Trace Elements Present in Human Body | Mineral Metabolism

The following points highlight the eleven main trace elements present in human body. The trace elements are: 1. Iron 2. Copper 3. Iodine 4. Fluorine 5. Zinc 6. Cobalt 7. Manganese 8. Molybdenum 9. Selenium 10. Chromium 11. Lead.

Human Body: Trace Element # 1. Iron:

The total iron content of the normal adult is about 4 to 5 gm. About 60 to 70 per cent of the total iron is present in hemoglobin; about 51 per cent is in storage as ferritin; 3 per cent as myoglobin and only about 0.1 per cent is carried in the plasma in combination with the β-globulin transport protein transferrin.

The hemoprotein and flavoprotein en­zymes together make up less than 1.0 per cent of the total iron. Large amounts are present as hemosiderin.

Physiological Function:

a. Iron functions mainly in the transport of oxygen to the tissues (hemoglobin).

b. It is also involved in the processes of cel­lular respiration.

c. It is an essential component of hemoglo­bin, myoglobin, cytochromes and the res­piratory enzyme systems (cytochrome oxidase, catalase and peroxidase).

d. The nonheme iron is completely protein- bound which exists in the form of storage and transport.

e. The nonheme iron is also utilized in the structure of xanthine dehydrogenase and succinate dehydrogenase and also in the iron-sulfur proteins of the respiratory chain.

Sources:

Distribution:

Daily Requirement:

About 10 per cent of the ingested iron is only ab­sorbed.

In adult women, the average loss of blood dur­ing a menstrual period, which is a monthly loss, of 16-32 mg of iron or an additional average loss of 0.5-1.0 mg per day. This amount is easily obtained from the diet.

In excessive menstrual blood loss and in chronic iron-deficiency anemia, a supplement of 100 mg of iron per day is sufficient to respond. So during growth, pregnancy and lactation, iron de­mand is more.

In healthy adult male or in healthy women af­ter menopause, the dietary requirement is negligi­ble unless any deficiency or loss of iron occurs.

The iron deficiency occurs as a result of mal­absorption from the gastrointestinal tract. A defect in hemoglobin synthesis in anemia is commonly found in copper deficiency.

Iron in the Blood:

The nor­mal concentration of iron in blood is 65-170 ng/100 ml.

Absorption:

Under normal conditions, very little dietary iron is absorbed (less than 10 per cent), the amount excreted in the urine are minimal. Infants and children absorb a higher percentage of iron from foods than adults. Iron deficiency in in­fants is due to a dietary deficiency. Iron-deficient children absorb twice as much as normal children.

Most of the iron in food occurs in the ferric (Fe⁺⁺⁺) state either as Fe(OH)₃ or as ferric organic compounds. These compounds are broken down into free ferric ions or loosely bound organic iron. The gastric hydrochloric acid and the organic ac­ids of the foods are both important for this purpose. Reducing substances in foods, such as cysteine and ascorbic acid convert ferric ion into the ferrous (Fe⁺⁺) state.

In this form it is more soluble and, there­fore, readily absorbed. Iron absorption is enhanced by proteins of low molecular weight digestive prod­ucts (peptides, amino acids) forming iron chelate. Heme enters the mucosal cells without being re­leased from the porphyrin ring. In humans, dogs and rats, heme is broken down in the mucosa and iron appears in the plasma transferrin.

Factors Affecting Iron Absorption:

a. Absorption of iron occurs mainly in the stomach and the duodenum. Impaired ab­sorption takes place in patients who have total removal of stomach or a removal of the considerable amount of the intestine.

b. A diet high in phosphate causes decreased absorption due to the formation of insolu­ble ferric phosphate (FePO₄). Very low phosphate favours increased absorption of iron.

c. Phytic acid (present in cereals) and oxalates interfere absorption.

d. Vitamin C increases absorption.

e. Gastric acidity increases absorption by converting Fe(OH)₃ to Fe⁺⁺⁺. Achlorhydria and administration of alkali decrease ab­sorption.

f. Proteins of low molecular weight favour absorption.

g. Copper deficiency also causes decrease in absorption.

h. Alcohol ingestion favours iron absorp­tion.

Previously, “Mucosal Block” theory was consid­ered to be the controlling of iron absorption. The iron-binding protein, apoferritin, in the mucosal cells, was the controlling factor. Ferrous ion being oxidized to ferric ion combines with apoferritin to form iron containing protein.

