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Let us make an in-depth study of the water and mineral metabolism.
Water Metabolism:
Distribution of water in the body:
Water is the major constituent of human body. The average body water is 50-70% of the body weight. Females have little less water than males.
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1. The water content of intracellular fluid is 50% of total body weight.
2. The water content of extracellular fluid is 20% of the body weight, which is distributed as follows:
Factors influencing the distribution of body water:
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The distribution of water is continuously changing. Osmotic forces are the principal factors for controlling the amount of fluid in various compartments of the body. These are maintained by the solutes of the body. Solutes are of three types.
1. Organic molecules of small molecular size (glucose, urea, amino acids etc.):
Since these diffuse freely across the cell membrane, they are not important in the distribution of water. If they are present in large quantities, they can help retaining water.
2. Organic substances of large molecular size {proteins):
These substances can throw effect in the transport of fluids from one compartment to the other.
3. The inorganic electrolytes:
These inorganic electrolytes are the most important both in the distribution and in the retention of body water.
Intake and Loss of Body Water:
A. Water intake:
Water is supplied to the body by the following processes:
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1. Water taken orally.
2. Along with food.
3. Oxidation of food stuffs i.e. fats, proteins and carbohydrates yield water after combustion.
B. Water loss:
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Water is lost from the body by 4 routes
1. Evaporation from lungs.
2. Kidneys eliminate water as urine.
3. The intestines excrete in the feces.
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4. Perspiration.
C. Additional water loss in diseases:
1. Water loss is more in diarrhea and vomiting. These losses can be fatal in infants.
2. In kidney disease, renal water loss is more.
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3. In fever, insensible losses may rise much higher than normal.
4. Patients in high environmental temperatures sustain extremely high external water loss.
Water Balance:
An equilibrium persists between the intake and output of water in the body. In addition to other factors, certain hormones such as ADH, vasopressin, oxytocin and aldosterone influence the regulatory mechanism.
There is a continuous excretion of water in the form of digestive juices from the body into the alimentary canal. This water (except 100 ml) is reabsorbed with the water of the food and drinks. The amount of this internal secretion is 7 to 10 liters/day.
Physiological Functions of Water:
1. Specific heat:
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Heat is required to raise the temperature of 1 gm. of water through one degree Celsius is more than for almost any other solid or liquid. The high specific heat of water helps in minimizing the rise in body temperature due to the heat emitted out of chemical reactions.
2. Latent heat of evaporation:
Water has the highest latent heat of evaporation than any other liquid. A certain amount of water can cause maximum cooling by evaporation, so that body temperature does not rise.
3. Solvent power:
Water forms true solutions as well as colloidal solutions. Even water insoluble substances are made water soluble by the hydrotropic action. Therefore, it is the most suitable solvent for cellular components; water thus brings various substances in contact for chemical reactions to proceed.
4. Dielectric constant:
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Oppositely charge particles can coexist in water. Therefore, it is a good ionizing medium. This stimulates the chemical reactions.
5. Catalytic action:
A large number of chemical reactions in the body are accelerated by water due to its ionizing power. All chemical reactions in the body proceed in presence of water only.
6. Lubricating action:
Water acts as a lubricant in the body to prevent friction in joints, pleura, conjunctiva and peritoneum.
Regulation of Passage of Water:
1. If capillary pressure is increased, more water will flow into the tissues.
2. A fall in blood pressure helps in passage of water form the tissues to the blood.
3. If the plasma proteins are decreased, water will flow into the tissues.
4. Dilution of blood by excessive ingestion of water can lower the osmotic pressure of the plasma proteins and thus may increase capillary pressure.
Dehydration:
When the loss of water exceeds the intake, the body’s water content is reduced. This means that the body is in negative water balance and the condition is known as dehydration.
Causes:
1. Primary dehydration:
(a) Deprivation of water during desert travel, extreme weakness and mental patients refraining to drinking water causes dehydration. Occurs more quickly in fever and in high environmental temperatures.
(b) Excessive water loss due to vomiting, prolonged diarrhoea, excretion of large quantities of urine and sweat. In water depletion, the concentration of extracellular fluid increases. Water is drawn from the cells and both extracellular and intracellular compartments shrink. Extreme thirst results; individual complains of hot and dry body. The tongue becomes dry.
2. Secondary dehydration:
Concentration of electrolytes of the body fluids is maintained constant through the elimination or retention of water. The reduction or increase in the total electrolytes which affects, chiefly the basic radical Na (extracellular) or K (intracellular) and the acid radicals HCO3 and CI is accompanied by a corresponding increase or decrease in the volume of body water. This causes intracellular edema, slowing of circulation and impairment of urinal function. The individual becomes weak.
3. Dehydration due to injection of hypertonic solution:
When a highly concentrated sugar or salt solution is injected into the body, the osmotic pressure of blood will increase. This results in the flow of fluid from the tissues into the blood until equilibrium sets in. Consequently, the blood volume increases. This increased blood volume soon returns to normal by the loss of excess material through urination. This causes a net loss of body water producing dehydration.
