Phr.

Bholakant Raut
Quality Control Officer

TRACE ELEMENTS
Big elements e.g. Oxygen, Hydrogen, Nitrogen

Elements in
the human
body

Major elements e.g. Calcium, Phosphorus,

Potassium,
Sulfur,
Sodium,
Chloride,
Magnesium
Trace elements e.g. Boron, Chromium, Iodine,
Iron, Copper, Cobalt, Manganese, Molybdenum,
Selenium, Tin, Silicon, Vanadium

Trace elements are naturally occurring, homogeneous, inorganic substance required in humans in
amounts less than 100 mg/day.
The human body needs a number of minerals in trace (milligram) quantities. These include iron,
copper and zinc. Other minerals are required in ultra-trace (microgram) amounts. These are
chromium, manganese, fluoride, iodide, cobalt, selenium, silicon, arsenic, boron, and vanadium.
Trace elements are vital for human body to maintain normal yet complex physiological functions
related to bodys growth & development. They also balance toxicity levels.
They are called trace elements because of their body concentration, which are few milligrams per
kg or less. The daily requirement of dietary trace elements is few milligrams. They are also
known as micronutrients
Trace elements are categorized as essential, probably essential or non-essential based upon their
biological effect, diseases.
Essential trace elements includes iron, zinc, copper, cobalt, chromium, fluorine, iodine,
manganese, molybdenum and selenium
Probably essential trace elements include nickel, tin, vanadium, silicon, boron etc.
Non-essential trace elements include aluminum, arsenic, barium, bismuth, bromine, cadmium,
germanium, gold, lead, lithium, mercury, rubidium, silver, strontium, titanium and zirconium is
all found in plant and animal tissue.
Essential Trace Elements are divided into two sub-groups
Trace Elements: Iron, Zinc and Copper
Ultra Trace-Elements: Manganese, Selenium, Cobalt, Chromium, Fluorine, Iodine and
Molybdenum
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Phr. Bholakant Raut

Quality Control Officer

Iron
Iron is considered to be one of the essential constituents of the body. Its usual contents are about
45 mg/kg body weight. The total body content of iron is estimated to be about 3-4 gm. The main
portion of body iron (70%) occurs in haemoglobin and myoglobin. The remaining portion of the
body iron is in the form of storage iron, transport iron and enzyme iron. In normal adults, about 1
mg of iron is lost from the body daily. Iron containing foods are beef, poultry, fish, soybean
flour, spinach, beans and fortified cereals.
Dietary Source: Liver, kidneys, heart and spleen, egg yolk, fish and oyster
The amount of iron in the body is controlled by regulating the absorption but not excreation.
The reason for this is that body recycles the iron obtained from breakdown of RBC and thereby
daily requirement of iron is quite low.
Iron requirement increases during pregnancy, growth and lactation (about 10-12 mg for male
and 12-18 mg for female). Large amount of iron gets lost in haemorrhage and in menstrual flow.
The iron loss has been reported to be more in case of female as compared to male. Iron loss
becomes still more during pregnancy as it gets transported to placenta, thus iron preparation
are generally given during pregnancy. A small amount of iron gets excreted into urine and faeces
(about 1 mg daily) and the bulk of iron excreted through faeces has been in the form of
unabsorbed iron from food.
Iron is essential to the elementary metabolic processes. It is responsible for the transport of
molecular oxygen from the respiratory chain.

Functions:

As a component of hemoglobin in blood, one of the most important functions of iron is to

transport oxygen from the lungs to different parts of the body.

In myoglobin, iron enables storage of oxygen in muscle cells. Iron is also part of many
enzymes and is essential for growth, healing, immune function and synthesis of DNA.

Heme respiratory carrier, essential component of catalases, cytochromes and peroxidases.

Essential component of haemoglobin and the cytochromes. Severs in the expression of genes
for receptors of ferritin, transferritin and metallothioneins.

Iron is essential for the formation of haemoglobin in the RBCs. It is also essential for tissue
oxidation.

Deficiency:
Anaemia, fatigue, abnormalities in epithelial tissues, low level of ferritin, haemoglobin
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Phr. Bholakant Raut

Quality Control Officer

Toxicity: bloody diarrhoea, vomiting and sometimes liver failure.

Iron deficiency anemia occurs when body doesn't have enough iron to produce hemoglobin.
Hemoglobin is the part of red blood cells that gives blood its red color and enables the red blood
cells to carry oxygenated blood throughout body. If there is lack of iron consumption, or if there
is loss of too much iron, the body can't produce enough hemoglobin, and iron deficiency anemia
will eventually develop.
Causes of iron deficiency anemia include:
Blood loss. Blood contains iron within red blood cells. Iron loss also increases during
bleeding and hemorrhage. Women with heavy periods are at risk of iron deficiency anemia
because they lose blood during menstruation. Slow, chronic blood loss within the body
such as from a peptic ulcer, a hiatal hernia, a colon polyp or colorectal cancer can cause
iron deficiency anemia. Gastrointestinal bleeding can result from regular use of some overthe-counter pain relievers, especially aspirin.

