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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 body’s 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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Catalase . body can become iron deficient. infants and children need iron from their diet.  A lack of iron in your diet. Slow.2% Other iron compounds 3. Women with heavy periods are at risk of iron deficiency anemia because they lose blood during menstruation. eggs. leading to difficulty in digesting food. 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. For proper growth and development. and iron deficiency anemia will eventually develop. a colon polyp or colorectal cancer — can cause iron deficiency anemia. which affects your intestine's ability to absorb nutrients from digested food. Causes of iron deficiency anemia include:  Blood loss. Blood contains iron within red blood cells. too. An intestinal disorder. If there is lack of iron consumption. Body regularly gets iron from the foods eaten. such as celiac disease a disease in which the small intestine is hypersensitive to gluten. Hemoglobin 68% Ferritin 13% Haemosiderin 12% Myoglobin 3% Iron enzymes 0. If part of small intestine has been bypassed or removed surgically. vomiting and sometimes liver failure.  An inability to absorb iron. that may affect the ability to absorb iron and other nutrients. Consuming too little iron over time. especially aspirin. 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. Gastrointestinal bleeding can result from regular use of some overthe-counter pain relievers. leafy green vegetables and iron-fortified foods.6% •Iron dependent enzymes (enzymes that require iron as cofactor): Cytochrome oxidase. Occurrence in the following forms:        3 One of the most essential trace elements. Examples of iron-rich foods include meat.  Pregnancy. chronic blood loss within the body — such as from a peptic ulcer. Bholakant Raut Quality Control Officer Toxicity: bloody diarrhoea. Xanthine oxidase and peroxidase. a hiatal hernia. Iron from food is absorbed into the bloodstream in small intestine. Iron deficiency anemia occurs when body doesn't have enough iron to produce hemoglobin. Body content is 4-6g and is found in the following forms.). can lead to iron deficiency anemia. Without iron supplementation. Iron loss also increases during bleeding and hemorrhage. the body can't produce enough hemoglobin. or if there is loss of too much iron.Phr.

Transferrin transports iron to various organs and tissues. Ferritin in serum is derived from the breakdown of macrophages of the RES (liver. It binds 4000 iron molecules which accounts for a larger iron storage. odour. 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. bone marrow.3 mg/day is absorbed from digested food however the absorption increases during growth and pregnancy. it may give rise to anaemic conditions. may contain soft lumps that produce a yellow streak when crushed. spleen and bone marrow). Identification 4 . It is filtered and dried. Wt. It is stored mainly in the form of ferritin and haemosiderin. •Iron is absorbed in Ferrous (Fe2+) form. Only ~1. In case of iron deficiency the iron absorption from food increases to 4 mg/day. Ferritin is a protein. Iron binds to transferrin for transportation in plasma. 169. slight. In the body. Bholakant Raut Quality Control Officer •Body conserves iron very well. which is measurable in blood as free iron. liver and spleen. The sparingly soluble ferrous Fumarate gets separated.Phr. iron is mainly concentrated in the liver. macrophages and some respiratory enzymes such as catalases and cytochromes. Whereas the storage occurs in hepatoparenchymal cells.9 Ferrous Fumarate contains not less than 93. Its measurement is used to assess iron stores in the body. Each transferrin molecule binds to two iron atoms. reticuloendothelial cells.0 per cent and not more than 101. 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. If the storage sites of iron are depleted and the serum iron level falls below 60µg/100 ml. calculated on the dried basis. It is synthesized by cells that store iron and is later used to synthesize heme. fine powder. Description: A reddish orange to reddish brown.0 per cent of C4H2FeO4.