Effects of dehydration:
1. Loss of weight due to the reduction in tissue water.
2. Disturbances in acid-base balance.
3. Rise in the non-protein nitrogen of blood.
4. Rise in the plasma protein concentration and of chloride.
5. Rise in body temperature due to reduction in circulating fluid.
6. Increased pulse rate and reduced cardiac output.
7. Dryness, wrinkling and looseness of skin.
8. Exhaustion and collapse.
Correction of dehydration:
1. Ordinary NaCl solution may be given parenterally to repair the losses.
2. In case of excretion of fluid high in Na and HCO3 resulting in fluid and electrolyte loss, a mixture of 2/3 isotonic saline and 1/3 Na lactate should be administered intravenously.
3. Dehydration in diabetes mellitus, Addison’s disease, uremia, extensive burns and shock cannot be corrected by the above methods.
Water intoxication:
Caused by excessive water retention due to renal failure, hyper secretion of ADH, excessive administration of fluids parenterally.
Symptoms:
Headache, nausea and muscular weakness.
Mineral Metabolism:
Living beings have organic and inorganic types of chemical constituents. The organic constituents i.e. proteins, carbohydrates, fats etc. are made up of C, H, O and N. The inorganic constituents described as ‘minerals’ comprise of the elements present in the body other than C, H, O and N. Although they constitute a relatively small amount of the total body tissues, they are essential for many vital processes.
There are 31 elements present in the body.
They are divided into two classes:
(1) Essential elements and
(2) Non-essential elements.
Essential elements:
Those which are essential to maintain the normal living state of a tissue.
They are again divided into two sub groups:
Macro elements:
They are required to be present in the diet, more than 1 mg.
Ex. Ca, P, Mg, Na, K, CI and S.
Micro elements:
They are 8 in number and utilized in trace quantities (in microgram or Nano-gram). Hence they are called trace elements. These are Fe, Cu, Zn, Co, Mo, F, I and Mn.
Non-essential elements:
They are 8 in number. They are present in tissues but their functions if any are not clearly defined. They include Al, B, Se, Cr, Br, As, Ti and Pb. Four additional elements, Ni, Tin, Vanadium and Silicon have been suggested as essential trace elements in nutrition but their implications for human nutrition are unknown.
The mineral elements present in the body are supplied in the diet. In poor diets consumed by a large majority of people, calcium and iron deficiency occur commonly. Iodine deficiency occurs in people living in certain hilly tracts, where the soil and water are deficient in iodine. In tropical countries, addition of sodium chloride in the diet is of great importance, because of the loss of NaCl in sweat. The deficiencies of other minerals do not occur normally in average diets.
i. Sodium, potassium and chlorine are involved mainly in the maintenance of acid-base balance and osmotic control of water metabolism.
ii. Calcium, phosphorus and magnesium are constituents of bone and teeth.
iii. Phosphorus is the constituent of body cells of the tissues, such as muscle, liver etc.
iv. Sulphur is present in cysteine, methionine, thiamine, biotin, lipoic acid and coenzyme A.
Calcium:
Source:
Milk (0.2 gm./100 ml) and cheese are important dietary sources. Other sources-are egg yolk, lentils, nuts, cabbage, cauliflower and asparagus, etc.
Requirement:
(1) Men and women after 18 years of age require 800 mg/day.
(2) During lactation and in pregnancy of 2nd and 3rd term 1.2 gm./day is required.
(3) Infants under 1 year require-360-540 mg/day.
(4) Children of 1-18 years need 800-1200 mg/day.
Absorption:
Calcium is taken in the diet as calcium phosphate, carbonate, tartarate and oxalate. Calcium is absorbed actively in the upper small intestine. The active process is regulated by 1,25 dihyrocholecalciferol, a metabolite of vitamin D which is produced in the kidney in response to low plasma Ca++ concentrations. Absorption of calcium by the intestine is never complete. Ca is absorbed by an active transport process occurring mainly in the upper small intestine.
Calcium absorption is influenced by the following factors:
1. Vitamin D promotes absorption of Ca.
2. Acidic pH favous calcium absorption because Ca salts (phosphate and carbonates) are quite soluble in acid solution arid are relatively insoluble in alkaline solutions. Hence an increase in acidophilic flora, e.g. lactobacilli is recommended to lower pH which favours the absorption of Calcium.
3. Organic acids, lactose and basic amino acids in the diet favour calcium absorption.
4. Higher levels of proteins in the diet help to increase the absorption of calcium. On a high protein diet, about 15% of the dietary calcium is absorbed, compared with 5% absorption on a low protein diet. Certain calcium salts are much more soluble in aqueous solution of amino acids than in water and thus absorption of calcium is increased in presence of amino acids.