A lack of iron in your diet. Body regularly gets iron from the foods eaten. Consuming too
little iron over time, body can become iron deficient. Examples of iron-rich foods include
meat, eggs, leafy green vegetables and iron-fortified foods. For proper growth and
development, infants and children need iron from their diet, too.

An inability to absorb iron. Iron from food is absorbed into the bloodstream in small
intestine. An intestinal disorder, such as celiac disease a disease in which the small intestine
is hypersensitive to gluten, leading to difficulty in digesting food.), which affects your
intestine's ability to absorb nutrients from digested food, can lead to iron deficiency anemia.
If part of small intestine has been bypassed or removed surgically, that may affect the ability
to absorb iron and other nutrients.

Pregnancy. Without iron supplementation, iron deficiency anemia occurs in many pregnant
women because their iron stores need to serve their own increased blood volume as well as
be a source of hemoglobin for the growing fetus.

Occurrence in the following forms:

One of the most essential trace elements. Body content is 4-6g and is found in the following
forms;
Hemoglobin
68%
Ferritin
13%
Haemosiderin
12%
Myoglobin
3%
Iron enzymes
0.2%
Other iron compounds
3.6%
Iron dependent enzymes (enzymes that require iron as cofactor): Cytochrome oxidase,
Xanthine oxidase and peroxidase, Catalase

Phr. Bholakant Raut

Quality Control Officer

Body conserves iron very well. Only ~1.3 mg/day is absorbed from digested food however the
absorption increases during growth and pregnancy. In case of iron deficiency the iron absorption
from food increases to 4 mg/day.
Iron is absorbed in Ferrous (Fe2+) form, which is measurable in blood as free iron. In the body,
iron is mainly concentrated in the liver, macrophages and some respiratory enzymes such as
catalases and cytochromes. It is stored mainly in the form of ferritin and haemosiderin. If the
storage sites of iron are depleted and the serum iron level falls below 60g/100 ml, it may give
rise to anaemic conditions.
Iron binds to transferrin for transportation in plasma. Whereas the storage occurs in
hepatoparenchymal cells, reticuloendothelial cells, bone marrow, liver and spleen. Each
transferrin molecule binds to two iron atoms. Transferrin transports iron to various organs and
tissues.
Ferritin is a protein. It binds 4000 iron molecules which accounts for a larger iron storage. It is
synthesized by cells that store iron and is later used to synthesize heme. Ferritin in serum is
derived from the breakdown of macrophages of the RES (liver, spleen and bone marrow). Its
measurement is used to assess iron stores in the body. Low Ferritin levels indicate depletion of
iron stores and used as an early indication of iron deficiency
Compounds of iron:
1) Ferrous Fumarate
Molecular Formula: C4H2 FeO4

Mol. Wt. 169.9

Ferrous Fumarate contains not less than 93.0 per cent and not more than 101.0 per cent of
C4H2FeO4, calculated on the dried basis.
Description: A reddish orange to reddish brown, fine powder; may contain soft lumps that
produce a yellow streak when crushed; odour, slight.
Preparation: It is obtained by double decomposition in which a hot aqueous solution of ferrous
sulphate is added slowly to a solution of sodium Fumarate with constant stirring. The sparingly
soluble ferrous Fumarate gets separated. It is filtered and dried.

Identification

Phr. Bholakant Raut

Quality Control Officer

A. Heat 1 g with 25 ml of a mixture of equal volumes of hydrochloric acid and water on a

water-bath for 15 minutes, cool and filter. Reserve the precipitate for test B; the filtrate gives
reaction A of ferrous salts.
B. Wash the precipitate reserved in test A with a mixture of 1 volume of dilute hydrochloric
acid and 9 volumes of water and dry at 105. Suspend 0.1 g of the residue in 2 ml of sodium
carbonate solution and add dilute potassium permanganate solution dropwise; the
permanganate is decolorised and a brownish solution is obtained.
C. Mix 0.5 g with 1 g of resorcinol. To 0.5 g of the mixture in a crucible, add a few drops of
sulphuric acid and heat gently; a deep red semi-solid mass is formed. Add the mass to a large
volume of water; an orange-yellow solution without any fluorescence is obtained.
Test for purity: It has to be tested for As, heavy metal, lead, Ferric iron, sulphates, and loss on
drying.
Assay: Weigh accurately about 0.3 g and dissolve in 15 ml of dilute sulphuric acid with the aid
of gentle heat. Cool, add 50 ml of water and immediately titrate with 0.1 M ceric ammonium
sulphate using ferroin sulphate solution as indicator. 1ml of0.1 M ceric ammonium sulphate is
equivalent to 0.01699 g of C4H2FeO4.
Uses: It finds use as haematinics, as other iron salts. When other prepartions do not get tolerated,
this salt gives better results. Ferrous Fumarate is given in the form of tablets.