Add the mass to a large volume of water. lead. Reserve the precipitate for test 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°.1 g of the residue in 2 ml of sodium carbonate solution and add dilute potassium permanganate solution dropwise.5 g with 1 g of resorcinol. calculated on the dried basis. 482. B. C.2 Category: Haematinic (A hematinic is a nutrient required for the formation of blood cells in the process of hematopoiesis. the filtrate gives reaction A of ferrous salts.01699 g of C4H2FeO4. When other prepartions do not get tolerated.1 M ceric ammonium sulphate using ferroin sulphate solution as indicator. the permanganate is decolorised and a brownish solution is obtained. Then barium carbonate is added to get the barium salt.Phr. sulphates. 2H2O Mol. Ferric iron. The main hematinics are iron. a deep red semi-solid mass is formed. heavy metal.0 per cent and not more than 102. Uses: It finds use as haematinics. Cool.) Ferrous Gluconate contains not less than 95. this salt gives better results.0 per cent of C12H22FeO14 . 2) Ferrous Gluconate Molecular formula: C12H22 FeO14. as other iron salts. To 0. Suspend 0. Test for purity: It has to be tested for As.1 M ceric ammonium sulphate is equivalent to 0. Ferrous Fumarate is given in the form of tablets.3 g and dissolve in 15 ml of dilute sulphuric acid with the aid of gentle heat. Assay: Weigh accurately about 0. an orange-yellow solution without any fluorescence is obtained. This is treated with ferrous sulphate and the 5 . Heat 1 g with 25 ml of a mixture of equal volumes of hydrochloric acid and water on a water-bath for 15 minutes. and loss on drying. B12. Preparation: Gluconic acid is first prepared by oxidation of glucose by dilute nitric acid. and folate. add a few drops of sulphuric acid and heat gently. Mix 0. add 50 ml of water and immediately titrate with 0. Wt. cool and filter. 1ml of0.5 g of the mixture in a crucible. Bholakant Raut Quality Control Officer A.

coating the plate with Silica gel G. 6 . The solution of ferrous Gluconate is concentrated to yield a grey powder or granules. It is soluble in water and almost insoluble in alcohol. Its aqueous solution is acidic in nature. barium. chloride. sucrose. fine powder or granules. Determine by thin-layer chromatography. Bholakant Raut Quality Control Officer precipitated barium sulphate is removed and the filtrate is concentrated and cooled to get crystals. resembling that of burnt sugar. dextrose. Identification A. The principle spot in the chromatogram obtained with the test solution corresponds to that in the chromatogram obtained with the reference solution. 1ml of the resulting solution gives reaction A of ferrous salts. and loss on drying. B. arsenic.Phr. cool and dilute to 50 ml with water. It can also be prepared by double decomposition reaction between calcium Gluconate and ferrous sulphate. odour. heavy metals. ferric ion. The calcium sulphate is insoluble and filtered off. oxalic acid. Dissolve 5 g in carbon dioxide-free water at 60°. slight. Test for purity: It has to be tested for acidity. Description: A yellowish grey or pale greenish-yellow. sulphate.

concentrated and cooled. Storage: It is stored in well closed containers which are protected from light. When effervescence ceases.0 per cent of FeS0 4. Fe + H2 SO4 7 FeSO4 + H2 . After effervescence ceases. accurately weighed. Uses: Similar to any other ferrous salt. 278. using 0. Wt. It is used for the preparation of ferrous Gluconate tablets. Preparation Ferrous sulphate is obtained by dissolving iron in excess of dilute sulphuric acid. On exposure to moist air.). 1ml of 0. odourless. the crystals rapidly oxidise and become brown. Identification It gives the characteristic reaction of ferrous salts and sulphates. crystalline powder. until the red colour disappears. Description: Bluish green crystals or a light green. if kept open.1 M ceric ammonium nitrate. of the substance under examination. Bholakant Raut Quality Control Officer Ferrous compound. Efflorescent in air. 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.0 Ferrous Sulphate contains not less than 98.0 g.1 ml of ferroin solution as indicator. 7H2O Mol. add about 1. 7H20.5 g of sodium bicarbonate in a mixture of 70 ml of water and 30 ml of 1 M sulphuric acid. the liquid is filtered. 3) Ferrous Sulphate Molecular Formula: FeSO4. it finds use as a haematinic.0 per cent and not more than 105. gets oxidised into ferric by the oxygen of air. Fe2+ Fe3+ Assay: Dissolve 0.Phr.1 M ceric ammonium nitrate is equivalent to 0.04461 g of C12H22 FeO 14. 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. The green crystals are separated by filtration at room temperature. shake gently to dissolve and titrate with 0. It is regarded to cause fewer side effects than other ferrous salts including ferrous sulphate. That is why the tablets of ferrous sulphate are kept in a closed container. Category: Haematinic.