Ferritin:

It was believed that the absorption depended on the formation of ferritin. When apo­ferritin was saturated with iron, no further uptake of iron could take place. More recently, evidences show that ferritin is involved in the major regulation of iron absorp­tion.

Iron taken into the mucosal cell is bound to specific carriers which regulate its passage across the cell to the blood. Intestinal ferritin, therefore, acts as a storage compound rather than the control­ling of absorption.

Transport in the Plasma:

All the iron released from the mucosal cell enters the portal blood in the ferrous state. In the plasma, ferrous is oxidized to ferric state by ceruloplasmin (a copper binding plasma protein) exerts a cata­lytic activity (serum ferroxidase) in plasma. Hu­man serum also contains a yellow cuproprotein (ferroxidase 11) which catalyzes the oxidation of ferrous ions.

Feme ion is then incorporated into a specific iron binding protein, transferrin or siderophilin, which is a glycoprotein of molecular weight 76,000 containing 5.3 per cent carbohy­drate. Transferrin can bind 2 atoms of ferric ions per molecule of protein to form a red ferric-protein complex. Iron release from the mucosal cell is fa­cilitated by a low degree of transferrin saturation by iron.

Under normal circumstances, almost all of the iron bound to transferrin is taken up readily by bone- marrow. Only the reticulocytes can utilize the fer­ric ion bound to transferrin, although reticulocytes and the mature erythrocytes can take up unbound ferric ion. The iron with transferrin makes a com­plex which is not filterable by the kidney. The total iron binding capacity in both sexes is about 250- 450 µg/dL.

Losses of iron into the urine occur in proteinu­ria. In nephrosis, iron (1.5 mg/day) with protein may be excreted in the urine. In hepatic disease, both the bound iron and the total iron-binding ca­pacity of the plasma is low.

Excretion:

The body stores of iron are conserved very effi­ciently. Only minute amounts are excreted in the urine, feces and sweats. Relatively large amounts are lost in the menstrual flow. The bulk of the iron of the feces is unabsorbed food iron. In the tropics, iron loss is often much greater. During pregnancy, iron is lost to the fetus. Iron is also lost from the skin by means of sweat, hair loss and nail clippings.

The daily excretion of iron is as follows:

Abnormal Iron Metabolism:

Ferritin and hemosiderin, the storage forms of iron, act as an internal iron reserve to protect against sudden losses of iron by bleeding. Ferritin is present not only in the intestine but also in liver (about 700 mg), spleen and bone-marrow.

If more iron is administered parenterally exceeding the capacity of the body to store as ferritin, it accumulates in the liver as hemosiderin, a form of colloidal iron oxide in association with protein. The iron con­tent of hemosiderin is 35 per cent by weight.

Iron metabolism is disturbed mainly by the following causes:

a. Decreased formation of hemoglobin.

b. Decrease in circulating hemoglobin.

c. Abnormalities in the serum iron concen­tration.

d. Abnormal deposition of iron-containing pigment in the tissues.

The disorders of iron metabolism are:

a. Siderosis;

b. Nutritional siderosis;

c. Hemochroma­tosis.

a. Siderosis:

When excessive amounts of iron are released in or introduced into the body beyond the capacity for its utiliza­tion, the excess is deposited in the vari­ous tissues, mainly in the liver. This may occur due to repeated blood transfusion, excessive breakdown of erythrocytes in hemolytic types of anemia and inad­equate synthesis of hemoglobin as in per­nicious anemia.

b. Nutritional siderosis:

The disorder is found among Bantus in South Africa. Bantus cook their food in large iron pots and consume iron-rich food. The absorp­tion of iron appears to be high leading to the development of nutritional siderosis. Livers of the Bantus contain large amounts of iron.

c. Hemochromatosis:

Hemochromatosis is a rare disease in which large amounts of iron are deposited in the tissues, especially the liver, pancreas, spleen and skin pro­ducing various disorders. Accumulation of iron in the liver, pancreas and skin pro­duces hepatic cirrhosis, bronze diabetes and bronze-state pigmentation, respec­tively.

Iron Deficiency Anemia:

Iron deficiency anemia is widely prevalent among children, adolescent girls and nursing mothers. The hemoglobin content of the blood is 5 to 9 gm/100 ml.

Women of Child Bearing Age:

The clinical symptoms are breathlessness on exertion, giddiness and pallor of skin. In severe cases, there may be edema of the ankles.

Weaned Infants and Young Children:

The hemoglobin level is 5 to 9 gm./100 ml blood. The children are dull, and inactive and show pallor of the skin. The appetite is poor and growth and de­velopment are retarded.