5. If calcium: phosphorus ratio is much high, Ca3(PO4)2 will be formed and absorption of calcium is reduced. The optimal ratio for both elements is about 1:1 (1:2 to 2:1) and with ratios outside these limits, absorption is decreased. This is because of formation of insoluble calcium phosphate.
6. When fat absorption is impaired much free fatty acids are formed due to hydrolysis. These fatty acids react with free calcium to form insoluble calcium soap and then Ca is lost in faeces.
7. Absorption of calcium is inhibited by a number of dietary factors that cause formation of insoluble calcium salts, i.e. phytate (cereal grain), oxalate, phosphate and iron, etc.
8. High concentration of Mg in the diet decreases absorption of Ca.
9. Presence of excess fibre in the diet interferes with the absorption of Ca.
10. Percentage of calcium absorption decreases as its intake increases.
11. Parathyroid hormone increases the intestinal absorption of calcium.
12. Adrenal glucocorticoids diminish intestinal transport of Ca.
13. After the age of 55 to 60 there is gradual diminution of intestinal transport of calcium. During menopause many women develop negative calcium-phosphorus balance leading to a type of osteoporosis. This is usually accompanied by pain and fractures. The negative balance of calcium and phosphorous are markedly improved by administration of estrogen or by androgens such as testosterone. A combination of estrogen and androgen is more effective.
14. Kidney threshold regulates the blood calcium level. In a normal adult any extra calcium absorbed from the intestine is readily excreted in the urine. In hypocalcaemia kidney threshold also becomes abnormal.
15. Excess of iron also dis-favours absorption of calcium and phosphorus, as ferric phosphate is highly insoluble. The net result is an upset in the Ca:P ratio.
16. Oxalate in certain foods precipitate calcium in the intestine as insoluble calcium oxalate. The phytic acids of food form insoluble salt with calcium and reduce calcium absorption.
17. Vitamin D increases calcium and phosphorus absorption from the intestine. Vitamin D promotes synthesis of specific calcium binding protein which participates in the active transport of calcium across the small intestinal mucosa. Lack of vitamin D, excess of phytates, low Ca/P ratio in diet, increased pH of upper intestine and malabsorption syndromes influence the amount of calcium absorption adversely.
Biological role:
Calcium is involved in the following biological processes:
1. Constituent of bones and teeth:
Calcium along with phosphate constitutes the mineral part of the skeleton and teeth where it is present to the extent of 99% of the total calcium present in the body. It is primarily in the form of crystals of hydroxyapatite, while some is in combination with phosphate (calcium phosphate) in the form of amorphous crystals.
2. Neuromuscular functions:
This involves excitability of nerve function, neural transmission, and contractility of cardiac and skeletal muscle. Normal concentration of calcium ions is required for the normal excitability of heart muscle.
3. Blood coagulation:
It plays a vital role in blood clotting process since it activates the enzymic conversion of prothrombin into thrombin and production of thromboplastin. The removal of calcium from the blood can prevent blood coagulation and because of this reason EDTA, oxalates, citrates are used as anticoagulant because these ions can precipitate calcium into the respective insoluble salts.
4. Membrane function:
It controls the permeability of all membranes and is often bound by lecithine in the membrane, i.e. it decreases the permeability and balances the opposite action of sodium and potassium capillary permeability. This involves transfer of inorganic ions across cell membranes and release of neurotransmitters at synaptic junction.
5. Selected enzymatic reactions:
Calcium acts as activator for number of en2ymes like ATPase, succinic dehydrogenase, lipase, etc. It also antagonizes the effect of magnesium on many enzymes. It releases cellular enzymes such as amylase from the parotid and increases the level of activity of intracellular enzymes such as—Isocitric dehydrogenase, phosphorylase and phosphof ructokinase.
6. Regulation of secretion of certain peptide hormones:
Pituitary hormones, parathyroid hormone, calcitonin and vasopressin are regulated through calcium ionic concentration. Calcium along with zinc plays a vital role in release of insulin from pancreas. Calcium homeostasis: Normal blood values are 9.5-10.5 mg/100 ml. 35-45% of this is bound to proteins, mostly to the albumin fraction. In the extracellular fluid nearly all the calcium is in ionized form (55-65%). 0.5 (5-10%) mg is complexed to organic acids, phosphate, citrate, etc., while in renal failure, it may be complexed to other organic ions as well.
The skeleton is in a dynamic state of equilibrium to maintain calcium homeostasis. 4-8 gm. of calcium in bone is rapidly exchangeable with that in plasma and is present on the surface of the bone crystals—labile calcium storage pool. The remaining 99% of bone calcium is more firmly fixed in bone tissue and exchanges at a very slow rate.
Metabolism:
The blood cells contain very little amount of calcium, most of the blood calcium is therefore, in the plasma, where it is present in 3 fractions:
(1) Ionized about 2 mg/100 ml.
(2) Non-diffusible (protein bound) above 3.5 mg/100 ml.
(3) A small amount as calcium complex of citrate and phosphate.