etc. arsenic. Uses: Ferrous sulphate finds use as a hematinic. Ferrous sulphate when heated decomposes to yield ferric oxide. When effervescence ceases.  These enzymes mainly regulate normal growth. cell growth. Many oral preparations.1 ml of ferroin solution as indicator. carboxypeptidase etc. It effloresces (to change to a powder from loss of water of crystallization) in dry air. wound healing. zinc.02780 g of FeSO4 . Orally it is administered in the form of capsule or tablets.5 g of the substance under examination. for promoting formation of haemoglobin in anaemias caused due to deficiency. collagen synthesis. Excessive use or consumed mistakenly by children may cause gastrointestinal irritation. 2HgCl2 + 2Fe2+ Hg2Cl2 + 2Fe3+ + 2Cl- Tests for purity: It has to be tested for acidity. it gets oxidised to ferric salt which is having a brownish yellow colour. i. taste. copper. shock. bone metabolism. Assay: Dissolve 2. Bholakant Raut Quality Control Officer Properties: It occurs in the form of greenish crystals or crystalline powder having an astringent taste. immune system. When exposed to air. ferric ions. smell and vision. including liquids are marketed. reproduction. 2(FeSO4. manganese. 1 ml of 0.5 g of sodium bicarbonate in a mixture of 150 ml of water and 10 ml of sulphuric acid. shake gently to dissolve and titrate with 0. alkaline phosphatase. 7H20. It is soluble in water but is insoluble in alcohol.Phr. chlorides etc. lead. certain reducing agents such as hypophosphorus acid and dextrose are included in such formulations.1 M ceric ammonium nitrate is equivalent to 0. Ag+ +Fe2+ Ag + Fe3+ Au3+ + 3Fe2+ Au + 3Fe3+ In presence of light. ferrous sulphate reduces mercuric chloride to mercurous chloride. Zinc (Zn) Distribution and transportation  Second most abundant trace element  It acts in the body mainly as a cofactor for 100 diverse zinc. until the red colour disappears. accurately weighed.1 M ceric ammonium nitrate.e. sulphur dioxide and sulphuric acid. In order to stabilize the ferrous form.dependent enzymes such as DNA polymerase.7H2O) Fe2O3+ SO2+H2SO4+ 13H2O Ferrous sulphate reduces the salts of silver and gold to their corresponding metals. 8 . using 0.. add about 0.

Infection. 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. transportation and storage • Copper is the third most abundant trace element in the human body. Post absorption it’s found in the blood bound to erythrocytes (75-80%). Some toxic compounds such as ZnCl2 if ingested may cause generalized necrosis.5g and is distributed as 60% in muscle. liver cirrhosis. burns and ulcers if applied excessively on skin. loss of appetite.5-19 mol/L Urine: 12 mol/L Erythrocytes: 185-200 mol/L Copper (Cu) Source. the rest is complexed with albumin.Phr. 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. fish and sea food 20-30% of the dietary zinc is absorbed mainly by small intestine. water pumped through copper pipes and chocolates. development of abnormal skin lesions and excessive hair loss Zn toxicity occurs due to: Excessive ingestion of Zn. 30% in bone and remaining 10% in other body tissues and organs. • The daily dietary requirement is between 2-6mg which is mainly obtained from red meat. Bholakant Raut Quality Control Officer             Body content is 2. hepatitis. Daily requirement is 3-14mg. shell-fish. 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. sickle cell anemia. 9 . 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. cocoa.

