228 Introduction to Human Nutrition
and skin. The major excretory route of molybdenum
after ingestion is the urine, with signifi cant amounts
also excreted in bile.
Metabolic functions and essentiality
Molybdenum functions as a cofactor for the iron- and
fl avin-containing enzymes that catalyze the hydroxyl-
ation of various substrates. The molybdenum cofac-
tor in the enzymes aldehyde oxidase (oxidizes and
detoxifi es purines and pyrimidines), xanthine oxidase/
hydrogenase (production of uric acid from hypoxan-
thine and xanthine), and sulfi te oxidase (conversion
of sulfi te to sulfate) has molybdenum incorporated as
part of the molecule.
Defi ciency symptoms
Although there is a clear biochemical basis for the
essentiality of molybdenum, defi ciency signs in
humans and animals are diffi cult to induce. Naturally
occurring defi ciency, uncomplicated by molybdenum
antagonists, is not known with certainty. In animal
experiments, where large amounts of the molybde-
num antagonist tungsten have been fed, defi ciency
signs are depressed food consumption and growth,
impaired reproduction, and elevated copper concen-
trations in the liver and brain.
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 sulfi te and decreased
urinary excretion of uric acid and sulfate.
Assessing status
Determining the body status of molybdenum is dif-
fi cult. Homeostatic control of molybdenum ensures
that plasma concentrations are not elevated, except
after extremely high dietary intakes. Decreased
urinary concentrations of sulfi te, 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.9.14 Fluoride
Fluorine occurs chiefl y in fl uorspar and cryolite, but
is widely distributed in other minerals. Fluoride is the
ionic form of fl uorine, a halogen, and the most elec-
tronegative of the elements in the periodic table; the
two terms are often used interchangeably. Fluorine
and its compounds are used in producing uranium
and more than 100 commercial fl uorochemicals,
including many well-known high-temperature plas-
tics. Hydrofl uoric acid is extensively used for etching
the glass of light bulbs, etc. Fluorochlorohydrocarbons
are extensively used in air conditioning and refrigera-
tion. Fluorine is present in small but widely varying
concentrations in practically all soils, water supplies,
plants and animals, and is a constituent of all diets.Absorption, transport and
tissue distribution
Fluoride appears to be soluble and rapidly absorbed,
and is distributed throughout the ECF in a manner
similar to chloride. The concentrations of fl uorine in
blood, where it is bound to albumin, and tissues are
small. The elimination of absorbed fl uoride occurs
almost exclusively via the kidneys. Fluoride is freely
fi ltered through the glomerular capillaries and under-
goes tubular reabsorption in varying degrees.
Fifty percent of orally ingested fl uoride is absorbed
from the gastrointestinal tract after approximately 30