All these forms of calcium in the serum are in equilibrium with one another. A decrease in ionized calcium in the serum causes tetany. This may be due to an increase in the pH of blood or lack of calcium because of poor absorption from the intestine, decreased dietary intake, increased renal excretion as in nephritis or parathyroid deficiency.
Factors influencing blood calcium level:
1. Parathyroid hormone:
In fasting condition or state there is no absorption from the intestine, the normal plasma Ca concentration is maintained by its rate of excretion and its mobilization from bones through the action of the parathyroid hormone.
2. Vitamin D:
It enhances absorption of Ca from the intestine and thus maintains normal Ca concentration.
3. Plasma proteins:
Half of the blood Ca (non-diffusible) is bound to plasma proteins and thus any decrease in these proteins will be accompanied by a decrease in the total calcium level.
4. Plasma phosphate:
A reciprocal relationship exists between the concentration of Ca and phosphate ions in plasma. The marked increase in serum phosphate causes a fall in serum calcium concentration.
5. Calcitonin:
An increase in the ionized Ca levels in the plasma is the stimulus for the production of calcitonin which then causes a deposition of Ca in bone.
Excretion:
Calcium is excreted in the urine, bile and digestive secretion. About 75% of dietary calcium is absorbed and rest is excreted as fecal calcium. Nearly 10 g of Ca is filtered by the renal glomeruli in 24 hours. But only 200 mg appear in the urine, which is in the ionic state as well as in the complexes with citrate and other organic anions. A very small amount of Ca is excreted into the intestine after absorption. About 15 mg of Ca is excreted in the sweat. Vigorous physical exercise increases the loss of Ca by way of sweat.
Disease state:
Calcium metabolism is highly influenced by parathyroid hormones. In hyperparathyroidism serum calcium rises (12-22 mg/100 ml) (hypercalcaemia), phosphatase activity is increased, urinary calcium is decreased and phosphorus rises in serum. The calcium, phosphorus ratio is important in ossification. In the serum the product of calcium and phosphorus (in mg/100 ml) is normally 50 in children and may be below 30 during rickets.
The following are the diseases related to calcium in the body:
(a) Effects of parathyroid:
1. In hyperparathyroidism, the following changes occur:
(i) Hypercalcemia (12-22 mg/dl).
(ii) Decrease in serum phosphate.
(iii) Diminished renal tubular reabsorption of phosphate.
(iv) Increased phosphatase activity.
(v) Renal urinary Ca and phosphorus found from bone decalcification and dehydration.
(vi) Extra Ca and P are lost from soft tissue and bones by increased bone destroying activity.
2. In hypoparathyroidism, the following changes occur:
(i) The concentration of serum Ca may drop below 7 mg/100 ml.
(ii) Increased serum phosphate and decreased urinary excretion of calcium and phosphorus.
(iii) Normal or occasionally raised serum phosphatase activity.
(iv) Normal acid-base equilibrium.
(v) Probably increased bone density.
(b) Tetany:
Decreased ionized fraction of serum Ca causes tetany.
This may be due to:
1. Increase in the pH of blood.
2. Poor absorption of Ca from the intestine.
3. Decreased dietary intake of Ca.
4. Increased excretion of Ca as in hepatitis.
5. Parathyroid deficiency.
6. Increased retention of phosphorus as in renal tubular disease.
Symptoms:
Muscles lose tone and become flabby.
Affects the face, hands and feet.
(c) Rickets:
This is characterized by faulty calcification of bones in children showing serum phosphate values of 1 to 2 mg/100 ml.
This may be due to:
1. Vitamin D deficiency.
2. A deficiency of Ca and P in the diet or a combination of both.
3. Poor absorption of Ca from the intestine.
4. Parathyroid deficiency.
5. Increased alkaline phosphatase activity.
(d) Osteoporosis:
This disease occurs in adults due to the following causes:
1. Decalcification of bones as a result of Ca deficiency in the diet.
2. Hypoparathyroidism.
3. Low vitamin D content of the body.
Symptoms:
Fractures of the brittle bones occur even after minor accidents.
Pain due to fracture of vertebrae (may radiate round the trunk, to the buttocks or down the legs).
Renal rickets:
It is a hereditary disease. It is called familial hypophosphatemia rickets. Affected persons show severe rickets with hypophosphatemia.
The causes are:
(i) Defective transport of phosphate by the intestine and the renal tubules
(ii) Lowered serum phosphorus and hyperphosphaturia
(iii) Reduced intestinal absorption of calcium and phosphorus. Vitamin D in ordinary doses does not relieve the disease. Hence, it is referred to as vitamin D resistant rickets.
Phosphorus:
Source:
Phosphorus is present in nearly all foods therefore a dietary deficiency is not known to occur in man. Dairy products, cereals, egg yolk, meat, beans and nuts are usually rich sources. The daily average intake is 800-1000 mg and is about twice that of calcium.
