Page 496 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

VetBooks.ir Chapter 32

Molybdenum

Jeffery O. Hall

INTRODUCTION can occur in a variety of oxidation states that range from
(-II) to (VI) (IMOA, 2006), but valence states IV, V, and
Molybdenum (Mo) is an essential nutrient in plants and
VI are the most common in biological systems (Johnson,
animals. Thorough reviews on Mo have been published
1997). Mo is utilized in the production of oxidation cata-
(Dick, 1956; Underwood, 1977; Ward, 1978; Friberg
lysts, pigments, corrosion-resistant steel, smoke suppres-
and Lener, 1986; Mills and Davis, 1987; Rajagopalan,
sants, lubricants, fertilizers, and metal alloys. Although
1988; Nielsen, 1996; Johnson, 1997; NRC, 2006; Gould
uniformly found in nature, the United States has the great-
and Kendall, 2011). In plants and microbes, reduction of est producible Mo reserves.
nitrate to nitrite and nitrogen fixation requires Mo
Mo is commonly found in low concentrations in most
(Williams and daSilva, 2002). Higher animals require Mo
dietary constituents (Rajagopalan, 1988), but excess
for oxygen transfer reactions of aldehyde oxidase, sulfite
intake can occur from plants grown on soils naturally
oxidase, and xanthine oxidase, where Mo is bound to a
high in Mo or from areas contaminated by mining or
pterin nucleus (Johnson et al., 1980). Although dietary
smelting operations. Naturally high soil and forage
clinical deficiencies have not been reported under natural
molybdenum concentrations have been reported in local-
conditions (Mills and Davis, 1987), deficiency has been
ized areas of several states in the western United States,
produced in animals fed purified Mo deficient diets (Mills
as well as Canada, England, Australia, and New Zealand
and Bremner, 1980; Anke et al., 1985). Functional Mo
but likely occurs in other countries as well. In addition,
deficiency has been caused by genetic disorders in
high molybdenum forages have been identified from con-
humans (Reiss, 2000) and competitive replacement of
taminated areas associated with mining and industrial
tungsten for Mo in enzymes (Nell et al., 1980). Iatrogenic
operations (King et al., 1984). Daily dietary requirements
Mo deficiency, resulting in aberrant sulfur-containing
for all species are such that requirements are met, even
amino acid metabolism, has been reported following pro-
with low intake.
longed total parenteral nutrition (Abumrad et al., 1981).
Mo toxicity is intricately tied to interactions with copper
and sulfur. Predominant manifestations of Mo poisoning are PHARMACOKINETICS/TOXICOKINETICS
associated with secondary copper deficiency, but not all clin-
ical signs are alleviated by copper supplementation, as some Absorption
of the effects can be related to direct thiomolybdate binding
to the copper dependent enzyme systems (Gould and Mo absorption differs between monogastrics and
Kendall, 2011). The copper sulfur molybdenum interac- ruminants. In monogastrics, Mo absorption occurs from
tions are complex and vary greatly in degree of severity the stomach throughout the intestinal tract (Bell et al.,
among species. 1964; Miller et al., 1972; Nielsen, 1996). In contrast, rumi-
nant absorption likely depends on the chemical form of
the molybdenum. Historically, Mo absorption in ruminants
was thought to occur in the intestinal tract, as an extensive
BACKGROUND
delay in peak blood concentration would indicate that
Mo is a transition metal within group VI of the periodic rumen absorption did not occur. However, some delay in
table. It has an atomic number of 42, an atomic weight of overall total Mo absorption could be due to the time
95.95, and has seven different naturally occurring atomic necessary for the conversion of the molybdates to
masses from 92 to 100 (Rosman and Taylor, 1998). Mo thiomolybdates in the rumen, as preformed thiomolybdates
Veterinary Toxicology. DOI: http://dx.doi.org/10.1016/B978-0-12-811410-0.00032-5
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