ceruloplasmin. and is required for women's fertility and to maintain pregnancy.Phr. • Copper is closely related to estrogen metabolism. erythrocyte function and regulate erythrocyte survival • Copper is critical for energy production in the cells. • Copper stimulates production of the neurotransmitters epinephrine.g. connective tissue. It is also involved in nerve conduction. • Acts as a catalyst for copper-containing enzymes such as. ascorbic acid oxidase. ascorbic acid. 9% is bound to carrier proteins such as albumin and only 1% is free Cu²+. Bholakant Raut Quality Control Officer • • • Typically 40-60% copper is absorbed by the duodenum and is transported via metalloenzymes e. Body content of copper is 80-120mg. dopamine-β-hydroxylase. Hypercuperaemia is associated with: • Pregnancy • Estrogen therapy • Thelassemia and anemia • Leukemia and Lymphoma particularly Hodgkin’s 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 Wilson’sdisease • 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 10 . norepinephrine and dopamine. the cardiovascular system and the immune system.genetic disorder where copper absorption leads to a brain disease which then causes characteristic wiry-steel hair. Body functions OF Copper (Cu) • Copper is involved in the process of erythropoiesis. • Nephrosis • Hypoproteinemia. In plasma 90% is bound to a conjugated metalloenzyme known as ceruloplasmin. cytochrome oxidase and tyrosinase Clinical significance: Hypocuperaemia is associated with • Anemia in infants • Malnutrition in infants • Menkes’kinky-hair syndrome….

inhibition of vit-K dependant clotting and altered cholesterol transport and utilization Manganese toxicity occurs due to inhalation of manganese dust. liver. •Vitamin B6 supplements (pyridoxine) Anti-copper agents * Zinc acetate (a chelating agent for Cu. R Nase and glucosyl-and glactosyltransferase Average daily intake is 20 μg/day however daily body requirement is 2-5μg/day Manganese is absorbed via small intestine in similar process as iron. loss of appetite and speech difficulties.5 -1μg/l . chocolate. 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. sterility.05-0. Excessive manganese have also been associated with psychological and neurological disturbances Manganese is normally NOT tested in routine diagnostic laboratories. Normal values: 0. mushrooms.Phr. super oxide dimutase. Beta-microglobulins carry Manganese to mitochondrial rich organs such as liver. peroxidase. 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. balances Cu levels) * Trientine hydrochloride * Penicillamine and D-penicillamine Normal Values of Cu: Serum = 12-26 μmol/L Urine = 0. Treatment of Wilson’s disease •Lifelong treatment is recommended •Low-copper diet -avoid shellfish. and various other foods. pancreas. nuts. loss of weight.55 μmol/day Manganese (Mn)-Ultra-trace element • • • • • • • • • • • 11 Important role in regulating metabolic processes which mainly include lipid and carbohydrate metabolism. however it’s known to increase in case of myocardial infarction. such as hair color and growth alterations. bone and tissue formation. 5’nucleotidase. where minors are known to suffer from headaches. Reduced levels have been observed in children suffering from epilepsy and other convulsive disorders. skeletal growth and reproduction Over 50 Manganese dependent enzymes have been identified and these include: catalase.

Phr. also plays a crucial role in the control of oxygen metabolism.e. Selenium deficiency occurs due to: • Hemolytic anemia • Clansman's thrombasthenia (platelet disorder) • Carcinoma • Gastrointestinal cancer • Malnutrition 12 . It catalyzes the breakdown of H2O2 and liquid hydroperoxides in body tissues and fluids. 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). Low Selenium also leads to Keshan’s disease. Reduced GTH-Px due to reduced Selenium also leads to neuron damage. Only about 3 per cent of an ingested dose is absorbed. which is a type of cardiac myopathy discovered in china where soil Selenium was absent. spleen. Animal products and sea foods are relatively low in manganese. inhibits cataract formation). Vegetables and fruits contain moderate amounts. heart. fish and grains –Recommended intake for adults 50-200 μg/day as in USA however intake may vary in other countries where soil Selenium levels are low. Nuts and unrefined grain are rich sources of manganese. hence protects body from oxidative damage. –It’s widely distributed in the human body however highest levels are found in the liver. Functions in human body: Selenium is incorporated in the enzyme Glutathione peroxidase (GTH-Px) that plays important role in normal immune system function. In RBCs the enzyme GTH-Px prevents peroxidation of Hemoglobin and cell membrane. GTH-Px accumulates in high concentration in liver to de-toxify hyper-oxides GTH-Px protects eye lens tissues from damage (i. pancreas and lungs. 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. Bholakant Raut Quality Control Officer • • Manganese is required for the synthesis of mucopolysaccharides through the enzymes polymerase and galacto-transferase. SELENIUM (Se) Ultra-trace element • • • • • • • • • • • • • • • Least abundant however the most toxic of all the essential elements –Dietary source is meat. Therefore people with cataract have 1/6 of normal Selenium levels in their eye lens tissues. kidney.