Absorption:
Like calcium, phosphorus is also absorbed by upper small intestine and factors influencing the absorption are also similar. The normal range for plasma inorganic phosphorus is 3.0-4.5 mg/dl. In children values are higher (5-6 mg/dl) and remain so up-till puberty.
Distribution:
Phosphorus is distributed more widely than calcium. 15% is found in muscle and other soft tissues and 85% in the inorganic mineral phase of bone. It is an integral part of many macromolecules. Ex. Phospholipids, phosphoproteins and nucleic acids.
Functions:
It has no physiological effects comparable to that of calcium but it has many other functions which are as follows:
1. Formation of bone and teeth.
2. Formation of phospholipids essential to every cell.
3. Formation of nucleic acids and derivatives.
Ex. Adenylic acid and is thus significant in (RNA and DNA) protein synthesis and from genetics point of view.
4. Formation of organic phosphates as intermediate in metabolic processes.
Ex. In glycolysis, Glucose + ATP → G-6-P + ADP.
5. Formation of energy rich phosphate compounds.
Ex. ATP (energy currency of the cell).
6. Both inorganic and organic phosphates can take part in buffering the cell.
Ex, Sodium-potassium-phosphates.
7. Formation of coenzymes.
Ex. TPP, NADP.
8. Formation of phosphoprotein.
Ex. Casein.
Excretion:
Urinary excretion is equivalent to dietary phosphate intake. It varies diurnally, more being excreted at night. The usual daily loss is 600-800 mg, tubular resorption being 85-95%. Renal loss of phosphate can be of significant magnitude to lower serum phosphorus values and enhance osteoid demineralization.
Homeostasis:
There is a greater fluctuation observed in blood phosphate values due to easy shift between extracellular fluid and intracellular compartments. Thus it is quite dependent on dietary phosphorus. Inorganic phosphate affects the net movement of calcium into and out of bone.
Raised phosphate will lead to depression of the solubility of the calcium of bone crystals and thus shift equilibrium towards bone. In this manner it opposes the effect of the parathyroids. Ingestion of heavy dose of phosphate can lower serum calcium and increase excretion of calcium in urine. Lowered phosphorus on the other hand will make parathyroid activity more apparent.
Hormonal factors are not directly linked. However renal phosphate clearance is very vital in homeostasis and seems to be secondarily involved in certain endocrinopathies, e.g. involving parathormone, growth hormone and corticosteroids.
Disease state:
The following are the disease states of phosphorus in the body:
1. In rickets, serum phosphate is as low as 1-2 mg/100 ml (There is a temporary decrease in serum P during absorption of carbohydrates and some fats).
2. Organic P content is low but inorganic content is high in the serum in diabetes.
3. P retention causes acidosis in severe renal diseases. This results in increase of serum P.
4. Serum P levels are increased in hypoparathyroidism and decreased in hyperparathyroidism and celiac disease.
5. In renal rickets, blood P is very low with an increased alkaline phosphatase activity.
6. The deficiency of vitamin D is the cause of low serum P and the defects in the calcification of bones (referred to as vitamin D resistant rickets).
Magnesium:
Source:
Magnesium is present in milk, egg, cabbage, cauliflower etc.
Daily requirement:
Infants—100-150 mg; Children—150-200 mg and Adults—200-300 mg.
Absorption:
A greater part of the daily ingested Mg is not absorbed. A very high intake of fat, phosphate, calcium and alkalies diminish its absorption. Parathyroid hormone increases its absorption.
Distribution:
Whole blood it is 2-4 mg/dl, CSF it is 3 mg/100 ml and muscle it is 2 mg/100 ml.
Functions:
1. 70% of the total magnesium content (21g) of the body is combined with calcium and phosphorus in the complex salts of bone. The remainder is in the soft tissues and body fluids. It is the principal cation of the soft tissue.
2. Magnesium ions act as activators for many of the phosphate group transfer enzymes.
3. It is found in certain enzymes, such as co-carboxylase.
4. It functions as a cofactor for oxidative phosphorylation.
Disease state:
The following are the disease states of magnesium in the body:
1. Magnesium deficiency causes depression, muscular weakness and liability to convulsions. Its deficiency has also been observed in chronic alcoholics with low serum mg and muscular weakness.
2. Low in Kwashiorkor, causing weakness.
Low levels of Mg are reported in uremia, normal and abnormal pregnancy, rickets, growth hormone treatment, hypercalcemia and recovery phase of diabetic coma.
Sodium, Potassium, Chloride:
Substances whose solutions conduct an electric current are called ‘electrolytes’. They are about 11 in general. Na, K, Ca and Mg are cations whereas CI, HCO3, HPO4, SO4, organic acids and proteins are anions. Among these sodium, potassium and chloride are important in the distribution and the retention of body water, thus have close relationship among them. Hence these three elements appear as a single question in the university exams.
Source:
The most important source of Na and CI in the diet is common table salt (NaCl). The good source of K are chicken, calf flesh, beef liver, dried apricot, dried peaches, bananas, the juice of orange and pineapple, potatoes etc.