Treatment:

Anemic women should take fer­rous sulphate tablets. For a child of below 12 months, a mixture of ferrous ammonium citrate sweetened with glycerine and for children of 1 to 5 years ferrous ammonium citrate mixture should be given in curing.

Human Body: Trace Element # 2. Copper:

Physiological Functions:

a. It has an important role in hemoglobin synthesis.

b. It is required for melanin formation, phos­pholipid synthesis, and collagen synthe­sis.

c. It has a role in bone formation and in main­tenance in the integrity of myelin sheath.

d. It is a constituent of several enzymes, such as tyrosinase, cytochrome oxidase, ascor­bic acid oxidase, uricase, ferroxidase 1 (ceruloplasmin) and ferroxidase 11.

e. It is a constituent of superoxide dismutase, amine oxidase and dopamine hydroxylase.

f. Three copper containing proteins namely cerebrocuprein, erythrocuprein and hepatocuprein are present in brain, RBC and liver, respectively.

Sources:

Distribution:

The adult human body contains 100-150 mg of copper.

The concentration of copper in the fetal liver is 5-10 times higher than that in liver of an adult.

Daily Requirements:

A nutritional deficiency of copper has never been demonstrated in man, although it has been suspected in case of nephrosis.

Blood Copper:

The normal concentration of copper in serum is 75- 160 µg/100 ml. Both the red blood cells and serum contain copper. In 80 per cent of the red blood cell copper is present as superoxide dismutase (erythrocuprein). The copper in plasma occurs in firmly bound and loosely bound forms. The firmly bound copper consists of ceruloplasmin.

The loosely bound copper is known as direct reacting copper and is loosely bound to serum albumin. The plasma copper levels increase in pregnancy because of their estrogen content. Oral contraceptives have a similar effect.

Absorption:

Absorption of copper occurs in the human duode­num. 30 per cent of the normal daily diet of copper is absorbed in the duodenum.

Excretion:

Only 0 to 32 µg of copper is excreted in normal urine in 24 hours. The daily biliary excretion of copper is 0.5 to 1.3 mg and 0.1 to 0.3 mg is ex­creted across the intestinal mucosa into the bowel lumen.

Effects of Copper Deficiency:

a. Although iron absorption is not disturbed, the release of iron into the plasma is pre­vented due to the decreased synthesis of ceruloplasmin. As a result, hypoferrimia occurs which leads to the depressed syn­thesis of heme developing anemia in se­vere deficiency of copper.

b. The experimental animals on a copper-deficient diet lose weight and die.

c. In copper-deficient lambs, low cytochrome oxidase activity results in neonatal ataxia.

d. Copper deficiency produces marked skel­etal changes, osteoporosis and spontane­ous fractures.

e. Elastin formation is impaired in the defi­ciency of copper. Because a copper- con­taining enzyme plays an important role in the connective tissue metabolism, espe­cially in the oxidation of lysine into alde­hyde group which is necessary for cross- linkage of the polypeptide chains of elas­tin and collagen.

f. Copper deficiency results in the myocar­dial fibrosis in cows. It is suggested that reduction in cytochrome oxidase activity may lead to cardiac hypertrophy.

Disorders of Copper Metabolism:

Wilson’s Disease (Hepatolenticular degeneration):

Wilson’s disease is a rare hereditary disorder of copper metabolism.

The following disorders have been observed in this disease:

a. The absorption of copper from the intes­tine is very high (about 50 per cent), whereas 2 to 5 per cent copper is absorbed in normal subjects.

b. Ceruloplasmin formation is very less. Hence, a greater part of serum copper re­mains loosely bound to serum protein—notably albumin and, therefore, copper can be transferred to the tissues, such as brain and liver or to the urine.

c. Excessive deposition of copper in the liver and the kidney causes hepatic cirrhosis and renal tubular damage, respectively. The renal tubular damage results in the increased urinary excretion of amino ac­ids, peptides and glucose.

Clinical Symptoms:

a. Progressive hepatic cirrhosis of a coarse nodular type gradually leads to portal hypertension and finally to hepatic failure.

b. There is dysfunction of the lenticular re­gion of the brain necrosis and sclerosis of the corpus structures cause basal ganglion syndromes in adolescence.

c. Defects in renal tubular reabsorption and glomerular filtration.

d. Copper deposition in Descemet’s mem­brane of the eye causes a golden brown, yellow or green ring round the cornea. This lesion is called Kayser-Fleischer ring.

e. There is occasional pigmentation of the nails and skin.

