TRACE/MICROMINERALS

They are required in small amount by the body compared to the macro elements
Iron
Iron was discovered in the body by Lemmery and Geofgroy in 1713. Nicholas Monarde, a
16th century physician of Seville, indicated that iron produced “great effects and marvellous
works”, he used iron for a large number of unrelated ailments including gout, acne and
alopecia. (Alopecia areata is an autoimmune disorder that usually results in unpredictable,
patchy hair loss).
Antoine Lavoisier (1743–1794), considered by many as the “father of modern chemistry”
and a prominent chemist and leading scientist in the 18th century chemical revolution,
developed an experimentally based theory of the chemical reactivity of oxygen and Iron. He
referred oxygen as iron’s intimate partner in innumerable biochemical processes. He
discussed their interaction in more and indicated that this interaction (of iron with oxygen)
could generate extremely toxic radical species,
Iron is the most abundant element on earth, yet only trace elements are present in living cells.
Iron is found in in every living cell and is essential to all cells of the human body. The total
body content is about 5grams; varying slightly with age, sex, body size, nutritional status and
general health. It is the only nutrient for which adult women have greater requirements than
adult men
Iron is a micro-mineral that has a number of key functions. It’s a major part of hemoglobin in
red blood cells; as it carries oxygen from the lungs to all parts of the body and facilitates
oxygen use and storage in muscles. In addition, every cell in the body needs iron to produce
energy
Almost 1/4 of the worldwide population is affected by anemia, of which iron deficit is the
primary cause. Its deficiency is linked with impaired physical work ability reduced mood and
cognitive function, and poor pregnancy related outcomes. An individual’s iron condition falls
on a range (ranging from replete to depleted iron stores), iron deficiency and iron deficiency
anemia. Therefore, individuals with iron deficiency are at increased risk of developing iron
deficiency anemia
Iron chemistry and physiology
Iron has two ordinary aqueous oxidation states namely ferrous (Fe2+) and ferric (Fe3+).
These states enable iron to take part in oxidation/reduction reactions that are crucial to energy
metabolism by accepting or donating electrons. On the other hand, this property also enables
free iron to catalyze oxidative reactions, ensuing in reactive and damaging free radicals.
Hence, body iron is required to be chemically bound to assist appropriate physiological
role,of transport, and storage, with minimal opportunity for free ionic iron to catalyze harmful
oxidative reactions. The majority of the body’s iron functions in heme protein complexes that
transport oxygen as hemoglobin and myoglobin. Approximately 2/3 of the body iron is in
hemoglobin. For transport by hemoglobin, oxygen binds directly to the iron atom, stabilized
in a Fe2+ oxidation state surrounded by the protoporphyrin ring and histidine residues.
Hemoglobin iron easily binds and releases oxygen, circulating in blood erythrocytes.
Myoglobin, consisting of a single heme molecule and globin, enables oxygen transfer from

1
erythrocytes to cellular mitochondria in muscle cytoplasm. Lesser amounts of iron in the
heme form, function in mitrochondrial cytochromes involved with electron transfer, oxygen
utilization, and the production of ATP. A small fraction of body iron functions in heme-
containing hydrogen peroxidases such as catalase that protect against excessive hydrogen
peroxide accumulation by catalyzing its conversion to hydrogen and oxygen.
Other important functions of iron include;

 Catalyzing the conversion of beta carotene into vitamin A.

 The synthesis of purines which form integral part of nucleic acid
 The removal of lipids from the blood.
 Collagen synthesis.
 Antibody production needed for proper immune formation.
 Detoxification of drugs in the liver.
Iron absorption and metabolism
The new born infant has a total of about 250mg in the body. The total body iron in an adult
male is 3000 to 4000 mg. In contrast, the average adult woman has only 2000-3000 mg of
iron in her body. This difference may be attributed to lesser iron reserves in women, lower
concentration of hemoglobin and a smaller vascular volume than men. Of this approximately
two-thirds are utilized as functional iron such as that in hemoglobin (60%), myoglobin (5%)
and various heme and nonheme enzymes (5%). The remainder is found in storage as ferritin
(20%) and hemisoderin (10%).
Control of iron uptake is undoubtedly of principal importance due to the lack of a regulated
means of excreting iron. Once the food is consumed and digested, dietary iron is mainly
absorbed in the duodenum and proximal jejunum. Reasonably, haem iron is absorbed more
effi ciently than non-haem iron, apparently by endocytosis of the intact iron– protoporphyrin
complex at the enterocyte brush border. After the digestion iron from all dietary sources
enters a common intracellular pool from which depending on the iron status of individuals it
is either stored as ferritin in the enterocyte or exported from the enterocyte via the ferroportin
transporter on the basal side of the cell. Ferroportin transports ferrous iron which is
immediately oxidized to Fe3+ and picked up by transferrin to be transported to cells
expressing transferrin receptors.
The body uses several mechanisms to regulate iron absorption because the body cannot easily
eliminate excess iron once it is absorbed.5-10% of iron in food is absorbed in healthy
people.10-20% of iron in food is absorbed in by people with iron deficiency. The extent of
iron absorption depends on a variety of factors, the most important being the amount of
current iron stores in the body. Iron in food occurs in several forms which differ in their
absorption by the body. Iron that is part of haemoglobin and myoglobin molecules in animal
flesh is about 40% of total iron present called heme iron and is readily absorbed more than
twice as efficiently as simple elemental iron known as non-heme iron. Non-heme iron
provided from plant sources and elemental iron components of animal tissues. It is less
efficiently absorbed than heme iron. The difference in absorption of heme and non heme iron