2) Ferrous Gluconate
Molecular formula: C12H22 FeO14, 2H2O

Mol. Wt. 482.2

Category: Haematinic (A hematinic is a nutrient required for the formation of blood cells in the
process of hematopoiesis. The main hematinics are iron, B12, and folate.)
Ferrous Gluconate contains not less than 95.0 per cent and not more than 102.0 per cent of
C12H22FeO14 , calculated on the dried basis.
Preparation: Gluconic acid is first prepared by oxidation of glucose by dilute nitric acid. Then
barium carbonate is added to get the barium salt. This is treated with ferrous sulphate and the
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Phr. Bholakant Raut

Quality Control Officer

precipitated barium sulphate is removed and the filtrate is concentrated and cooled to get
crystals.

It can also be prepared by double decomposition reaction between calcium Gluconate and
ferrous sulphate. The calcium sulphate is insoluble and filtered off. The solution of ferrous
Gluconate is concentrated to yield a grey powder or granules.

Description: A yellowish grey or pale greenish-yellow, fine powder or granules; odour, slight,
resembling that of burnt sugar. It is soluble in water and almost insoluble in alcohol. Its aqueous
solution is acidic in nature.
Identification
A. Dissolve 5 g in carbon dioxide-free water at 60, cool and dilute to 50 ml with water. 1ml of
the resulting solution gives reaction A of ferrous salts.
B. Determine by thin-layer chromatography, coating the plate with Silica gel G. The principle
spot in the chromatogram obtained with the test solution corresponds to that in the chromatogram
obtained with the reference solution.
Test for purity: It has to be tested for acidity, arsenic, barium, ferric ion, heavy metals, chloride,
sulphate, oxalic acid, dextrose, sucrose, and loss on drying.

Phr. Bholakant Raut

Quality Control Officer

Ferrous compound, if kept open, gets oxidised into ferric by the oxygen of air. That is why the
tablets of ferrous sulphate are kept in a closed container.
Fe2+
Fe3+

Assay: Dissolve 0.5 g of sodium bicarbonate in a mixture of 70 ml of water and 30 ml of 1 M

sulphuric acid. When effervescence ceases, add about 1.0 g, accurately weighed, of the
substance under examination, shake gently to dissolve and titrate with 0.1 M ceric ammonium
nitrate, using 0.1 ml of ferroin solution as indicator, until the red colour disappears. 1ml of 0.1 M
ceric ammonium nitrate is equivalent to 0.04461 g of C12H22 FeO 14.
Storage: It is stored in well closed containers which are protected from light.
Uses: Similar to any other ferrous salt, it finds use as a haematinic. It is regarded to cause fewer
side effects than other ferrous salts including ferrous sulphate. It is generally given in the form of
tablets or as elixirs (a sweetened liquid usually containing alcohol that is used in medication
either for its medicinal ingredients or as a flavoring.). It is used for the preparation of ferrous
Gluconate tablets.

3) Ferrous Sulphate
Molecular Formula: FeSO4, 7H2O

Mol. Wt. 278.0

Ferrous Sulphate contains not less than 98.0 per cent and not more than 105.0 per cent of FeS0 4,
7H20.
Category: Haematinic.
Description: Bluish green crystals or a light green, crystalline powder; odourless. Efflorescent in
air. On exposure to moist air, the crystals rapidly oxidise and become brown.
Identification
It gives the characteristic reaction of ferrous salts and sulphates.
Preparation
Ferrous sulphate is obtained by dissolving iron in excess of dilute sulphuric acid. After
effervescence ceases, the liquid is filtered, concentrated and cooled. The green crystals are
separated by filtration at room temperature. In all these operations undue exposure to air is
prevented because ferrous sulphate is oxidised readily on exposure to moist air and the crystals
get coated with brownish yellow ferric sulphate.
Fe + H2 SO4

FeSO4 + H2

Phr. Bholakant Raut

Quality Control Officer

Properties: It occurs in the form of greenish crystals or crystalline powder having an astringent
taste. It effloresces (to change to a powder from loss of water of crystallization) in dry air. When
exposed to air, it gets oxidised to ferric salt which is having a brownish yellow colour. It is
soluble in water but is insoluble in alcohol. Ferrous sulphate when heated decomposes to yield
ferric oxide, sulphur dioxide and sulphuric acid.
2(FeSO4.7H2O)

Fe2O3+ SO2+H2SO4+ 13H2O

Ferrous sulphate reduces the salts of silver and gold to their corresponding metals.
Ag+ +Fe2+

Ag + Fe3+

Au3+ + 3Fe2+

Au + 3Fe3+

In presence of light, ferrous sulphate reduces mercuric chloride to mercurous chloride.