F Post absorption vitamin B12 is converted to cobalamine and stored in the liver.1μg/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. 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. cardiomyopathy •Laboratory testing is rarely carried out however normal plasma levels are 0. •Cobalt deficiency has never been reported.5 –4.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.0 μg/L 13 . nausea. Bholakant Raut Quality Control Officer Increased Selenium may occur due to: • •Reticuloendothelial neoplasia • •Poisoning (toxicity) Normal Values of Se: • whole blood 57-340 μg/L • RBC 71-340 μg/L • Serum 78-320 μg/L • Urine 5-100 μg/L • Hair 0.6-2. however vitamin B12 deficiency may occur mainly due to the absence of I.6 μg/L Cobalt (Co) Ultra-trace element Biological function is limited •Vitamin B12 is the only cobalt containing compound •Beef.Phr.

Bholakant Raut Quality Control Officer 14 .Phr.

It forms a complex compound made up of chromium-amino acid-nicotinic acid which is referred to as the glucose tolerance factor.Phr. Small quantities are present in fish. This trace mineral helps transport protein where it is needed in your body. Major losses of chromium occur during milling of wheat and refining of sugar. and kidney. . vegetables. It can also deter diabetes because it works with insulin in the metabolism of blood sugar. Body functions of Chromium     15 Chromium helps to prevent and lower high blood pressure. liver. Chromium is used in the metabolism and storage of fats. Food sources of chromium are yeast. It is believed that chromium crosses the placenta only as the glucose tolerance factor. 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. and fruits. proteins. A large proportion of chromium is absorbed from organic chromium complexes present in food. The urine contains 80 per cent of excreted chromium. and carbohydrates by the body. Major excretory route is the kidney.

Iodine is necessary for the synthesis of the thyroid hormone. The usual intake of iodine is an average man is about 140 micrograms and for female about100 micrograms daily. Enlargement of the thyroid gland occurs when iodine intake is less than 15 μg/day. which results in developmental delays and other health problems.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.Phr. chronic renal failure Iodine Iodine (as iodide) is considered to be one of the essential trace elements. Iodine deficiency is a lack of the trace element iodine. Iodine can be administered internally which is reduced to iodide in the intestinal track. Corn oil . The levels of thyroid stimulating hormone are raised causing enlargement of the thyroid gland. negative nitrogen balance hyperglycemia and weight loss reverse with IV supplementation in TPN. hence the goitre. as well as cretinism. Iodine is an essential constituent of the thyroid hormones. Sources: Brewers' yeast. Of the two types of thyroid hormones circulating in the blood of such persons T4 decreases but T3 remains normal. Chicken. thyroxine and tri-iodo thyronine. impaired glucose tolerance. Iodine is an essential trace element. The thyroid gland contains large amount of iodine (0.Whole grains Signs of Deficiency:      Adult-onset diabetes increased insulin levels and decreased insulin binding altered CHO metabolism. It may result in goiter (so-called endemic goiter). This amount is usually obtained for diet. peripheral neuropathy. the thyroid hormones thyroxine and triiodothyronine contain iodine. the salts of iodine like sodium iodide are preferred for internal administration. Meat products. 16 . Bholakant Raut Quality Control Officer Other Benefits: Helps improve glucose uptake in elderly people when loss comes as natural result of aging. but due to insolubility of iodine . glycosuria. fasting hyperglycemia impaired growth. especially clams. The daily requirement of iodine depends on the individual metabolic rate. May help prevent hardening of the arteries. Shellfish.