2
make animal flesh a rich source of dietary iron, considering both its iron content and the
increased efficiency of absorption of the heme iron present. Consuming heme iron and non
heme iron together increases non-heme iron absorption e.g. eating meat with vegetables and
grain products.
Iron status, iron deficiency and iron overload
Infants, children, teenagers, and women of childbearing age are commonly affected by iron
deficiency; whereas healthy adult males are seldom deficient. Deficiency is caused by several
factors, usually by a combinations of increased need (rapid growth in the young population,
menstruation and pregnancy in fertile women) and insufficient uptake, which in turn may
depend on other factors such as a decreased caloric intake and/ or a larger fraction of calories
derived from food ingredients which contains less absorbed iron.
The earliest stage of iron deficiency is characterized by loss of storage iron (indicated by
ferritin) and is called iron depletion or prelatent iron deficiency. The concentrations of serum
iron and the iron-carrying serum protein transferrin are normal at this stage. When iron stores
are exhausted (serum ferritin.
Symptoms frequently associated with iron deficiency anemia include palor, weakness,
fatigue, dyspnea, palpitations, sensitivity to cold, abnormalities in the oral cavity and
gastrointestinal tract, and reduced capacity for work [33]. It further appears that even
mid/prelatent iron deficiency may have significant health consequences which can be
attributed to decreases in essential body iron and limitations in tissue oxidative capacity.
Iron overload is associated with increases in non-protein bound iron resulting from the
physiologic iron-binding capacity being overwhelmed. Disadvantages with overload are for
example increased risk for bacterial infection and cardiomyopathy. Overload can result from
inborn errors in metabolism leading to hyper-absorption of iron or inadequate synthesis of the
iron-binding proteins. Overload can also result from excessive absorption of dietary iron due
to various causes including chronic ingestion of greater than adequate amounts of dietary
iron, especially heme iron. These observations concerning of iron overload have raised the
question as to whether or not general fortification of food with inorganic iron is beneficial.
Dietary and non-dietary factors affecting iron absorption
Dietary factors contribute a significant role in the development of iron defi ciency and then
iron deficiency anemia.
 Iron absorption by the gut enterocytes controls iron balance but there is no route of
controlled iron excretion. This means that iron absorption is regulated by dietary and
systemic factors. Dietary iron is largely non-heme iron with about 5%–10% in the
form of heme iron in diets containing meat. Even though heme iron constitutes a
smaller part of dietary iron, it is highly bioavailable and 20%–30% of heme iron is
absorbed. Contrary, the absorption of non-heme iron is much more variable and
signifi cantly affected by other components of the diet; with 1%–10% of non-heme
iron absorbed [38]. Moreover, iron in the environment and the diet is primarily ferric
iron (Fe3+) which is insoluble and so not bioavailable. Thus, before it can be
absorbed the non-heme iron has to be reduced from ferric (Fe3+) to ferrous (Fe2+)
iron by dietary reducing agents, such as ascorbic acid or by endogenous ferri-

3
reductases, such as duodenal cytochrome B (dcytB) [39]. Ferrous iron is transported
across the apical membrane of the duodenum by the divalent metal transporter 1
(DMT1), which is localized on the brush border membrane close to dcytB. The uptake
of ferrous ions by dcytB is driven by proton co-transport, so an acidic duodenal pH
facilitates iron uptake, and is competitively inhibited by other divalent cations.
Ascorbic acid is one of the most effective enhancer of nonheme iron absorption. Other
dietary factors such as citric acid and other organic acids, alcohol and carotenes
similarly enhance non-heme iron absorption. Furthermore, animal based proteins such
as meat, fish, and poultry, enhance iron absorption but the bioactive component of the
“meat factor” has yet to be identified. Meat also promotes non-heme iron absorption
by activating gastric acid production. Conversely, absorption of non-heme iron is
inhibited by phytic acid (inositol hexaphosphate and inositol pentaphosphate) in
grains and cereals and by polyphenols in some vegetables, coffee, tea, and wine.
These inhibitors bonded to non-heme iron so it is not available for uptake.

Dietary factors inhibiting iron absorption

Calcium:
Calcium does inhibit both non-heme iron and heme iron absorption. Calcium inhibits
the absorption of both heme and nonheme iron in a comparable way and thus, it is
likely that this inhibition by calcium occurs after the heme iron is freed from the
porphyrin ring. Calcium has been shown to inhibit iron absorption in both rats and
man.
Calcium supplements in amounts greater than 300 mg/d can reduce iron absorption.
Calcium supplements should be taken several hours before or after an iron rich meal.