2HgCl2 + 2Fe2+

Hg2Cl2 + 2Fe3+ + 2Cl-

Tests for purity: It has to be tested for acidity, arsenic, copper, lead, zinc, manganese, ferric
ions, chlorides etc.

Assay:

Dissolve 2.5 g of sodium bicarbonate in a mixture of 150 ml of water and 10 ml of

sulphuric acid. When effervescence ceases, add about 0.5 g of the substance under examination,
accurately weighed, shake gently to dissolve and titrate with 0.1 M ceric ammonium nitrate,
using 0.1 ml of ferroin solution as indicator, until the red colour disappears. 1 ml of 0.1 M ceric
ammonium nitrate is equivalent to 0.02780 g of FeSO4 , 7H20.
Uses: Ferrous sulphate finds use as a hematinic, i.e., for promoting formation of haemoglobin in
anaemias caused due to deficiency. Excessive use or consumed mistakenly by children may
cause gastrointestinal irritation, shock, etc. Orally it is administered in the form of capsule or
tablets. Many oral preparations, including liquids are marketed. In order to stabilize the ferrous
form, certain reducing agents such as hypophosphorus acid and dextrose are included in such
formulations.

Zinc (Zn)
Distribution and transportation
Second most abundant trace element
It acts in the body mainly as a cofactor for 100 diverse zinc- dependent enzymes such as
DNA polymerase, alkaline phosphatase, carboxypeptidase etc.
These enzymes mainly regulate normal growth, immune system, cell growth, collagen
synthesis, wound healing, bone metabolism, reproduction, taste, smell and vision.
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Phr. Bholakant Raut

Quality Control Officer

Body content is 2.5g and is distributed as 60% in muscle, 30% in bone and remaining 10% in
other body tissues and organs.
Daily requirement is 3-14mg, age and sex dependent (infants and children require as little as
3-5mg whereas adult males require more than adult females however during lactation
demand in females increases to 14mg/day)
Diet rich in zinc includes: red meat, fish and sea food
20-30% of the dietary zinc is absorbed mainly by small intestine.
Post absorption its found in the blood bound to erythrocytes (75-80%), the rest is complexed
with albumin, transferrin and immunoglobulins
Zinc is mainly excreted through GIT in the stool and to a lesser extent in urine
Zinc levels will decrease substantially in: leukemia, liver cirrhosis, hepatitis, sickle cell
anemia, Infection, pernicious anemia and malnutrition
Common symptoms of zinc deficiency that must be noted include:
In children: growth retardation and skeletal abnormalities are typical symptoms in which zinc
deficiency should be considered
In adults: reduced sense of taste and smell, loss of appetite, development of abnormal skin
lesions and excessive hair loss
Zn toxicity occurs due to:
Excessive ingestion of Zn. Some toxic compounds such as ZnCl2 if ingested may cause
generalized necrosis, burns and ulcers if applied excessively on skin. This compound is
found mostly in deodorants
Prolonged exposure to industrial compounds such as ZnO may lead to pneumonitis and
sometimes even cancers
Normal Values of Zn:
Serum:
11-23 mol/L
Plasma:
15.5-19 mol/L
Urine:
12 mol/L
Erythrocytes:
185-200 mol/L

Copper (Cu)
Source, transportation and storage
Copper is the third most abundant trace element in the human body.
The daily dietary requirement is between 2-6mg which is mainly obtained from red meat,
cocoa, shell-fish, water pumped through copper pipes and chocolates.
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Phr. Bholakant Raut

Quality Control Officer

Typically 40-60% copper is absorbed by the duodenum and is transported via

metalloenzymes e.g. ascorbic acid oxidase.
In plasma 90% is bound to a conjugated metalloenzyme known as ceruloplasmin, 9% is
bound to carrier proteins such as albumin and only 1% is free Cu+.
Body content of copper is 80-120mg.

Body functions OF Copper (Cu)

Copper is involved in the process of erythropoiesis, erythrocyte function and regulate
erythrocyte survival
Copper is critical for energy production in the cells. It is also involved in nerve conduction,
connective tissue, the cardiovascular system and the immune system.
Copper is closely related to estrogen metabolism, and is required for women's fertility and to
maintain pregnancy.
Copper stimulates production of the neurotransmitters epinephrine, norepinephrine and
dopamine.
Acts as a catalyst for copper-containing enzymes such as; ceruloplasmin, ascorbic acid,
dopamine--hydroxylase, cytochrome oxidase and tyrosinase
Clinical significance:
Hypocuperaemia is associated with
Anemia in infants
Malnutrition in infants
Menkeskinky-hair syndrome.genetic disorder where copper absorption leads to a brain
disease which then causes characteristic wiry-steel hair.
Nephrosis
Hypoproteinemia.
Hypercuperaemia is associated with:
Pregnancy
Estrogen therapy
Thelassemia and anemia
Leukemia and Lymphoma particularly Hodgkins disease
Rheumatoid arthritis
Copper toxicity may occur due to ingestion of excess copper or as a result of
environmental exposure and this is characterize by increased tissue and serum levels
Wilsonsdisease
Autosomal recessive genetic disorder with onset in the 2 nd or 3rd decade
Onset in children aged 4-5yrs is also reported but rarely
Serum ceruloplasmin and serum copper is low
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Phr. Bholakant Raut

Quality Control Officer

Increased urine and tissue copper due to excessive deposition of copper in tissues particularly
in the hepatocytes and basal ganglia of the brain leading to their steady degeneration.