due to lack of dietary iodine to make it.[1] Seafood is also a well-known source of iodine. squint. 17 . 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. gives rise to high levels of thyroid stimulating hormone (TSH). the cochlea. In mild iodine deficiency. Iodine deficiency during the foetal and early neonatal period adversely affects the growing brain. The best way of providing iodine is by the use of iodised salt. disorders of stance and gait. Maternal iodine deficiency during pregnancy gives rise to cretinism. Bholakant Raut Quality Control Officer Prevention includes adding small amounts of iodine to table salt — a product known as iodized salt. without an elevated TSH. ―neurologic‖ and ―myxoedematous‖. the cellular growth and proliferation can result in the characteristic swelling or hyperplasia of the thyroid gland. This explains the combination of mental deficiency. as the body converts more of the levothyroxine to triiodothyronine as compensation. 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 is a condition associated with iodine deficiency and goiter. of which two types have been described. levels of triiodiothyronine (T 3) may be elevated in the presence of low levels of levothyroxine. Iodine compounds have also been added to other foodstuffs. and the basal ganglia all of which grow rapidly during the second trimester and are vulnerable to iodine deficiency. The retardation of physical and mental development and deafness in hypothyroid subjects disappears rapidly when provided with adequate amounts of iodine. dwarfism) happens to be a clinical condition of deficiency of thyroid hormones since birth. stunted growth. Some such patients may have a goiter. such as flour. which stimulates the thyroid gland to increase many biochemical processes. Supplementation with iodine through salt has been used as the main plank of the strategy of prevention. deafness. The main function of thyroxine is to increase the metabolic rate by increasing the oxidative process in the body. Hyperthyroidism occurs due to the excessive secreation of thyroid hormones and severe form of this may get manifested by exopthalmous (enlargement of eye balls). commonly characterised by mental deficiency. A low amount of thyroxine (one of the two thyroid hormones) in the blood. deaf-mutism and motor rigidity found in cretinism. The parts most affected are the cerebral neocortex. Cretinism (mental retardation.Phr. water and milk in areas of deficiency. or goiter.

thyroxine and triiodothyronine and to prevent goiter. probably as an antioxidant. The thyroid gland actively absorbs iodine from the blood to make and release these hormones into the blood. pregnancy. respectively. and are stored prior to release in an iodine-containing protein called thyroglobulin. soybeans) ***severe deficiency during gestation and early postnatal growth: cretinism—mental deficiency. quadriplegia. 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). but also. and blood it’s only function is related to thyroid hormone Iodine is required for synthesis of thyroid hormones   Thyroxine (T4) --. spastic diplegia. Bholakant Raut Quality Control Officer Health education of the public and vigilance in the enforcement of using iodized salt are additional aspects of prevention. shuffling gait. short stature. dysarthria.3atoms of iodine per molecule Required not only for the synthesis of thyroid hormones. 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). hypothyroidism goiters are more prevalent in women and with increased age .Phr. peanuts. These are made from addition condensation products of the amino acid tyrosine. gastric mucosa. processed foods. or relative—adolescence. actions which are regulated by a second hormone TSH from the pituitary gland. deaf mutism. T4 and T3 contain four and three atoms of iodine per molecule. lactation goitrogens occurring naturally in foods can cause goiter by blocking absorption or utilization of iodine (cabbage. iodized salt Deficiency      18 goiter—enlargement of the thyroid gland deficiency may be absolute—in areas of deficiency. turnips.4 atoms of iodine per molecule Tri-iodothyronine (T3) ---.    body normally has 20-30 mg of iodine and more than 75% is in the thyroid gland the rest is in the mammary gland.

000 . 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 (50.80.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.000 mg/day) Toxicity: Iodine has wide margin of safety     19 Usually asymptomatic Acute pain from thyroidal hemorrhage Dysphagia (trouble swallowing) Dyspnea (trouble breathing) .