Phytate:
During digestion, the phytate molecule can be negatively charged, indicating a
potential for binding positively charged metal ions like iron [48]. The negative
consequence of phytate in bran on iron absorption was first demonstrated by Sharpe et
al. (1950). Several methods of preparations of cereal grains including soaking,
germination and fermentation have been shown to completely reduce the phytate
content of cereals and vegetables under optimal conditions.
Phenolic ( Polyphenols)
Polyphenols compounds: Include tannins in tea and caffeine in coffee. During
digestion, the phenolic compounds from the food or beverage released and can form
complex with Fe in the intestinal lumen making it unavailable for absorption. Nearly
all beverages reduced iron absorption depending on the amount of total polyphenols,
with the inhibition of black tea the greatest at 79–94%. Other beverages with high
phenolic include red wine, coffee cocoa while vegetables with high phenolic include,
spinach and aubergine.
Dietary factors enhancing iron absorption
Ascorbic acid:
Ascorbic acid appears to be the factor which is most potent in enhancing of iron
absorption particularly the non-heme iron in single-meal studies. There are two
mechanisms for this effect of nonheme iron on absorption. Firstly, it prevents the

4
 formation of insoluble and bonded iron compounds and secondly reduces ferric iron
(Fe 3+) to ferrous (Fe2+) iron states
Meat:
Meat increases the absorption of nonheme and heme iron. The mechanism behind this
enhancing effect of meat on both heme and nonheme iron absorption is as yet
unknown. It has however been reported by Hurrell et al. (2006), that meat
enhancement of iron absorption is by multiple mechanisms involving both gastric
acidity effects and chelation. Meat may enhance nonheme iron absorption by
stimulating production of gastric acid, and thereby promoting iron solubilization
within the stomach. Thereafter, a meat factor(s) may chelate the solubilized iron in the
acidic (lower pH) environment of the stomach and thereby maintain iron solubility
during intestinal digestion and absorption. Fish and poultry also have an enhancing
effect on nonheme iron absorption.
Alcohol:
Alcohol increases the absorption of non-heme iron slightly in man. It has been shown
that chronic alcohol abusers have increased serum ferritin concentrations and
calculated total body iron compared with non-drinkers although it is controversial
whether the alcohol affects the actual absorption process of iron.
 oxalic acid in vegetables bind iron thus reducing its absorption.
 Dietary fibre intakes above 35g/day bind iron and other trace elements.
Form of dietary iron
Heme iron is better absorbed compared to non-heme iron.
Iron needs

Iron needs differ for different age groups and sex. Pregnant women and adolescent girls need
twice as much as iron compared to adult men. Iron needs are determined by need to replace
losses through sweat, hair, nails, dead skin cells, masturbation or other forms of bleeding.
Growth increases iron needs due to increased blood volume and tissue mass. The adult
recommendations for iron are 10mg/d for men and 15mg/d for women to account for
menstruation losses.

Pregnant women require 30mg/d daily. This takes care of the increased placenta blood
volume and the foetal needs. New borns are born with enough iron stores to last for the first
4-6months until supplementary feeding is introduced. Human milk is a poor source of iron
15mg/d. Infants and children: Reserve of iron last 4–6months after delivery hence
complementary foods introduced at 6 months need to be rich in iron.

Dietary sources of iron

Liver is the richest source, lean meat, chicken, eggs, lean pork, dark green vegetables,
legumes, nuts, molasses and cereals.

Iron deficiency

5
Continued iron deficiency leads to nutritional anaemia caused by lack of dietary essentials
involved in haemoglobin formation or poor absorption of these dietary essentials. Some types
of anaemia have been reported to be caused by a lack of either dietary iron or high quality
protein; lack of pyridoxine (vitamin B6), which catalyses the heme portion of the
haemoglobin molecule, by a lack of vitamin C which influences the rate of iron absorption
and the release of iron from transferring to the tissues; and by lack of vitamin E, which
affects the stability of the red blood cell membrane. Copper is not part of the haemoglobin
but aids in its synthesis by influencing the absorption of iron, its release from the liver, or its
incorporation into haemoglobin.
Nutritional anaemia is characterised as both hypochromic and microcytic. Hypochromic
suggests a lack of red pigment haemoglobin and microcytic indicates the presence of small
red blood cells. When red blood cells synthesis is reduced, the amount of oxygen carried to
the blood is decreased. There are many types of anaemia but the major type found in the
world is iron deficiency anaemia. It is common in adolescent girls (growth and menstrual
demands), young infants and women of child bearing ages.
Iron toxicity
Excess intake may lead to hemosiderosis i.e. increased iron reserves due to excessive
supplements. Hemochromatosis: A genetic disorder of iron metabolism characterized by
increased absorption, saturation and deposition of iron in the liver tissues.