Absorption:
Normally Na, K and CI are completely absorbed from the gastro-intestinal tract. About 95% of sodium which leaves the body is excreted in the urine.
Distribution:
In the tissues both Na and K occur in a relatively large amount as compared to chloride and other inorganic salts as well as protein and organic salts. Sodium is present in extra cellular fluid and in a very low concentration inside the cells whereas potassium is mainly found inside the cells and in a very low concentration in the extracellular fluid.
Functions of sodium and potassium:
These electrolytes maintain normal osmotic pressure in the body and protect the body against excessive loss of fluid.
1. They maintain the acid base balance in the body. Sodium bicarbonate, sodium phosphate, potassium phosphate form the buffer system of extracellular and intracellular fluids.
2. They maintain normal water balance.
3. Na also functions in the preservation of normal excitability of muscle and the permeability of the cells. K inhibits ‘muscular contraction’ in general.
4. High intracellular potassium concentrations are essential for several important metabolic functions, including protein biosynthesis by ribosomes.
5. Sodium and Potassium chlorides maintain the viscosity of blood. A number of enzymes including glycolytic enzymes, such as pyruvate kinase, require K+ for maximal activity.
6. Na helps in the formation of the gastric juice. NaCl takes part in the series of reactions as a result of which HC1 is manufactured by the stomach.
7. K of KHb in the red cells helps in carbon dioxide transport.
8. K ions inhibit cardiac contraction and prolong relaxation.
9. K ions exert important effect on the function of nervous system.
Functions of chloride:
1. It provides 2/3rd of the anion of plasma and is the main factor for regulating body reactions.
2. NaCl and KCl are important agents in regulation of osmotic pressure in the body.
3. HCl of gastric juice is ultimately derived from the blood chlorides.
4. Chloride ions are essential for the action of ptyalin and pancreatic amylase.
5. It is essential in acid-base regulation. Chloride plays a role in the body by chloride shift mechanism.
Metabolism:
The metabolism of these elements is influenced by the following factors:
Hormones:
Mainly adrenocortical steroids and some of the sex hormones facilitate the retention of sodium and chloride in the body and excretion of potassium by kidneys in the urine. In adrenocortical deficiency, serum sodium decreases because excretion increases.
Temperature:
When atmospheric temperature is high as in summer, large amounts of sodium and chloride are lost in perspiration (sweating) and this loss may be checked when temperature is low (in winter).
Renal function:
In renal disease, with acidosis, Na and CI ion excretion in urine is increased due to poor tubular reabsorption of sodium whereas that of K ion is decreased leading to hyponatraemia and hypochloraemia but hyperkalaemia.
Average requirement of Na and K in human body is 5-15 and 4 gm. per day, respectively.
Disorders:
Hyponatraemia:
On sodium deficient diet, young ones grow slowly, lack fat deposit, there is muscle and testicular atrophy, lung infection and deficiency of osteoid tissues. There will also be loss of water, which will be evident by rapid weight loss.
Hypokalaemia:
Extreme potassium depletion in circulating blood causes hypokalemia in young one, they grow slowly and both sexes become sterile. The heart rate is slow, muscle weakness, irritability and paralysis are seen. Bone growth is retarded and in becomes excessively fragile and kidney hypertrophy is exhibited.
Hyperkalemia:
Hyperkalemia paralysis occurs due to excessive amount of potassium in blood. The disease is characterized by periodical attacks of weakness or paralysis. The symptoms of hyperkalaemia are chiefly cardiac and central nervous system depression. They are related to the elevated plasma potassium level and not to increase in intracellular potassium levels.
A dietary chlorine deficiency produces no symptom except a subnormal growth rate. Under normal dietary condition human beings are not subject to a deficiency of sodium, potassium or chlorine. However excessive diarrhoea, vomiting or extreme sweating over long period may bring about a NaCl deficiency. Sometimes the metabolism of individual minerals is asked as a separate question in the university exams. Hence each one is described separately in detail, hereunder.
Sodium:
Physiological functions:
1. Major component of extracellular fluids and exists in the body in association with anions chloride, bicarbonate, phosphate and lactate.
2. In association with chloride and bicarbonate it plays a role in acid base equilibrium.
3. Maintains osmotic pressure of the body fluids and thus protects the body against excessive fluid loss.
4. Plays an important role in the absorption of glucose and galactose from small intestine.
5. Maintains normal water balance and distribution.
6. Maintains the normal neuromuscular function.
7. Functions in permeability of cells.
Distribution:
About 1 /3rd of the total sodium content of the body is present in the inorganic portion of the skeleton. Most of the sodium is present in the extracellular fluid.
Plasma — 330 mg/100 ml
Muscles — 60 to 160 mg/100 gm.
Cells — 85 mg/100 gm.
Nerve — 312 mg/100 gm.
Daily requirement:
Adults require 5-15 gms/day. In temperate region, NaCl intake is less. In tropical region, NaCl intake is more. Hypertension patients should not take more than 1 gm. of Na per day.