Treatment of Wilsons disease

Lifelong treatment is recommended
Low-copper diet -avoid shellfish, chocolate, liver, mushrooms, nuts, and various other foods.
Vitamin B6 supplements (pyridoxine)
Anti-copper agents
* Zinc acetate (a chelating agent for Cu, balances Cu levels)
* Trientine hydrochloride
* Penicillamine and D-penicillamine
Normal Values of Cu:
Serum = 12-26 mol/L
Urine = 0.05-0.55 mol/day

Manganese (Mn)-Ultra-trace element

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Important role in regulating metabolic processes which mainly include lipid and
carbohydrate metabolism, bone and tissue formation, skeletal growth and reproduction
Over 50 Manganese dependent enzymes have been identified and these include: catalase,
peroxidase, super oxide dimutase, 5nucleotidase, R Nase and glucosyl-and glactosyltransferase
Average daily intake is 20 g/day however daily body requirement is 2-5g/day
Manganese is absorbed via small intestine in similar process as iron.
Beta-microglobulins carry Manganese to mitochondrial rich organs such as liver, pancreas,
kidney and pituitary gland
Major excretion is through bile and pancreas into GIT
Deficiency of Manganese is rare however its etiology is not well known
Several defects have yet been associated with it; such as hair color and growth alterations,
loss of weight, inhibition of vit-K dependant clotting and altered cholesterol transport and
utilization
Manganese toxicity occurs due to inhalation of manganese dust, where minors are known to
suffer from headaches, sterility, loss of appetite and speech difficulties. Excessive manganese
have also been associated with psychological and neurological disturbances
Manganese is normally NOT tested in routine diagnostic laboratories, however its known to
increase in case of myocardial infarction. Reduced levels have been observed in children
suffering from epilepsy and other convulsive disorders.
Normal values: 0.5 -1g/l

Phr. Bholakant Raut

Quality Control Officer

Manganese is required for the synthesis of mucopolysaccharides through the enzymes

polymerase and galacto-transferase. Only about 3 per cent of an ingested dose is absorbed.
Nuts and unrefined grain are rich sources of manganese. Vegetables and fruits contain
moderate amounts. Animal products and sea foods are relatively low in manganese.

SELENIUM (Se) Ultra-trace element

Least abundant however the most toxic of all the essential elements
Dietary source is meat, fish and grains
Recommended intake for adults 50-200 g/day as in USA however intake may vary in other
countries where soil Selenium levels are low.
Its widely distributed in the human body however highest levels are found in the liver,
kidney, heart, spleen, pancreas and lungs.
Functions in human body:
Selenium is incorporated in the enzyme Glutathione peroxidase (GTH-Px) that plays
important role in normal immune system function, also plays a crucial role in the control of
oxygen metabolism.
It catalyzes the breakdown of H2O2 and liquid hydroperoxides in body tissues and fluids,
hence protects body from oxidative damage.
In RBCs the enzyme GTH-Px prevents peroxidation of Hemoglobin and cell membrane.
Vitamin-E also catalyses the activity of GTH-Px
Low GTH-Px in platelets leads to bleeding disorders
Low GTH-Px in plasma leads to edema due to damage to capillary membranes
In phagocytic cells (leukocytes and macrophages), there is increased activity of GTH-Px
which protects these cells from destruction due to the pre-oxidase which is generated by the
oxidative destruction of foreign bodies.
GTH-Px accumulates in high concentration in liver to de-toxify hyper-oxides
GTH-Px protects eye lens tissues from damage (i.e. inhibits cataract formation). Therefore
people with cataract have 1/6 of normal Selenium levels in their eye lens tissues.
Reduced GTH-Px due to reduced Selenium also leads to neuron damage.
Low Selenium also leads to Keshans disease, which is a type of cardiac myopathy
discovered in china where soil Selenium was absent.