Conclusion
Iron is a vital element in the body. It is also toxic when consumed in excess. Hence, its effect
in the body is like a two edged sword. Iron deficiency result in anemia,
ZINC (Zn)
Zinc is an essential element
Zinc is present in all body tissues and fluids .The total human body zinc content has been
estimated to be 30 mmol (2grams). Skeleton muscle accounts for approximately 60% of the
total body content and bone mass, with a zinc concentration of 1.5-3.0mol/g (100-200g/g) for
approximately 30%. The concentration of zinc in lean body mass is approximately 0.46 mol/g
(30(g/1). Plasma zinc has a rapid turn over and represent only about 0.1% of total body zinc
content. This level appears to be under close homeostatic control. High concentrations of zinc
are found in the choroids of the eye (4.2 mol/g or 274 g/g) and in prostastic fluids (4.6-7.7
mmol/l or 300-500mg/l). Zinc is lost through faeces, urine and shed tissues. High tissue
losses are from the skin, the mucosal cells, menstrual fluids and semen.
History:
Zinc was first shown to be biological important more than 100 years ago when it was found
to be needed for the growth of certain bacteria. In the 1920s, it was demonstrated to be
required for the growth of experimental rats.
Absorption/Metabolism/Excretion:
Absorption- Zinc is poorly absorbed less than 10% of dietary zinc is taken into the body,
primarily in the duodenum. It appears that metallic and zinc in its carbonate, sulfate, and

6
oxide forms are all absorbed equally well. Large amounts of calcium, phytic acid, fibre and
copper inhibit zinc absorption.
Metabolism - After Zinc is absorbed in the small intestine, it combines with plasma proteins
for transport to the tissues. Relatively large amounts of zinc are deposited in bones, but these
stores do not move into rapid equilibrium with the rest of the organism. The body pool of
biologically available zinc appears to be small and to have a rapid turnover, as evidenced by
the prompt appearance of deficiency signs in experimental animals.
Excretion - Most of the zinc derived from metabolic processes is excreted in the intestine - in
pancreatic, intestinal, and bile secretions. Only small amounts are excreted in the urine.
Functions:
Over 300 enzymes require zinc as a co-factor for optimal activity. Adequate zinc is necessary
to support many bodily functions such as;
1. It is involved in nucleic acid synthesis and function (some factors that control
expression of genes contains zinc-rich regions that bind DNA).
2. It is involved in protein metabolism, growth and wound and burn healing.
3. Immune function.
4. Development of sexual organs and bone.
5. Involved in storage, release and function of insulin.
6. Cell membrane structure and function.
Required for the transfer of carbon dioxide in red blood cells, for proper calcification of
bones, for the synthesis and Metabolism of proteins and nucleic acids; for the development
and functioning of reproductive organs;
Deficiency Symptoms/Toxicity:
Deficiency Symptoms- Loss of appetite and stunted growth, bone problems, improper
development of the male gonads , severe delays in wound healing, and an impairment of
glucose tolerance.
Poor hair development,
Toxicity-Toxicity of zinc is characterized by anemia, depressed growth, stiffness,
hemorrhage in bone joints resorption, depraved appetite, and in severe cases, death. The
anemia appears to result from an interference with iron and copper utilization because
addition of these two elements can overcome the anemia caused by excessive zinc.
Major interrelationships: zinc is involved in many relationships in the metabolism of
carbohydrates, fats, proteins, and nucleic acids. In interference with the utilization of copper,
iron, and other trace minerals, when there are excess dietary levels of zinc, in protection
against the toxic effects of cadmium (a zinc by product) , when there is ample dietary zinc, in
reduced absorption, when there are high dietary levels of calcium, phosphorus, and copper.
Also, there is indication that added dietary zinc may partially alleviate lead toxicity in some
species.

7
Recommended daily requirements for zinc
The adult recommended daily requirement is 15 mg/day for men and 12 mg/day for women.

Dietary sources of zinc

In general, protein-rich diets are also rich in zinc. Lean meats especially beef and other red
meats, eggs and shell fish are the best sources. Cereals and legumes contain significant
amounts of zinc but contain phytic acid and other substances that can interfere with intestinal
absorption of zinc.
Zinc deficiency
Zinc deficiency is associated with;
 Severe growth retardation and arrested sexual maturation.
 Altered taste acuity.
 Impaired immune function.
 Slow wound healing.
 Impaired central nervous system function.
IODINE (I)
Iodine is recognized as an essential nutrient for all animal species., ,
Iodine is present in the body in minute amounts, 15-23 mg and 75% of this is concentrated in
the thyroid gland that uses it to synthesize the where it is an integral component of the thyroid
hormones, thyroxin and triiodothyronine both of which have important metabolic roles. The
remainder is in other tissues particularly in the salivary, mammary and gastric glands and in
the kidney. It is present in food as iodide and other non elemental forms. Iodine was linked to
the presence of an enlarged thyroid gland (goitre) during World War I.
One of the factors affecting the output of thyroid glands is iodine availability. In the absence
of sufficient iodine, the gland attempts to compensate for the deficiency by increasing its
secretory activity, and this causes the gland to enlarge. This condition is known as simple, or
endemic, goiter.
History:
Iodine was the first nutrient to be recognized as essential for animals and humans. As early as
3000 B.C. the Chinese treated goiter by feeding seaweed and burnt sponge. Also, Hippocrates
(460 to 370 B.C.) a Greek physician, used the same treatment for enlarged thyroid glands.
The name iodine is derived from the Greek word iodes, meaning violet color, from the color
of the fumes of iodine.
In 1811, Bernard Courtois, a French chemist, discovered iodine in seaweed and described
some of its basic properties. Five years later, potassium hydriodate was introduced by Prout
as a treatment for goiter. However, the widespread appearance of goiter continued in much of
the world for many years.