Treatment:

Improvement can be achieved by removing the excess of tissue copper by adminis­tering the copper chelating agent penicillamine. This brings about marked increase in the urinary secretion of the metal.

Increased values of serum ceruloplasmin occur in many acute and chronic infectious diseases, hepatic and biliary tract dis­ease, leukemia and other forms of malignancy, iron deficiency anemia, hyperthyroidism, myocardial in­farction, and certain neurological diseases.

Menkes Disease:

It is an X-linked disorder of intestinal copper ab­sorption. The absorption of copper and its uptake in the mucosal cells and its intracellular transport within the mucosal cells are normal in patients with this disease.

But the transport of copper across the serosal aspect of the mucosal cell membrane is de­fective. The clinical features show that unless therapy is started promptly at birth, many severe symptoms like mental retardation, temperature instability, abnormal bone formation and susceptibility to in­fection are not to be cured.

Ceruloplasmin:

a. It is a copper-binding plasma protein.

b. Its molecular weight is about 151,000.

c. It contains about 8 atoms of copper per mole.

d. Normal plasma contains 30 mg of this pro­tein per dl.

e. It functions as a ferroxidase enzyme dur­ing iron transport.

Superoxide Dismutase:

a. It is an enzyme which catalytically scav­enges the toxic free radical superoxide ion (0₂) formed during aerobic metabolism.

b. Its molecular weight is about 32,000 and consists of two identical subunits.

c. It contains one Cu⁺⁺ and one Zn⁺⁺ per subunit.

d. Recent studies have shown that the cop­per proteins erythrocuprein, hepatocuprein and cerebrocuprein present in RBC, liver and brain, respectively, are identical with this enzyme.

Human Body: Trace Element # 3. Iodine:

Physiological Functions:

Iodine is required for the formation of thyroxine and triiodothyronine hormones of the thyroid gland. These thyroid hormones are involved in cel­lular oxidation, growth, reproduction, and the ac­tivity of the central and autonomic nervous sys­tems. Triiodothyronine is more active than thyrox­ine in many respects.

Sources:

Rich sources are sea water, marine vegetation, sea foods, and vegetables as well as fruits grown on the seaboard. Plants (and animal tissues) grown at high altitudes are deficient in iodine because of its low concentration in the water. In such regions, iodide is commonly added to the drinking water or table salt in concentration of 1 : 5000-1 : 200,000.

Daily Requirements:

Distribution:

The body normally contains about 10 to 20 mg of iodine. 70 to 80 per cent of this is present in the thyroid gland. Muscles contain large amount of iodine. The concentration of iodine in the salivary glands, ovaries, pituitary gland, hair and bile is greater than that in muscle. All the iodine in saliva is inorganic, but most tissues contain less amount of iodine in the inor­ganic form and most of the iodine is present in the organic form.

Blood Iodine:

Practically all of the iodine in the blood is in the plasma. The normal concentration of iodine in the plasma or serum is 3 to 6 µg/100 ml. Iodine protein bound is 3.5-7.5 µg/dL. 0.08 to 0.60 µg/100 ml is in the inorganic form and 4 to 8 µg/100 ml is in the organic form.

The organic form is bound to protein and precipitated by protein-precipitating agents. 90 per cent of the organic form consists of thyroxine and the remain­der is tri- and di-iodothyronine. About 0.05 per cent of the thyroxine is in the free state. Erythrocytes contain no organic iodine.

Absorption:

Iodine and iodides are absorbed most readily from the small intestine. Organic iodine compounds (diiodotyrosine and thyroxine) are absorbed as such and a part is broken down in the stomach and intes­tine with the formation of iodides. Absorption also takes place from other mucous membranes and the skin.

Storage:

90 per cent of the iodine of the thyroid gland is in organic combination and stored in the follicular colloid as “thyreoglobulin” a glycoprotein of mo­lecular weight 6,50,000 containing thyroxine, diiodotyrosine and smaller amounts of triiodothyronine. On demand, these substances are mobilized and thyroxine as well as triiodothyronine are passed into the systemic circulation. They undergo meta­bolic degradation in the liver.

Excretion:

a. Inorganic iodine is mostly excreted by the kidneys, liver, skin, lungs and intestine and in milk.

b. About 10 percent of circulating organic iodine is excreted in feces. This is entirely unabsorbed food iodine.

c. 40 to 80 per cent is usually excreted in the urine; of which 20 to 70 µg daily in adults and 20 to 35 µg in children. The urinary elimination is largest when the intake is lowest.

d. Urine iodine is increased by exercise and other metabolic factors.