Selenium deficiency occurs due to:

Hemolytic anemia
Clansman's thrombasthenia (platelet disorder)
Carcinoma
Gastrointestinal cancer
Malnutrition
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Phr. Bholakant Raut

Quality Control Officer

Increased Selenium may occur due to:

Reticuloendothelial neoplasia
Poisoning (toxicity)
Normal Values of Se:
whole blood 57-340 g/L
RBC
71-340 g/L
Serum
78-320 g/L
Urine
5-100 g/L
Hair
0.6-2.6 g/L

Cobalt (Co) Ultra-trace element

Biological function is limited
Vitamin B12 is the only cobalt containing compound
Beef, sea food and dairy products are major source of vitamin B12
Similar to Manganese the daily intake of cobalt significantly exceeds the required dose that is
0.1g/L
Deficiency of cobalt is related to diminished vitamin B12 absorption
>70% dietary vitamin B12 is absorbed in the presence of an intrinsic factor through the
intestinal mucosa
<5% is absorbed in the absence of I.F
Post absorption vitamin B12 is converted to cobalamine and stored in the liver.
Cobalt deficiency has never been reported, however vitamin B12 deficiency may occur mainly
due to the absence of I.F which subsequently affects intestinal absorption followed by
depletionof liver stores later on leading to pernicious anemia
Toxicity may occur due to excessive inhalation or ingestion which may lead to: pulmonary
edema, nausea, cardiomyopathy
Laboratory testing is rarely carried out however normal plasma levels are 0.5 4.0 g/L

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Phr. Bholakant Raut

Quality Control Officer

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Phr. Bholakant Raut

Quality Control Officer

Chromium
Chromium acts as a cofactor for insulin by facilitating attachment of insulin to receptors on the
surface of the target cell as well as within the cell. It forms a complex compound made up of
chromium-amino acid-nicotinic acid which is referred to as the glucose tolerance factor. It is
believed that chromium crosses the placenta only as the glucose tolerance factor.
A large proportion of chromium is absorbed from organic chromium complexes present in food.
Major excretory route is the kidney. The urine contains 80 per cent of excreted chromium.
Food sources of chromium are yeast, liver, and kidney. Small quantities are present in fish,
vegetables, and fruits. Major losses of chromium occur during milling of wheat and refining of
sugar.
Body functions of Chromium

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Chromium helps to prevent and lower high blood pressure.

It can also deter diabetes because it works with insulin in the metabolism of blood sugar.
This trace mineral helps transport protein where it is needed in your body.
Chromium is used in the metabolism and storage of fats, proteins, and carbohydrates by the
body.

Phr. Bholakant Raut

Quality Control Officer

Other Benefits: Helps improve glucose uptake in elderly people when loss comes as natural
result of aging. May help prevent hardening of the arteries.

Sources: Brewers' yeast, Meat products, Chicken, Shellfish; especially clams, Corn oil ,Whole
grains

Signs of Deficiency:

Adult-onset diabetes
increased insulin levels and decreased insulin binding
altered CHO metabolism, impaired glucose tolerance, glycosuria, fasting hyperglycemia
impaired growth, peripheral neuropathy, negative nitrogen balance
hyperglycemia and weight loss reverse with IV supplementation in TPN, chronic renal
failure

Iodine
Iodine (as iodide) is considered to be one of the essential trace elements.
Iodine is an essential constituent of the thyroid hormones, thyroxine and tri-iodo thyronine. The
thyroid gland contains large amount of iodine (0.06%) almost all of which is firmly bound to the
protein.
Absorptions of iodine can occur at all levels of GIT and excreation of iodine is primarily via the
urine.
The daily requirement of iodine depends on the individual metabolic rate. The usual intake of
iodine is an average man is about 140 micrograms and for female about100 micrograms daily.
This amount is usually obtained for diet. Iodine can be administered internally which is reduced
to iodide in the intestinal track, but due to insolubility of iodine , the salts of iodine like sodium
iodide are preferred for internal administration.
Iodine is necessary for the synthesis of the thyroid hormone. Enlargement of the thyroid gland
occurs when iodine intake is less than 15 g/day. Of the two types of thyroid hormones
circulating in the blood of such persons T4 decreases but T3 remains normal. The levels of
thyroid stimulating hormone are raised causing enlargement of the thyroid gland, hence the
goitre.
Iodine deficiency is a lack of the trace element iodine. It may result in goiter (so-called endemic
goiter), as well as cretinism, which results in developmental delays and other health problems.
Iodine is an essential trace element; the thyroid hormones thyroxine and triiodothyronine contain
iodine.