8
In 1914, Kendall, at the Mayo Clinic, in Minnesota, reported the isolation of a crystalline
compound containing 65% iodine from the thyroid gland and named it thyroxin. From this
discovery and from other studies, the inclusion of iodine in the diets of animals and man led
to a greater reduction of goiter in the U.S. and other developed countries of the world.
Kendall received the Nobel Prize for his work on thyroxin and other hormones.
Absorption/Metabolism/Excretion:
Iodine absorption is very efficient (near 100%). Although it is absorbed throughout the entire
gastrointestinal tract, most absorption takes place in the small intestine. Following absorption,
iodine takes two main pathways within the body. Approximately 30% is removed by the
thyroid gland and used for the synthesis of the thyroid hormones; most of the remainder is
excreted in the urine, although small amounts are lost in the feces and sweat.
Functions:
1. The sole function of iodine is making the iodine-containing hormones, thyroxin and
triodothyronine, secreted by the thyroid gland, which regulate the rate of oxidation
within the cells; and in so doing influence growth, the functioning of the nervous and
muscles tissues, circulatory activity, and the Metabolism of all nutrients.
2. Regulation of growth and development as part of thyroxin hormone. Thyroxin can
stimulate metabolism by as much as 30%.
3. Conversion of carotene to vitamin A.
4. Synthesis of protein.
5. When thyroxin levels are normal, absorption of carbohydrates from the intestines is
more efficient.
6. Synthesis of cholesterol.
Recommended daily allowances:

For adults 150mg/day

Dietary sources of iodine

These include: Salt water, fish, sea foods, iodized salt, molasses, dark green leafy vegetables
especially spinach leaves.

Deficiency of iodine

Goitre

This is a condition characterised by swelling in the neck as a result of the enlargement of the
thyroid gland. The gland enlarges as it attempts to compensate for lack of iodine essential to
its major role in the synthesis of thyroxin. The pituitary gland hormone that stimulates the
thyroid hormone production, thyroid stimulating hormone also stimulates the growth of the
thyroid gland. Too much growth of the gland causes difficulties in breathing.

9
Goitre is also associated with the consumption of goitrogens (substance in foods such as the
cabbage family and water that interfere with thyroid gland metabolism and thus may cause
goitre if consumed in large amounts). Defects in the enzymes necessary for the synthesis and
release of thyroxin can also lead to goitre. Goitre is common in areas where the soil is poor in
iodine due to leaching. Goitre incidences are six times more in females than males with
adolescent girls and pregnant women being more susceptible.

Cretinism
If an expectant mother consumes iodine deficient diets during the early pregnancy, her infant
may be born with a short stature (dwarfed) and with mental retardation. Maternal iodine
needs take precedence over foetal needs. The retarded body growth is referred to as cretinism
characterized by physical drawfness, mental retardation, thick-dry skin and enlarged
protruding stomach.

Myxedema
This is a condition seen in adults who have had symptoms of hypothyroidism throughout
their development and growth period. It is characterized by coarse sparse hair, dry, yellowish
hair, poor tolerance to cold and low husky voice.
Hyperthyroidism
This is where basal metabolic rate is accelerated by as much as 100% above normal and is
associated with over activity of the thyroid gland and experience nervousness, weight loss,
increased appetite, intolerance to heat, tremors and protruding eyeballs.

SELENIUM (Se)
Selenium is named after selene, the moon goddess. It is needed in minute quantities, because
(1) only traces are present in most dietary sources, and (2) poisoning may result when the
dietary level increases to 0.0003% or more. However, adequate dietary Se is one of the keys
to the maintenance of health under stressful conditions such as (1) prematurity at birth, (2)
protein-energy malnutrition, and (3) the tissue disorders which accompany aging.
Selenium is deposited in all body tissues except fat. The highest concentrations occur in the
liver, kidney, heart and spleen. Serum levels are about 0.22 µg/dl. Most selenium in foods is
bound to derivatives of the amino acids; methionine and cysteine. Because these substances
are readily absorbed, bioavailability of selenium is considerably higher than that of zinc and
iron. About 50%-100 % of dietary selenium intake is absorbed. In addition, since no
physiological mechanism appears to control selenium absorption, selenium has a definite
potential for toxicity. Most selenium is excreted via the urine and faeces.