Iodine Deficiency in Human Beings:

a. In adults, the thyroid gland is enlarged, producing the disease goitre. If treatment is started very early, the thyroid becomes normal. If treatment is delayed, the en­largement of the gland persists.

b. In children, severe iodine deficiency re­sults in the extreme retardation of growth which is known as cretinism.

Prevention of Goitre:

Goitre can be prevented by the regular use of iodide salt or iodide added to the drinking water in the concentration of 1 : 5000 to 1 : 2,00,000.

Goitrogenic Substances in Foods:

Foods such as cabbage, cauliflower and radish con­tain substances 1 to 5, vinyl-2-thio oxazolidone which react with the iodine present in the food and make it unavailable to the body. These substances are known as “Goitrogenic” substances.

Human Body: Trace Element # 4. Fluorine:

Physiological Functions:

a. Fluoride, in trace quantities, is essential for the development of teeth and bones.

b. It is, in combination with vitamin D, re­quired for the treatment of osteoporosis.

c. Sodium fluoride is a powerful inhibitor of the glycolytic enzyme enolase.

d. Fluoroacetate acts as a powerful inhibitor of aconitase activity, responsible for the conversion of citrate to cis-aconitate, of the citric acid cycle.

e. Fluoride ions inhibit the metabolism of oral bacterial enzymes and diminish the local production of acids which are im­portant in the production of dental car­ies.

f. Fluorine forms a protective layer of acid-resistant fluoroapatite with hydroxyapatite crystals of the enamel.

Sources:

For humans, drinking water is the main sources of fluoride.

Daily Requirement:

Fluoride is present in small amounts in normal bones and teeth. Drinking water containing 1 to 2 ppm meet up the requirement of the body and pre­vent dental caries without producing any ill effect.

Distribution:

It occurs in many tissues, notably the bones, teeth and kidneys. The amounts of fluoride in the soft tissues are very low and do not increase with age. It remains mostly in the extracellular water.

Absorption:

Soluble fluorides are rapidly absorbed from the small intestine.

Excretion:

It is excreted in the urine, in the sweat, and by the intestinal mucosa. Most of the fluoride that escapes retention by the bones and teeth is excreted rap­idly into the urine.

Abnormalities:

a. Intake of excessive amounts of fluoride (3 to 5 parts per million) in childhood causes “dental fluorosis” (molted enamel). The enamel of the teeth loses its lustre and becomes rough. Chalky white patches with yellow or brown staining are found over the surface of the teeth.

The enamel becomes weak and in severe cases there occurs a profound loss of enamel with ‘pit­ting’ which gives both the surfaces a cor­roded appearance.

b. Highly excessive intake of fluorine (over 10 parts per million) results in increased density and hyper-calcification of the bone of spine, pelvis and Limbs. In addition, the ligaments of the spine become calcified and the collagen in the bone is also calci­fied. Neurological disturbances are com­mon. Such individuals are crippled and cannot exhibit simple daily tasks, such as bending, squatting, etc. as the joints be­come stiff.

c. Drinking water containing less than 0.5 ppm fluorine causes dental caries in chil­dren.

Prevention of Fluorosis:

Fluorosis can be prevented by removing fluorides from the water by treatment with activated carbon or by some other suitable absorbents.

Human Body: Trace Element # 5. Zinc:

Physiological Functions:

a. Zinc is an essential constituent of many enzymes, such as carbonic anhydrase, al­kaline phosphatase, pancreatic carboxy-peptidases, and erytosolie superoxide dismutase.

b. The retina contains a zinc metalloenzyme, relinene reductase which is required for the formation of retinene.

c. It maintains normal concentration of vita­min A in plasma.

d. It is required for the mobilization of vita­min A from the liver.

e. It is required for the preparation of insulin and increases the duration of insulin ac­tion when given by injection. Zinc is used in the P-cells of the pancreas to store and release insulin as required.

f. It is concerned with the healing of wounds.

g. It is essential for the normal growth and reproduction of animals.

Sources:

Distribution:

It is widely distributed in the tissues of the body. The whole body (70 kg weight) contains 1.4 to 2.3 gm. zinc. 20 per cent of the total is present in skin. A certain amount is also present in the bones and teeth. High concentrations of zinc are present in sperma­tozoa, prostate and epididymis. The highest con­centration occurs in the choroid of the eye.