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Phr. Bholakant Raut

Quality Control Officer

Prevention includes adding small amounts of iodine to table salt a product known as iodized
salt. Iodine compounds have also been added to other foodstuffs, such as flour, water and milk in
areas of deficiency.[1] Seafood is also a well-known source of iodine.
A low amount of thyroxine (one of the two thyroid hormones) in the blood, due to lack of dietary
iodine to make it, gives rise to high levels of thyroid stimulating hormone (TSH), which
stimulates the thyroid gland to increase many biochemical processes; the cellular growth and
proliferation can result in the characteristic swelling or hyperplasia of the thyroid gland, or
goiter. In mild iodine deficiency, levels of triiodiothyronine (T 3) may be elevated in the presence
of low levels of levothyroxine, as the body converts more of the levothyroxine to
triiodothyronine as compensation. Some such patients may have a goiter, without an elevated
TSH.
When the inorganic iodide ingested along with food after absorption reaches blood circulation it
exerts an important role in the synthesis of two important thyroid hormones called thyroxine and
tri-iodo thyronine which are essential for the normal growth and development and play vital role
in the energy metabolism.
Hyperthyroidism occurs due to the excessive secreation of thyroid hormones and severe form of
this may get manifested by exopthalmous (enlargement of eye balls).
The main function of thyroxine is to increase the metabolic rate by increasing the oxidative
process in the body. Deficiency of thyroid hormones is responsible for hypothyroidism a
condition in which all metabolic process are slowed down and goiter (enlargement of thyroid
gland) appears which is characterised by swelling of neck. Cretinism (mental retardation,
dwarfism) happens to be a clinical condition of deficiency of thyroid hormones since birth.
The retardation of physical and mental development and deafness in hypothyroid subjects
disappears rapidly when provided with adequate amounts of iodine. The best way of providing
iodine is by the use of iodised salt.

Cretinism is a condition associated with iodine deficiency and goiter, commonly characterised by
mental deficiency, deafness, squint, disorders of stance and gait, stunted growth.
Maternal iodine deficiency during pregnancy gives rise to cretinism, of which two types have
been described, neurologic and myxoedematous.
Iodine deficiency during the foetal and early neonatal period adversely affects the growing brain.
The parts most affected are the cerebral neocortex, the cochlea, and the basal ganglia all of which
grow rapidly during the second trimester and are vulnerable to iodine deficiency. This explains
the combination of mental deficiency, deaf-mutism and motor rigidity found in cretinism.
Supplementation with iodine through salt has been used as the main plank of the strategy of
prevention.

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Phr. Bholakant Raut

Quality Control Officer

Health education of the public and vigilance in the enforcement of using iodized salt are
additional aspects of prevention.

body normally has 20-30 mg of iodine and more than 75% is in the thyroid gland
the rest is in the mammary gland, gastric mucosa, and blood
its only function is related to thyroid hormone

Iodine is required for synthesis of thyroid hormones

Thyroxine (T4) --- 4 atoms of iodine per molecule

Tri-iodothyronine (T3) ---- 3atoms of iodine per molecule

Required not only for the synthesis of thyroid hormones, thyroxine and triiodothyronine and to
prevent goiter, but also, probably as an antioxidant, for extrathyroidal organs as mammary and
salivary glands and for gastric mucosa and immune system (thymus):
Iodine's main role in animal biology is as constituents of the thyroid hormones, thyroxine (T4)
and triiodothyronine (T3). These are made from addition condensation products of the amino
acid tyrosine, and are stored prior to release in an iodine-containing protein called thyroglobulin.
T4 and T3 contain four and three atoms of iodine per molecule, respectively. The thyroid
gland actively absorbs iodine from the blood to make and release these hormones into the blood,
actions which are regulated by a second hormone TSH from the pituitary gland.
Absorption and Excretion

iodine is absorbed in the form of iodide

occurs both as free and protein-bound iodine in circulation
iodine is stored in the thyroid where it is used for the synthesis of T3 and T4
the hormone is degraded in target cells and in the liver and the iodine is conserved if needed
excretion is primarily via urine
small amounts from bile are excreted in the feces

Food Sources: foods of marine origin (seaweed), processed foods, iodized salt
Deficiency

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goiterenlargement of the thyroid gland

deficiency may be absolutein areas of deficiency, or relativeadolescence, pregnancy,
lactation
goitrogens occurring naturally in foods can cause goiter by blocking absorption or utilization
of iodine (cabbage, turnips, peanuts, soybeans)
***severe deficiency during gestation and early postnatal growth: cretinismmental
deficiency, spastic diplegia, quadriplegia, deaf mutism, dysarthria, shuffling gait, short
stature, hypothyroidism
goiters are more prevalent in women and with increased age

Phr. Bholakant Raut

Quality Control Officer

Note normal man and three adult women with cretinism:

Short stature
Protuberant abdomen
Swollen features

Iodine Excess and Toxicity

Humans are remarkably tolerant to high iodine intakes

In iodine deficiency, repletion must be done slowly to prevent hyperthyroidism
Paradoxical goiter (enlarged thyroid as a result of very high intakes of iodine)

Occurs in Japan and China with high intake of seaweed (50,000 - 80,000 mg/day)
Toxicity: Iodine has wide margin of safety

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Usually asymptomatic
Acute pain from thyroidal hemorrhage
Dysphagia (trouble swallowing)
Dyspnea (trouble breathing)