Absorption/Metabolism/Excretion:
Ingested Se is absorbed in the duodenum. Thence, it is bound to a protein and transported in
the blood to the tissues, where it is incorporated into tissue protein as selenocysteine and
selenomethionine, in this later instance Se replaces sulphur in the amino acids cysteine,
cystine and methionine. Se is excreted mostly through the kidneys, a little in feces and sweat.
Functions:
1. Component of the enzyme glutathione peroxidase, the metabolic role of which is to
protect against oxidation of polyunsaturated fatty acids and resultant tissue damage.

10
 2. Protecting tissues from certain poisonous substances, such as arsenic, cadmium and
mercury.
3. Interrelation with vitamin E – they spare each other, and with sulphur containing
amino acids.
4. It functions as an integral component of an anti oxidant enzyme; glutathione
peroxidase that protects cells and lipid membranes against oxidative damage.
5. It also acts as a structural component, incorporated into the protein matrix of the teeth.
Recommended daily allowances for selenium
The recommended daily allowance estimated to be safe and adequate for an adult is about 50-
200 µg/day.

Dietary sources of selenium

Food sources vary with the selenium soil content. Good sources include sea food, legumes,
whole grains, low fat meats and dairy products with smaller amounts in vegetables.

Selenium deficiency
The signs and symptoms of selenium deficiency include pain, muscle wasting and
cardiomyopathy, a form of heart disease.

Selenium toxicity
High doses (a milligram or above daily is toxic. Selenium toxicity causes vomiting,
diarrhoea, loss of hair and nervous system.

Major interrelationships
The functions of Se are closely related to those of vitamin E and the sulphur containing
amino acids
Selenium protects against the toxic effects of arsenic, cadmium, silver, copper and mercury
A diet high in protein or high in sulphate provides some protection against selenium
poisoning
Diets rich in polyunsaturated fatty acids but poor in vitamin E may raise the requirements for
selenium.
FLUORINE (F)
Fluorine is present in small, but widely varying, concentrations in practically all soils, water
supplies, plants and animals. In small amounts, fluorine helps develop strong bones and teeth,

11
It is found mainly in the teeth and skeleton. Traces of fluorine in the teeth help to protect
against decay. When consumed in early adulthood, it becomes part of the enamel, making it
more resistant to the organic acids formed from foods that get stuck in between the teeth.
Fluorine is also known to harden and strengthen the bone especially later in life and thus slow
or inhibit the development of osteoporosis. Fluorine in excessive amounts bones become
porous and soft and teeth become mottled and easily worn down.

History:
Fluorine was first isolated in 1886 by Henri Moissan, a Frenchman, who obtained it by the
electrolysis of anhydrous hydrogen fluoride containing dissolved potassium fluoride. The
name fluorine is derived from the Latin fluo, meaning to flow, because from early times it
was used as a flux in metallurgy.
Absorption/Metabolism/Excretion:
A large portion (about 90%) of ingested fluorine is normally absorbed, primarily from the
small intestine. That portion of absorbed fluorine which is not taken up by the bones and
teeth (50% or more of the fluorine absorbed) is excreted mainly in the urine (although small
amounts are excreted in the sweat and the feces), with the result that the level of fluorine in
the blood plasma is quite constant.
Functions:
Constitutes 02 to .05% of the bones and teeth. Necessary for sound bones and teeth.
Mode of action
Fluorine forms crystals of flourapatite which replaces crystals of hydroxypatite normally
deposited during tooth formation. Flourapatite in the tooth enamel is more resistant to cavity
forming acids. Absorption is known to occur in the mouth through the tooth surface. Intakes
of 8ppm in adult life protects against osteoporosis (a condition where there is a reduction of
the bone density due to erosion of calcium).
Dietary sources of fluorine
 The main source is water. If it contains 1ppm (part per million), this will be adequate.
 Other sources include small fish when consumed whole.
 Tea has a high content.
 Foods grown in high fluoride water will have more than fresh foods.
Toxicity
Too much fluorine intake causes browning of teeth enamel and excessive amounts may cause
dental flourosis in which the teeth become mottled.
Major interrelationships:
Large amounts of dietary calcium, aluminum, or fat will lower the absorption of fluorine.
MANGANESE (Mn)