Blood zinc:

a. Zinc is present in higher concentration in erythrocytes than in plasma.

b. Normal plasma contains about 20 per cent of the zinc present in whole blood.

c. The concentration of zinc of human blood, plasma and erythrocytes are 0.8 mg 0.12 mg and 1.44 mg/100 ml, respectively.

d. About 3 per cent of zinc ion is contained in leukocytes. In certain types of chronic leukemia, there is a marked fall in the zinc content of peripheral leukocytes.

e. Most of zinc in erythrocyte is present in carbonic anhydrase.

f. The plasma concentration of zinc of hu­man falls to 10 per cent of the normal level during later part of pregnancy and among those taking oral contraceptives.

Daily Requirement:

Absorption:

a. Zinc present in animal foods are well ab­sorbed in the small intestine, especially from the duodenum.

b. Zinc present in cereals, pulses, nuts and oilseeds are poorly absorbed due to the presence of phytic acid which interferes its absorption.

Excretion:

a. Zinc given orally or by injection is mostly excreted in the feces.

b. Endogenous zinc is secreted into the small intestine in the pancreatic juice.

c. 90 per cent of zinc intake by healthy adult human is lost in the feces, about 5 per cent is excreted in the urine and 5 per cent is retained in the body.

d. Excessive sweating in the hot climate causes excessive loss of the metal.

Deficiency of Zinc:

a. Zinc deficiency in man results in dwarf- ism and hypogonadism (retarded genital development).

b. There is loss of taste acuity.

c. There is also poor growth, loss of appetite and hypogeusia in young malnourished children with subnormal hair zinc levels.

d. The deficiency of zinc causes hepatosplenomegaly, delayed closure of the epiphy­ses of the long bones, and anemia.

Human Body: Trace Element # 6. Cobalt:

a. Cobalt is an essential component of vita­min B₁₂, which is necessary for normal red blood cell formation.

b. Certain enzymes, such as methyl-malonyl-CoA mutase, methyl-tetrahydrofolate oxidoreductase, homocysteine methyltransferase, and ribonucleotide reductase re­quire vitamin B₁₂ for activity.

Sources:

It is highly available in food.

Distribution:

It is present in all tissues in small amounts. The total body content of cobalt is about 1.1 mg. The highest concentration occurs in liver, kidneys and bones. Most of the cobalt is present in vitamin B₁₂.

Daily Requirements:

Its requirement for man is very little. It is, required as vitamin B₁₂. As little as 1 to 2 µg of B₁₂, contain­ing 0.045 to 0.09 µg of cobalt, is sufficient to main­tain normal bone marrow function in pernicious anemia.

Absorption:

Cobalt is readily absorbed from the small intestine (70 to 80 per cent). Only minute amounts are present in the tissues. Cobalt administered as a soluble salt is poorly absorbed and, therefore, largely elimi­nated in the feces.

Excretion:

About 65 per cent of the amount ingested is ex­creted in the urine, the remainder in the feces. In­jected isotopic cobalt is eliminated rapidly and al­most completely by the kidneys into the urine.

Cobalt in Ruminant Nutrition:

Nutritional anemia in cattle and sheep living in cobalt poor soil areas can be treated successfully with cobalt. Microorganisms in the rumens of these animals use cobalt to synthesize vitamin B₁₂.

Cobalt Toxicity:

Cobalt administered in large amounts to man or animals becomes toxic. It develops a condition known as polycythemia (increased number of eiythrocytes in blood).

Cobalt Efficiency:

In ruminants only, cobalt deficiency causes ano­rexia, fatty liver, macrocytic anemia, wasting and hemosiderosis of spleen.

Human Body: Trace Element # 7. Manganese:

a. Manganese is essential for normal bone structure, reproduction, and the normal functioning of the central nervous system.

b. Manganese ions activate glycosyl-transferase which is concerned with the syn­thesis of the mucopolysaccharides of car­tilage and also associated with the syn­thesis of glycoproteins (e.g., prothrombin).

c. Pyruvate carboxylase and superoxide dismutase contain tightly bound manga­nese.

d. Arginase is activated by manganese ions.

e. It activates isocitrate dehydrogenase and phosphotransferases.

f. Manganese ions act as cofactor along with glucose-6-phosphate dehydrogenase.

g. Manganese ions inhibit lipid pero­xidation reaction.

Sources:

Distribution:

The body of a normal adult (70 kg. weight) con­tains 12-20 mg. manganese. It is present in all tis­sues of the body. The kidney and the liver are the main storage organs for manganese. Mitochondria are the principal intracellular sites of manganese uptake.

Daily Requirements:

In humans, deficiency of manganese is not known. The average dietary intake of 2.5-7.0 mg is quite sufficient.