Phr. Bholakant Raut

Quality Control Officer

Terminology
The transition elements are those elements having a partially filled d or f subshell in any common
oxidation state. The term "transition elements" most commonly refers to the d-block transition
elements. E.g. Cr, Mn, Fe ,Co, Ni, Cu, Zn etc.
Collagen is the main structural protein in the extracellular space in the various connective tissues in
animal bodies. As the main component of connective tissue, it is the most abundant protein in mammals,
making up from 25% to 35% of the whole-body protein content.
Collagen is most commonly found within the body in the skin, bones and connective tissues. The word
"collagen" is derived from the Greek "kolla," meaning glue. Collagen gives the skin its strength and
structure, and also plays a role in the replacement of dead skin cells.
Immunoglobulins, also known as antibodies, are glycoprotein molecules produced by plasma cells
(white blood cells). They act as a critical part of the immune response by specifically recognizing and
binding to particular antigens, such as bacteria or viruses and aiding in their destruction.
Erythrocyte: A cell that contains hemoglobin and can carry oxygen to the body. Also called a red blood
cell (RBC). The reddish color is due to the hemoglobin. Erythrocytes are biconcave in shape, which
increases the cell's surface area and facilitates the diffusion of oxygen and carbon dioxide.
Metalloenzymes are enzyme proteins containing metal ions (metal cofactors), which are directly bound
to the protein or to enzyme-bound nonprotein components (prosthetic groups). Metalloenzymes are
proteins which function as an enzyme and contain metals that are tightly bound and always isolated with
the protein. In proteins such as hemoglobins and cytochromes, the metal is Fe2+ or Fe3+, and it is part of
the heme prosthetic group.
Ceruloplasmin (or caeruloplasmin) is a ferroxidase enzyme that in humans is encoded by the CP
gene. Ceruloplasmin is the major copper-carrying protein in the blood, and in addition plays a role in
iron metabolism.
Menkes kinky hair syndrome is an X-linked recessive multisystemic lethal disorder of copper
metabolism. The clinical phenotype is marked by fine silvery wiry hair, doughy skin, connective tissue
disturbances, and progressive neurologic deterioration
oestrogen any of a group of steroid hormones which promote the development and maintenance of
female characteristics of the body. Such hormones are also produced artificially for use in oral
contraceptives or to treat menopausal and menstrual disorders.
Estrogen or oestrogen (see spelling differences) is the primary female sex hormone and is responsible
for development and regulation of the femalereproductive system and secondary sex characteristics.

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Phr. Bholakant Raut

Quality Control Officer

Erythropoiesis (from Greek 'erythro' meaning "red" and 'poiesis' meaning "to make") is the process
which produces red blood cells (erythrocytes). It is stimulated by decreased O 2 in circulation, which is
detected by the kidneys, which then secrete the hormone erythropoietin.

Neurotransmitters are endogenous chemicals that enable neurotransmission. They transmit signals
across a chemical synapse, such as in a neuromuscular junction, from one neuron (nerve cell) to another
"target" neuron, muscle cell, or gland cell. Neurotransmitters are the chemicals which allow the
transmission of signals from one neuron to the next across synapses. They are also found at the axon
endings of motor neurons, where they stimulate the muscle fibers. And they and their close relatives are
produced by some glands such as the pituitary and the adrenal glands.
E.G. Acetylcholine, Norepinephrine, Dopamine, Glutamate is an excitatory relative of GABA,
Serotonin, Endorphin etc
Nephrosis kidney disease, especially when characterized by oedema (a condition characterized by an
excess of watery fluid collecting in the cavities or tissues of the body.) and the loss of protein from the
plasma into the urine due to increased glomerular permeability (also called nephrotic syndrome).
Hypoproteinemia (or hypoproteinaemia) is a condition where there is an abnormally low level of protein
in the blood. There are several causes and all result in edema once serum protein levels fall below a
certain threshold.
Thalassemia is a blood disorder passed down through families (inherited) in which the body makes an
abnormal form of hemoglobin. Hemoglobin is the protein in red blood cells that carries oxygen. The
disorder results in large numbers of red blood cells being destroyed, which leads to anemia. Hemoglobin
is made of two proteins: Alpha globin and beta globin. Thalassemia occurs when there is a defect in a
gene that helps control production of one of these proteins.
Hodgkin disease is a type of lymphoma. Lymphoma is a cancer of a part of the immune system called
the lymph system. The first sign ofHodgkin disease is often an enlarged lymph node. The disease can
spread to nearby lymph nodes. Later it may spread to the lungs, liver, or bone marrow.
Rheumatoid arthritis a chronic progressive disease causing inflammation in the joints and resulting in
painful deformity and immobility, especially in the fingers, wrists, feet, and ankles.

Ferritin is a protein in the body that binds to iron; most of the iron stored in the body is bound
to ferritin. Ferritin is found in the liver, spleen, skeletal muscles, and bone marrow. Only a
small amount of ferritin is found in the blood. Inside cells, extra iron ions are locked safely in
the protein shell of ferritin. Iron ions are delivered in the blood by the protein transferrin
Metallothioneins (MTs) are intracellular, low molecular, low molecular weight, cysteine-rich
proteins.

A hematinic is a nutrient required for the formation of blood cells in the process of
hematopoiesis.

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