12
In nutrition, manganese is an essential element for many animal species. It is an activator of
several enzyme systems involved in protein and energy metabolism and in the formation of
mucopolysaccharides.
History:
Manganase was first recognized as an element in 1774 by the famed Swedish chemist, Carl
Scheele. It was isolated in the same year by his co-worker Johann Ghan. The name
manganase is a corrupted form the Latin word for a form of magnetic stone, magnesia. Over
95% of manganese is used in the steel industry. In 1931, University of Wisconsin researchers
reported that manganese is a dietary essential for growth of rats.
Absorption/Metabolism/Excretion:
Absorption: Mn is poorly absorbed in the small intestines. On average 45% of ingested Mn is
absorbed and 55% excreted through feces. Absorption can be depressed by excessive intake
of calcium, phosphorous or iron.
Metabolism: Mn is loosely bound to a protein and transported as transmaganin.
Excretion: Mn is mainly eliminated from the body in the feces and very little is removed
through urine.
Functions:
Formation of bone and growth of other connective tissues
Blood clotting
Insulin action
Cholesterol synthesis
Activator of various enzymes in the metabolism of carbohydrates, fats, proteins, and nucleic
acids (RNA & DNA)
Deficiency Symptoms/Toxicity:
Poor growth, lameness, shortening and bowing of the legs and enlarged joints. It is
associated with impaired glucose tolerance.
Toxicity: Mn is not toxic in moderated levels
Major interrelationships:
Excess Ca and P interfere with the absorption of Mn. Ma and vitamin K work together in the
clotting of blood.
Food Sources:
Rice, sorghums and wheat/wheat by-products.
CHROMIUM (Cr)
The mention of this element makes most people think of the chrome plating on the bumpers
and body trim of their automobiles. However, it was recently discovered that the tiny metal

13
can also exist in forms which function as(1)an essential element (2) a hormone (3) a vitamin
and (4) a poison.
HISTORY
Chromium was discovered by the French chemist Vauquel in 1791, while he was studying
the properties of crocoites, an ore which is rich in lead chromate. The common name of
chrome was derived from the Greek word chroma which means colour because the element is
present in different colored compounds. These compounds have long been used as pigments
in dyeing and in the tanning of leather. In the early 1900s chromium became an important
ingredient of corrosion-resistant metals-a use which has increased to the present.
It was not until 1959 that the medical scientists Mertz and Schwarz- who came to the United
States from Germany discovered that the feeding of Chromium salts corrected the abnormal
metabolism of sugar of rats which resulted from the feeding of diet based upon torula yeast.
Later work by these researchers and by Schroeder of the Dartmouth Medical School
established chromium as a co-factor with insulin necessary for normal glucose utilization and
for growth and longevity in rats and mice. Dr Schwarz has long studied the nutritional
effects of various types of yeasts; in 1957 he had discovered that Selenium was present as a
vital factor in American type brewers’ yeast).Shortly thereafter, it was found that the
inorganic salts of chromium were utilized well by both animals and humans. The chromium-
containing substance from yeast was named the glucose tolerance factor (GTF) because it
sometimes restored the metabolism of sugars to normal when diabetic-like tendencies were
present.
ABSORPTION/METABOLISM/EXCRETION
Absorption – studies have shown that only about 1% or less of the dietary intake of the
inorganic chromium is absorbed whereas as much as 10% to 25% of glucose tolerance factor
(GTF-Chromium) may be absorbed.
Metabolism-animal studies have shown that a greater proportion of chromium is stored in
the liver when it is supplied as GTF than when it is supplied as inorganic salt. Furthermore
chromium in the liver has been shown to have GTF activity. Next to the liver the kidney
appears to be one of the best sources of GTF Chromium.
Various stressful conditions such as malnutrition and loss of blood have long been known to
impair the body’s utilization of sugars. Likewise, it seems that the chromium needs of the
body become more critical under such conditions. For example the study on animal science
has shown that the effects of (1) low protein diets accompanied by controlled exercise, and
(2) the withdrawal of measured amounts of blood were more severe in chromium deficient
groups than in those given supplements containing the minerals.
Excretion –the predominant route of excretion of endogenous chromium is via the urine.
Functions-
Components of the glucose tolerance factor (GTF) which enhances the effect of insulin
Activator of certain enzymes most of which are involved in the production of energy from
carbohydrates fats and proteins

14
Stabilizer of nucleic acid (DNA and RNA)
Simulation of synthesis of fatty acids and cholesterol in the liver
Deficiency symptoms/Toxicity
Deficiency symptoms- Impaired glucose tolerance which may be accompanied by high
blood sugar and the spilling of sugar in the urine.
Disturbance in lipid metabolism
Toxicity-Chromium is seldom toxic because (1) only small amounts are present in most feeds
(2) the body utilizes it poorly (3) there is a wide margin of safety between helpful and
harmful dose
Note well - Excesses of inorganic chromium are much more toxic than similar amounts of
GTF-Chromium
Major Interrelationships
The following interrelationships are pertinent
1. Chromium functions best in the body when it is in the form of GTF-Chromium
2. Diets rich in carbohydrate may cause the supply of GTF-Chromium to be depleted
3. Inorganic Chromium is utilized but less efficiently than that in GTF.
4. The absorption of chromium is impeded by oxalates and phytates
5. Zinc antagonizes the effect of chromium
Dietary sources
Corn, liver milk, potatoes, , vegetable oil, wheat and wheat bran.
COPPER (Cu)
Copper and iron are mutually involved in the formation of hemoglobin- the red pigment in
blood which carries oxygen.
History:
Copper was discovered and first used by Neolithic man during the late stone-age. The exact
date of this discovery will probably never be known, but it is believed to have been about
8000BC. The late Bronze Age (3000 to 1000 B.C) takes its name from the use during this
period of bronze, an alloy of copper and tin.
As a result of a series of studies beginning in 1925 (and reported in 1928), Hart and the
associates at the University of Wisconsin discovered that a small amount of copper is
necessary, along with iron, for hemoglobin formation. Today, copper is considered as an
essential nutrient for all vertebrates and some lower animals’ species.
Absorption/Metabolism/Excretion:
Absorption- copper absorption is greatest in small intestine. Of the intake, about 30% is
absorbed.

