226 Introduction to Human Nutrition
while there are close metabolic relationships at the
molecular and transport levels between iodine and
vitamin A. Conversely, the widespread disruption of
metabolism in IDDs can affect the proper utilization
of a host of other nutrients.
9.12 Manganese
Manganese is widely distributed in the biosphere: it
constitutes approximately 0.085% of the Earth’s crust,
making it the twelfth most abundant element.
Manganese is a component of numerous complex
minerals, including pyroluosite, rhodochrosite,
rhodanite, braunite, pyrochite, and manganite.
Chemical forms of manganese in their natural depos-
its include oxides, sulfi des, carbonates, and silicates.
Anthropogenic sources of manganese are predomi-
nantly from the manufacturing of steel, alloys, and
iron products. Manganese is also widely used as an
oxidizing agent, as a component of fertilizers and fun-
gicides, and in dry cell batteries. The permanganate is
a powerful oxidizing agent and is used in quantitative
analysis and medicine.
Manganese is a transition element. It can exist in
11 oxidation states from −3 to +7, with the most
common valences being +2, +4, and +7. The + 2
valence is the predominant form in biological systems,
the +4 valence occurs in MnO 2 , and the +7 valence is
found in permanganate.
Absorption, transport, and
tissue distribution
The total amount of manganese in the adult human
is approximately 15 mg. Up to 25% of the total body
stores of manganese may be located in the skeleton
and may not be readily accessible for use in metabolic
pathways. Relatively high concentrations have been
reported in the liver, pancreas, intestine, and bone.
Intestinal absorption of manganese occurs through-
out the length of the small intestine. Mucosal
uptake appears to be mediated by two types of mucosal
binding, one that is saturable with a fi nite capacity
and one that is nonsaturable. Manganese absorption,
probably as Mn^2 +, is relatively ineffi cient, generally
less than 5%, but there is some evidence of improve-
ment at low intakes. High levels of dietary calcium,
phosphorus, and phytate impair the intestinal
uptake of the element but are probably of limited
signifi cance because, as yet, no well-documented
case of human manganese defi ciency has been
reported.
Systemic homeostatic regulation of manganese is
brought about primarily through hepatobiliary
excretion rather than through regulation of absorp-
tion (e.g., the effi ciency of manganese retention does
not appear to be dose dependent within normal dietary
levels). Manganese is taken up from blood by the liver
and transported to extrahepatic tissues by transferrin
and possibly α 2 -macroglobulin and albumin. Manga-
nese is excreted primarily in feces. Urinary excretion of
manganese is low and has not been found to be sensi-
tive to dietary manganese intake.Metabolic function and essentiality
Manganese is required as a catalytic cofactor for
mitochondrial superoxide dismutase, arginase, and
pyruvate carboxylase. It is also an activator of glycos-
yltransferases, phosphoenolpyruvate carboxylase, and
glutamine synthetase.Defi ciency symptoms
Signs of manganese defi ciency have been demon-
strated in several animal species. Symptoms include
impaired growth, skeletal abnormalities, depressed
reproductive function, and defects in lipid and carbo-
hydrate metabolism. Evidence of manganese defi -
ciency in humans is poor. It has been suggested that
manganese defi ciency has never been observed in
noninstitutionalized human populations because of
the abundant supply of manganese in edible plant
materials compared with the relatively low require-
ments of mammals. There is only one report of
apparent human manganese defi ciency. A male subject
was fed a purifi ed diet defi cient in vitamin K, which
was accidentally also defi cient in manganese. Feeding
this diet caused weight loss, dermatitis, growth retar-
dation of hair and nails, reddening of black hair, and
a decline in concentrations of blood lipids. Manganese
defi ciency may be more frequent in infants owing to
the low concentration of manganese in human breast
milk and varying levels in infant formulae.Toxicity
Manganese toxicity of dietary origin has not been well
documented. Toxicity has been observed only in
workers exposed to high concentrations of manga-
nese dust or fumes in air. For example, mine-workers
in Chile exposed to manganese ore dust developed,