Manganese in Blood:

Normal blood contains 4-20 µg./100 ml. In human serum, manganese is bound to a specific β-globulin,

Absorption:

Manganese is readily absorbed in the small intes­tine. Only 3 to 4 per cent of manganese present in the diet is absorbed.

Excretion:

95 to 96 per cent dietary manganese is excreted in the feces. Only traces of manganese is excreted in the urine.

Manganese Deficiency in Animals:

a. In manganese deficiency, the animals give birth to young ones which develop ataxia. In more severe deficiency, sterility results. In poultry, egg production and hatchability are decreased, even in mild deficiency of the metal.

b. The livers of manganese-deficient rats contain large amount of fat. This fat accu­mulation is prevented by manganese or chlorine.

c. Liver arginase activity and blood phos­phatase activity are reduced in manganese deficiency.

d. Bone deformities also occur in all animals in its deficiency.

Manganese Toxicity:

Miners who inhale large amount of manganese suf­fer from chronic manganese toxicity. There is the development of hepatolenticular degeneration re­sembling Parkinson’s disease.

Human Body: Trace Element # 8. Molybdenum:

Physiological Functions:

a. Molybdenum is an essential component of xanthine oxidase, aldehyde oxidase, and sulfite oxidase.

b. It is also present in nitrate reductase in plants, and nitrogenase, which functions in nitrogen fixation by microorganisms.

c. Traces of molybdenum are required for the maintenance of normal levels of xanthine oxidase in animal tissues.

Daily Requirements:

Adequate amounts of molybdenum are present in average diets. Therefore, exact requirement is un­known.

Absorption and Excretion:

About 50 to 70 per cent of the intake is readily absorbed in the small intestine. Half of the absorbed molybdenum is excreted in urine.

Toxicity:

a. Molybednum-rich diet consumption causes severe diarrhea and ill-health in cattle.

b. Rats, on high molybdenum diet, lose body weight with marked anorexia.

Human Body: Trace Element # 9. Selenium:

Physiological Functions:

a. Selenium is essential for normal growth, fertility and for the prevention of a wide variety of diseases in animals, although not known as essential for humans.

b. Glutathione peroxidase, a selenoprotein, catalyzes the peroxidation of glutathione. This enzyme is the protective agent against accumulation of H₂O₂, and organic peroxides within cells.

c. It is involved in immune mechanisms, ubiquinone synthesis, and mitochondrial ATP biosynthesis.

d. Selenoprotein also functions in the reductive deamination of glycine.

Sources:

Selenium is largely available in different foodstuffs. The variation depends on the differences in soil selenium content.

Distribution:

It is widely distributed in the animal body and high­est concentration is present in renal cortex, pan­creas, pituitary, and liver.

Daily Requirement:

Since average diet contains adequate amounts of selenium the requirement of it is not known.

Selenium Deficiency:

a. Selenium deficiency produces necrosis of the liver of rats.

b. Calves and lambs suffer from muscular dystrophy in selenium deficiency.

c. Chicks, on selenium-deficient diet, fail to grow and develop a diseased condition known as exudative diathesis.

Deficiency in Humans:

A. Keshan Disease:

This disease is reported from Keshan coun­try of north eastern China.

The disease affects mainly children and younger women.

It is manifested by an acute or chronic car­diac enlargement, arrhythmia and E.C.G. changes.

Prophylaxis with sodium selenite is highly effective.

B. Kaschinbeck Disease:

The disease is prevalent in several parts of eastern Asia and is characterized by de­generative osteoarthrosis affecting chil­dren between 5 and 13 years of age.

It retards growth by shortening fingers and bones with severe enlargement and dysfunction of the joints.

The disease becomes endemic in low sele­nium zones.

Relationship of Selenium to Vitamin E:

Both selenium and vitamin E are essential for cur­ing certain diseases in experimental animals.

When animals are given adequate amounts of vitamin E, selenium deficiency causes the following signs and symptoms:

a. Retardation of growth and muscular wast­ing in rats.

b. Retardation of growth and fertility in chicks.

These symptoms may be cured by the admin­istration of both selenium and vitamin E because of their close metabolic relationship.

Toxicity:

a. Chronic selenium poisoning develops “alkali disease”. The symptoms of alkali disease are dullness, lack of vitality, roughness of coat, loss of hair from the body and tail, stiffness and lameness, cir­rhosis of liver and anemia.

b. Acute selenium poisoning produces in animals salivation, grating of teeth, pa­ralysis and blindness. Death results due to respiratory failure.

