge
of not only molybdenum, but also copper and inorganic sulfate concentrations in
diet and in tissues. Suggested safe and adequate molybdenum intake levels for
infants are 0.015–0.04 mg day−1, 0.025–0.15 mg day−1 for children aged 1–10, and
0.075–0.25 mg day−1 for all individuals greater than the age of 10. Gastrointestinal
absorption is a significant portion of the ingested amount and depends on the
water solubility of the compound involved. Exposure to water-soluble molybdenum
increases absorption and toxicity may be greater than that from non-water-soluble
compounds.

The human body contains about 0.07 mg of molybdenum per kilogram, with higher
concentrations in the liver and kidneys and in lower concentrations in the vertebrae.
The average daily intake of molybdenum varies between 0.12 and 0.24 mg, but
it depends on the molybdenum content of the food. Pork, lamb, and beef liver
each have approximately 1.5 parts per million of molybdenum. Other significant
dietary sources include green beans, eggs, sunflower seeds, wheat flour, lentils,
cucumbers, and cereal grain. Little data on human toxicity of molybdenum are
available; however, in 1961, a goutlike syndrome was associated with excessive
exposure (10–15 mg day−1) to molybdenum. The disease occurred in Armenians
living in areas rich in molybdenum, which produced hyperuricemia, arthralgias,
erythema, edema, and deformity of the knees, hands, and feet. Although the exact
cause of this disease remains to be established, it is intriguing that the soil has
unusually high concentrations of molybdenum.

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Molybdenum
JUDITH R. TURNLUND, LARS T. FRIBERG, in Handbook on the Toxicology of Metals
(Third Edition), 2007

ABSTRACT
Molybdenum is an essential element for humans, and dietary recommendations
have been established. Dietary intakes in humans are usually within the range of
the recommendations. Soluble molybdenum compounds are readily absorbed when
ingested. The highest molybdenum concentrations are found in the kidneys, liver,
and bone. Excretion, primarily through the urine, is rapid. The biological half-life
ranges from a few hours to a few days. Turnover is much more rapid when intake is
high than when intake is low.
The metabolism of molybdenum is affected by copper and sulfur intake in some
species. In ruminants, copper generally has a beneficial effect on the symptoms
caused by excessive molybdenum, and thiomolybdates increase the excretion of
copper. Both positive and negative effects of the interaction between these three
elements have been reported. The effects and their magnitude vary between animal
species.

In livestock, chronic molybdenum poisoning known as “teart disease” is caused

by a diet high in molybdenum and low in copper. Symptoms include anemia,
gastrointestinal disturbances, bone disorders, and growth retardation. In laboratory
animals, excessive molybdenum may give rise to morphological and functional
changes in the liver, kidneys, and spleen. It has a growth-depressing action, and
deformities of bone may occur.

A few cases of pneumoconiosis have been reported among workers exposed to

metallic molybdenum and molybdenum trioxide. Increased blood uric acid values
and goutlike symptoms have been reported among workers exposed to molybde-
num in a copper-molybdenum plant, as well as among the general population living
in an area with high molybdenum and low copper content in soil and vegetables.

Molybdenum chemistry, metabolism, toxicity, and essentiality have been reviewed

by Friberg et al. (1975), Chappell and Petersen (1976; 1977), Mills and Davis (1987)),
Johnson (1997), Turnlund (2002), Institute of Medicine (2002), and Anke (2004).

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Molybdenum
Martin Kohlmeier, in Nutrient Metabolism, 2003

Transport and cellular uptake

Blood circulation: Molybdenum in blood (typical concentration 5 nmol/l) is largely
associated with alpha-2-macroglobulin as MoO2−4 as well as enzyme-bound in
erythrocytes (Nielsen, 1994). Uptake of MoO3-, to a lesser extent MoO2-4, by erythro-
cytes, leukocytes, fibroblasts, vascular smooth muscle, liver and other tissues pro-
ceeds via SLC4A1 (band 3 protein) which otherwise mediates exchange of chloride,
bicarbonate, sulfate, and glucose (Gimenez et al., 1993); several well-characterized
variants of this transporter account for the Diego blood group system antigens.
Tungstate is also transported by this system. An ATP cassette-binding (ABC) trans-
porter has been identified in bacteria that mediates molybdate transport (Neubauer
et al., 1999). There appears to be significant enterohepatic cycling.
Materno-fetal transfer: The molybdenum concentration in colostrum is eight-fold
higher than in maternal serum indicating an active, concentrative transport mech-
anism (Krachler et al., 1999).

Blood-brain barrier: The mechanisms for transport across the blood-brain barrier
have not yet been elucidated.