Absorption:
Normally, Na is completely absorbed from gastro-intestinal tract. Less than 2% is eliminated in feces. In persons suffering from diarrhoea, large amounts are lost in feces.
Excretion:
Urine — 5-35 gm.
Skin — 25-50 mg
Stool — 10-125 mg
Excessive loss of Na by sweating causes heat arrays.
Disease state:
1. Adrenal cortical steroids regulate the metabolism of Na. Insufficiency of adrenal cortical steroids decreases serum Na level with an increase in sodium excretion.
2. In chronic renal disease when acidosis exists, Na depletion occurs due to poor tubular reabsorption of Na as well as to the loss of Na in the buffering acids.
3. In persons not adapted to high environmental temperature large amount of Na is lost in the sweat, developing muscular cramps of extremities, oedema, headache, nausea and diarrhoea.
4. Hyponatremia causes dehydration and reduced blood pressure, decreased blood volume and circulatory failure.
This may be due to:
(a) Prolonged vomiting and diarrhoea resulting in excessive loss of digestive fluid.
(b) Chronic renal disease with acidosis due to poor tubular reabsorption of Na.
(c) Adrenocortical insufficiency.
(d) Loss of weight due to loss of water.
5. In Hypernatremia, serum Na is high.
This occurs in:
(a) Hyperactivity of adrenal cortex as in Cushing’s syndrome.
(b) Prolonged treatment with cortisone and ACTH as well as sex hormones, this results in—
(i) Increased retention of water in the body.
(ii) Increase in blood volume,
(iii) Increase in blood pressure.
6. Steroid hormones cause retention of Na and water in pregnancy.
Potassium:
Physiological junctions:
1. Potassium is largely present in intracellular fluid and it is also present in small amounts in the extra cellular fluid because it influences the cardiac muscle activity.
2. It plays an important role in the regulation of acid-base balance in the cell.
3. It maintains osmotic pressure.
4. It functions in water retention.
5. It is essential for protein biosynthesis by ribosomes.
6. The glycolytic enzyme pyruvate kinase requires K+ for maximal activity.
Sources:
High content of potassium is found in chicken, beef, liver, bananas, orange juice, pineapple, yam, potatoes etc.
Distribution:
Plasma — 20 mg/100 ml
Cells — 440 mg/100 gm.
Muscles — 250-400 mg/100g
Nerves — 530 mg/100g.
Daily requirement:
Normal intake of K+ in food is about 4 gm. It is so widely distributed that its deficiency is rare except in pathological condition.
Blood potassium:
Normal level of serum K is 14-20 mg/100 ml. Erythrocytes contain large amounts of K which avoids hemolysis. Serum K decreases during increased carbohydrate utilization following glucose or insulin administration. Aldosterone decreases serum K.
Absorption:
Normally, K is practically completely absorbed from gastrointestinal tract and less than 10% of K is eliminated in the feces. In subjects with diarrhea large amounts are lost in feces.
Excretion:
K is normally eliminated almost entirely in urine and a small amount in the feces. Aldosterone exerts an influence on potassium excretion. In normal kidney function; K is very promptly and efficiently removed from the blood.
Disease state:
1. K is not only filtered by the kidney but is also secreted by the renal tubules. Excretion of K is greatly influenced by changes in acid-base balance and also by adrenal cortex. The capacity of kidney to excrete K is very great and therefore hyperkalaemia does not occur even after ingestion of K, if kidney function is impaired K should not be given intravenously unless, circulatory collapse and dehydration are corrected.
2. Hyperkalaemia occurs in patients in the following conditions.
(a) Renal failure
(b) Severe dehydration
(c) Addison’s disease due to decreased excretion of K by the kidney
K deficiency occurs in chronic wasting diseases like malnutrition, prolonged negative nitrogen balance, gastrointestinal losses and metabolic alkalosis.
Chlorine:
Physiological functions:
1. As a component of sodium chloride, chloride ion is essential in acid-base balance.
2. As Cl– it is also essential in water balance and osmotic pressure regulation.
3. It is also important in the production of HCl in the gastric juice.
4. Cl– ion is an activator of amylase.
Sources:
Mainly as NaCl salt (table salt).
Distribution:
Plasma — 365 mg/100ml
Cells — 190 mg/ 100mg
CSF — 440 mg/100ml
Muscle — 40 mg/100g
Nerve — 171 mg/100g
Daily requirement:
5-20 gms. Excess consumption of NaCl increases blood pressure in hypertensive patients. Causes edema in protein deficiency.
Absorption:
Normally CI is practically completely absorbed from the GI tract.
Excretion:
CI is chiefly eliminated in the urine, also in sweat. Its concentration in sweat is increased in hot climates and decreased by aldosterone.