Human Body: Trace Element # 10. Chromium:

Physiological Functions:

a. Chromium potentiates the action of insu­lin in accelerating utilization of glucose in animal and humans.

b. It is effective in improving glucose toler­ance in some patients suffering from dia­betes mellitus.

c. It maintains the normal cholesterol level in blood of rats.

d. It regulates the incorporation of certain amino acids in heart muscle in rats.

Sources:

It is highly available in dietary foods.

Distribution:

The chromium content of adult human body is esti­mated to be 6 mg. It is widely distributed in tissues.

Chromium in Blood:

Normal blood contains about 0.009 to 0.055 parts per million.

Requirements:

Since average diet meets up the requirements, the exact necessity is unknown.

Absorption and Excretion:

It is readily absorbed in the small intestine. It is mobilized from the tissues in response to glucose administration.

Chromium is mainly excreted in urine, a small amount is lost in bile and feces.

Deficiency:

Its deficiency is characterized by impaired growth, disturbances in glucose, lipid and protein metabo­lism.

Toxicity:

Excessive amounts of chromium produces growth depression, liver and kidney damage in some ex­perimental animals.

Human Body: Trace Element # 11. Lead:

Lead is not an essential component of our body but it is always present in our body due to extensive use and easy absorption in the body in various forms.

Physiological Functions:

a. Lead is the inhibitor of enzymes and acts as a toxic substance against enzymes.

b. Prolonged use of lead may lead to impo­tence or sterility.

c. Lead may not cause any toxic effect when enters the body over a long period even in low dose but may cause harm when its concentration becomes high in different tissues due to its cumulative property.

d. Abortion pills are made up of lead.

e. Chronic poisoning with lead may cause sterility but not impotence.

f. Lead has got local irritating action on the tissues.

g. Chronic lead poisoning causes blue lin­ing in the gum.

h. Lead is extensively used in industries, ag­riculture, commerce, and for domestic pur­poses.

i. It is also used in the tin food container, batteries, paints, hair dyes, petrol, glass blowing and cosmetics as vermilion.

Sources:

It is available as lead acetate (sugar of lead), lead carbonate (used in painting), lead tetraoxide (used as vermilion), tetra-ethyl lead (used in petrol and gasoline), lead chromate, toxic compounds such as lead sulphide, lead chloride, lead sulphate and lead iodide, etc.

Distribution:

In chronic state, it is deposited in tissues, mostly in bones and also in liver and kidneys.

Absorption:

a. Most of the lead compounds are soluble in gastric juice and are absorbed through the gastrointestinal tract.

b. Lead dust and fume are well absorbed through the respiratory tract.

c. Tetra-ethyl lead, lead tetraoxide (vermil­ion), some other dyes and cosmetics are absorbed through the skin.

d. Lead acetate, although more injurious lo­cally, is soluble in water and easily ab­sorbed when swallowed.

Excretion:

a. It is mostly excreted through the urine al­though the excretion rate is very low 0 to 120 µg/24 hours.

b. It is also slightly excreted through bile and to a small extent through nails.

c. Much of the lead excreted through stool may be the unabsorbed ingested lead.

Lead in Blood:

The normal concentration of lead is 96-106 mEq/L of blood. The blood range between 0.1 mg% – 0.6 mg% usually shows clinical symptoms.

Toxicity:

a. Ingestion of lead acetate causes burning pain in the throat, abdominal pain and vomiting. There are cramps in the abdo­men, loose motion and the stool becomes dark due to lead sulphide. There may be thirst, dehydration, signs of collapse and death due to circulatory failure.

b. Chronic lead poisoning appears when the level of the accumulated lead exceeds the threshold level. This may occur in the in­dustrial environment due to inhalation of lead dust or lead vapour producing from burning of paints, battery, glass blowing and polishing, enamel factories, dye, cos­metic and colour factories.

Chronic lead poisoning in the early stage is manifested by facial pallor, anemia, blue line in the gum, basophilic stippling of red cells, reti­nal stippling and in the later stage there is constipation, palsy, encephalopathy, dis­turbance of genito-urinary and cardio-vas­cular system.

c. In acute poisoning with lead, the victims are usually children who chew substances painted with lead paints.

d. Chronic lead poisoning causes arterioscle­rosis with resultant hypertension and hy­pertensive cardiopathy. There may also be chronic interstitial nephritis and alopecia in this poisoning.

e. Chronic lead poisoning too causes degen­eration of anterior horn cells and demyelination leading to peripheral neuritis.