15
Metabolism-After absorption in the intestine, copper reaches the bloodstream where most of
it (80% or more) becomes bound in ceruloplasmin, a protein (globulin-copper) complex. The
reminder is loosely bound to albumen and transported to various tissues.
Excretion- Copper is excreted through the bile for elimination in the feces, but much of this
copper is reabsorbed.
Functions:
Facilitates the absorption of iron from the intestinal tract and releases it from storage in the
liver and the reticulo-endothelial system.
Essential for the formation of hemoglobin, although it is not a part of haemoglobin as such
Constituent of several enzymes systems
Development and maintenance of the vascular and skeletal structures (blood vessels, tendons,
bones)
Structure and functioning of the central nervous system
Required for normal pigmentation of the hair and wool
Component of important copper- containing proteins
Reproduction (fertility)
Deficiency Symptoms/ Toxicity:
Deficiency symptoms- Even though the requirement of copper is very small, many factors
relating to its absorption and utilization create copper deficiencies.
Fatigue and weakness, nutritional anaemia are signs of deficiencies
Toxicity: Excess copper is toxic; cause headaches, fever, vomiting blood in vomit, and
diarrhoea
Major interrelationships:
Copper, along with certain vitamins, is involved in iron metabolism.
Dietary excesses of cadmium, calcium, iron, lead, molybdenum plus sulphur, silver, and zinc
reduce the utilization of copper. There should not be less than 2 parts copper to 1 part
molybdenum.
An excess of molybdenum in the presence of sulfate causes a condition which can be cured
by administering copper.
In high- molybdenum areas, the copper level for horses and cattle should be about 5 times
higher than Normal.
Dietary sources: Corn, Oysters whole grains, beans, nuts, potatoes organ meats (kidneys and
liver). Dark green vegetables, dried fruits cocoa black pepper. The Copper content of plants
reflects the soil on which they were grown.

16
MOLYBDENUM (Mo)
Evidence that molybdenum is an essential trace element is based on the fact that it is part of
the molecular structure of two enzyme, xanthine oxidase (involved in the oxidation of
xanthine to uric acid and aldehyde oxidase involved in the oxidation of aldehyde to
carboxylic acids, and that diets low in molybdenum adversely affect growth in small animals.
Molybdenum is important in the ration in small amounts (about 2 ppm), but it is detrimental
in excessive quantities (about 20ppm).
History:
In 1778, Karl Scheele of Sweden recognized molybdenum as a distinct ore of a new element.
Then, in 1982, P.J. Hjolm obtained the metal by reducing the oxide with carbon and called it
molybdenum. The name molybdenum is derived from the Greek molybdos, meaning lead.
Molybdenum was long known as essential for the growth of all higher plants. Then, in 1963,
it was found in an essantial enzyme, xanthine dehydrogenase.
Absorption/Metabolism/Excretion:
Molybdenum is readily absorbed as molybdate in the small intestine, although some
absorption occurs throughout the intestinal tract. The rate of absorption can be dramatically
depressed by the presence of sulfates in feeds. There is little retention of this element except
in the liver, adrenals, kidneys and bones. Molybdenum is excreted rapidly in the urine, and in
limited amounts via the bile and feces.
Functions:
Molybdenum functions as a component of three different enzyme system which are involved
in the metabolism of carbohydrates, fats, proteins, sulfur- containing amino acids, nucleic
acid (DNA and RNA), and iron.
Molybdenum is a component of xanthine oxidase, an enzyme which is essential in the
formation of uric acid. Iron is also an important component of this enzyme.
Molybdenum is a component of the enamel of teeth.
Dietary sources,
Legumes, cereal grains, leafy vegetables, beef liver and milk
Deficiency Symptoms/Toxicity:
Deficiency symptoms- Seizures and lens dislocation, headaches, nausea, vomiting and coma.
Naturally occurring deficiency in animals is not known, unless utilization of the mineral is
interfered with the excess of copper and/or sulfate.
Toxicity- Toxicities of molybdenum are of greater practical concern than deficiencies.
Severe molybdenum toxicity: Symptoms are rear, they include headaches, nausea, vomiting
and coma.

17
Major interrelationships:
The utilization of molybdenum is reduced by excess copper, sulfate, and tungsten, an
environmental contaminant. Also even a moderate excess of molybdenum causes significant
urinary loss of copper, and toxicity due to excess copper is counteracted by molybdenum.

18