which increases the cell's surface area and facilitates the diffusion of oxygen and carbon dioxide. Menkes kinky hair syndrome is an X-linked recessive multisystemic lethal disorder of copper metabolism. the metal is Fe2+ or Fe3+. bones and connective tissues. Such hormones are also produced artificially for use in oral contraceptives or to treat menopausal and menstrual disorders. The term "transition elements" most commonly refers to the d-block transition elements. They act as a critical part of the immune response by specifically recognizing and binding to particular antigens. it is the most abundant protein in mammals. Zn etc. Fe . Ceruloplasmin is the major copper-carrying protein in the blood. 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." meaning glue. Erythrocyte: A cell that contains hemoglobin and can carry oxygen to the body. and in addition plays a role in iron metabolism. Collagen gives the skin its strength and structure. 20 . Collagen is the main structural protein in the extracellular space in the various connective tissues in animal bodies. Metalloenzymes are enzyme proteins containing metal ions (metal cofactors). and it is part of the heme prosthetic group. As the main component of connective tissue. In proteins such as hemoglobins and cytochromes. Cu. and also plays a role in the replacement of dead skin cells. The clinical phenotype is marked by fine silvery wiry hair.Phr. The reddish color is due to the hemoglobin. such as bacteria or viruses and aiding in their destruction. Metalloenzymes are proteins which function as an enzyme and contain metals that are tightly bound and always isolated with the protein. E. Ni. making up from 25% to 35% of the whole-body protein content. and progressive neurologic deterioration oestrogen any of a group of steroid hormones which promote the development and maintenance of female characteristics of the body. Also called a red blood cell (RBC). are glycoprotein molecules produced by plasma cells (white blood cells). The word "collagen" is derived from the Greek "kolla. which are directly bound to the protein or to enzyme-bound nonprotein components (prosthetic groups). doughy skin. Mn. connective tissue disturbances. Erythrocytes are biconcave in shape. also known as antibodies.g. Ceruloplasmin (or caeruloplasmin) is a ferroxidase enzyme that in humans is encoded by the CP gene. Collagen is most commonly found within the body in the skin.Co. Immunoglobulins. 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. Cr.

Thalassemia occurs when there is a defect in a gene that helps control production of one of these proteins. Ferritin is a protein in the body that binds to iron. Ferritin is found in the liver. Hodgkin disease is a type of lymphoma. E. Hypoproteinemia (or hypoproteinaemia) is a condition where there is an abnormally low level of protein in the blood. skeletal muscles. Acetylcholine. where they stimulate the muscle fibers. low molecular weight. especially in the fingers. Inside cells. or gland cell. and ankles. Lymphoma is a cancer of a part of the immune system called the lymph system. Thalassemia is a blood disorder passed down through families (inherited) in which the body makes an abnormal form of hemoglobin. Serotonin. or bone marrow. Hemoglobin is the protein in red blood cells that carries oxygen. spleen. most of the iron stored in the body is bound to ferritin. feet. They are also found at the axon endings of motor neurons. And they and their close relatives are produced by some glands such as the pituitary and the adrenal glands.) and the loss of protein from the plasma into the urine due to increased glomerular permeability (also called nephrotic syndrome). Later it may spread to the lungs. wrists. Norepinephrine. Endorphin etc… Nephrosis kidney disease. Glutamate is an excitatory relative of GABA. from one neuron (nerve cell) to another "target" neuron. such as in a neuromuscular junction. Iron ions are delivered in the blood by the protein transferrin Metallothioneins (MTs) are intracellular. which is detected by the kidneys. Dopamine. liver. Hemoglobin is made of two proteins: Alpha globin and beta globin. and bone marrow. The disease can spread to nearby lymph nodes. low molecular. A hematinic is a nutrient required for the formation of blood cells in the process of hematopoiesis. Neurotransmitters are the chemicals which allow the transmission of signals from one neuron to the next across synapses. 21 . There are several causes and all result in edema once serum protein levels fall below a certain threshold. The first sign ofHodgkin disease is often an enlarged lymph node. It is stimulated by decreased O 2 in circulation. Rheumatoid arthritis a chronic progressive disease causing inflammation in the joints and resulting in painful deformity and immobility.G. especially when characterized by oedema (a condition characterized by an excess of watery fluid collecting in the cavities or tissues of the body. Only a small amount of ferritin is found in the blood. muscle cell. extra iron ions are locked safely in the protein shell of ferritin. which then secrete the hormone erythropoietin. which leads to anemia. They transmit signals across a chemical synapse. 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). cysteine-rich proteins. Neurotransmitters are endogenous chemicals that enable neurotransmission.Phr. The disorder results in large numbers of red blood cells being destroyed.