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Metals
Rosalind Dalefield BVSc PhD DABVT DABT, in Veterinary Toxicology for Australia
and New Zealand, 2017

Circumstances of Poisoning
Molybdenum toxicity has occurred in Australian and New Zealand livestock grazing
on land where the soil molybdenum level is high and, less commonly, where
there has been excessive use of fertilizer containing molybdenum. Molybdenum
toxicosis has been observed secondary to use of sewage sludge as a fertilizer. Plants,
particularly legume species, absorb water-soluble molybdates from soil and fertilizer.

Excess molybdenum in soil may be naturally occurring or may be a result of

contamination from industries. Some industries that may cause molybdenum cont-
amination include aluminum smelters, steel mills, and brick manufacturers that use
clay high in molybdenum.

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Milk Salts | Trace Elements, Nutritional

Significance
K.D. Cashman, in Encyclopedia of Dairy Sciences (Second Edition), 2011

Molybdenum
Molybdenum is an essential component of several enzymes, including xanthine
oxidase, aldehyde oxidase (EC 1.2.3.1), and sulfite oxidase (EC 1.8.3.1), where it
occurs in the prosthetic group molybopterin. It is not known whether the human
requirement is for molybdenum per se or for molybopterin (or a precursor). Although
molybdenum deficiency has been reported in a patient on long-term total parenteral
nutrition therapy, dietary deficiency of molybdenum has not been observed in
humans.

The recently established RDAs for molybdenum in the United States are shown in
Table 6. Milk may contribute substantially to the intake of molybdenum (36% of
total molybdenum intake).

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Feed Ingredients | Feed Supplements:

Microminerals
J.W. Spears, T.E. Engle, in Encyclopedia of Dairy Sciences (Second Edition), 2011

Molybdenum
Molybdenum functions as a component of the enzymes xanthine oxidase, sulfite
oxidase, and aldehyde oxidase. Cattle requirements for molybdenum are not estab-
lished, but are obviously very low. There is no evidence that molybdenum deficiency
occurs in cattle under practical conditions. However, molybdenum supplementation
of ruminant diets has enhanced ruminal digestion in some studies, apparently by
altering ruminal microorganisms.

Toxicity of molybdenum can be a problem in cattle. Acute toxicity signs, including

severe diarrhea, loss of weight, anorexia, stiffness, and changes in hair color, may be
observed in cattle fed diets containing molybdenum at concentrations of 20 mg or
greater per kilogram. Molybdenosis can generally be overcome by providing large
amounts of copper. Concentrations of molybdenum much lower than those needed
to cause acute toxicity signs can result in copper deficiency, depending on the length
of time the cattle are exposed and the concentration of dietary copper.

Molybdenum levels in forages vary greatly depending on soil type and soil pH.
Neutral or alkaline soils with high moisture and organic matter favor molybdenum
uptake by forages. Cereal grains and protein supplements are less variable in molyb-
denum than forages.

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Metals and Minerals

 Konnie H. Plumlee DVM, MS, Dipl ABVT, ACVIM, in Clinical Veterinary Toxicology,
2004

Mechanism of Action.
Mo is required for metalloenzymes including xanthine oxidase, xanthine dehydro-
genase, aldehyde oxidase, and sulfite oxidase. In blood Mo binds with -macroglob-
ulin in the membranes of erythrocytes, where it enhances the resistance of the
membranes to rupture.3,4 Because of its requirement in metalloenzymes, Mo is an
essential nutrient for essentially all animals.

Mo has a three-way interaction with copper and sulfur.5 Ruminants are more sensi-
tive than nonruminant species to the toxicity of Mo, and this difference is generally
attributed to sulfur metabolism in the rumen. Dietary sulfur is converted to sulfide
in the rumen, which decreases the absorption of copper. Increasing Mo in the diet
increases the rate that microorganisms in the rumen convert the dietary sulfur to
sulfide. The thiomolybdates are absorbed and alter the postabsorptive metabolism
of Mo. The dithiomolybdates and trithiomolybdates are radially absorbed from the
rumen, but the total significance of this is not known.6

Increasing dietary Mo and sulfur increases the amount of trichloroacetic acid in-
soluble Mo-copper protein complex found in plasma. This occurs in both sheep
and cattle, and TCA solubility is a measure of available copper present in plasma.
However, clinical signs of copper deficiency can be observed even though plasma
and liver copper levels are within normal range. Mo may also alter zinc metabolism
in cattle.7

The desired ratio of copper to Mo is 4:1 to 10:1.8 The major factor that can result
in the calculated copper to Mo ratio being inadequate is dietary sulfur. Increasing
sulfur content in the diet, including sulfur in forage, increases the toxicity of Mo. A
dietary sulfur/Mo ratio of 100:1 may be considered safe, as long as neither Mo nor
sulfur is present in excess.

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