Diseases state:
1. CI deficit also occurs when losses of Na are excessive in diarrhoea, sweating and certain endocrine disturbances.
2. Loss of CI due to loss of gastric juice by vomiting or pyloric or duodenal obstruction.
3. Hypochloremia alkalosis may develop in Cushing’s syndrome or after administration of ACTH or cortisone.
Sulphur:
Sources:
Sulphur is taken mainly as cysteine and methionine present in proteins. Other compounds in the diet contribute small amounts of sulphur.
Absorption:
Inorganic sulphate is absorbed as such from intestine into the portal circulation. Small amount of sulphide may be formed in the bowel by the action of bacteria, but if absorbed into the blood stream, it is rapidly oxidized to sulphate.
Sulphur in blood (serum):
Inorganic — 0.5-1.1 mg/100 ml
Ethereal sulphate — 0.1-1.0 mg/100 ml
Neutral sulphur — 1.7-3.5 mg/100 ml
Physiological functions:
1. Sulphur is present primarily in the cell protein in the form of cysteine and methionine.
2. Cysteine plays important part in the protein structure and enzyme activity.
3. Methionine is the principal methyl group donor in the body. The ‘activated’ form of methionine, s-adenosyl methionine is the precursor in the synthesis of a large number of methylated compounds which are involved in intermediary metabolism and detoxification mechanism.
4. Sulphur is a constituent of coenzyme A and lipoic acid which are utilized in the synthesis of acetyl-CoA, malonyl CoA, Acyl-CoA and S-acetyl lipoate (involved in fatty acid oxidation and synthesis).
5. It is a component of a number of other organic compounds such as heparin, glutathione, thiamine, pantothenic acid, biotin, ergothionine, taurocholic acids, sulphocyamides, indoxyl sulphate, chondroitin sulphate, insulin, penicillin, anterior pituitary hormones and melanin.
Excretion:
Excreted in urine in 3 forms. Total sulphate excretion may be diminished in renal function impairment and is increased in condition accompanied by excessive tissue breakdown as in high fever and increased metabolism.
Disease state:
Serum sulphate is increased in renal function impairment, pyloric and intestinal obstruction and leukemia.
Marked sulphate retention in advanced glomerulo-nephritis causes the development of acidosis.
Increase in blood indica (indoxyl potassium sulphate) may occur in uremia.
Iron:
Iron is present in all organisms and in all the cells. It does not exist in the free state, instead is always present in organic combination, usually with proteins. It exists in two forms i.e. Fe2+ (ferrous) and Fe3+ (ferric). It serves as an oxygen and electron carrier and is incorporated into redox enzymes and substances which carry out the function of oxygen transport such as haemoglobin and cytochromes.
Total iron content in normal adult is 4 to 5 grams. 60-70% is present in hemoglobin, 3% in myoglobin and 0.1% in plasma combined with β-globulin transport protein transferrin. Hemoprotein and flavoprotein make up to less than 1% of total iron. Rest is stored as ferritin.
Source:
Rich – Liver, heart, kidney, spleen.
Good – Egg yolk, fish, nuts, dates, beans, spinach, molasses, apples, bananas, etc.
Poor — Milk, wheat flour, polished rice, potatoes etc.
Daily requirement:
Only about 10% of ingested iron is absorbed.
i. Infants – 10-15 mg..
ii. Children – 1-3 years 15 mg.
iii. 4-10 years – 10 mg.
iv. Older children and adults of 11 to 18 years — 18 mg.
v. 19 years and above — 10 mg.
vi. Females between 11 and 50 years of age and during pregnancy or lactation – 18 mg.
vii. After 51 years of age — 10 mg.
viii. In adult women the average loss of iron with blood during menstrual period is 16-32 mg per month or an additional loss of 0.5 to 1.0 mg per day. This amount is easily obtained from diet.
ix. In excessive menstrual blood loss and in chronic iron-deficiency anemia, a supplement of 100 mg of iron per day is sufficient to replenish.
x. During growth, pregnancy and lactation iron demand is more.
xi. In healthy adult male or post menopause women dietary iron requirement is negligible unless any deficiency or loss of iron occurs.
xii. Iron deficiency occurs as a result of malabsorption from gastro-intestinal tract.
xiii. A defect in hemoglobin synthesis in anemia is commonly found in copper deficiency.
Biologically active compounds that contain iron:
1. Haemic compounds:
In these compounds the protoporphyrin is combined with iron to form haem (divalent iron) and haematin.
Ex. Hemoglobin, myoglobin, cytochromes, catalases and peroxidases.
2. Non-haemic compounds:
These include Transferrin (siderophilin) to transport iron, ferritin and haemosiderin which are the stored forms of iron and miscellaneous compounds like enzymes.
Absorption:
Very little (less than 10%) of dietary iron is absorbed. Excretion in the urine is minimal. Infants and children absorb more iron as compared to adults. Iron deficiency in infants is due to dietary deficiency. Iron deficient children absorb approximately twice as much as normal children do. Absorption mainly occurs in the duodenum and the proximal jejunum.
(a) Most of the iron in food occurs in the ferric form (Fe3+), ex. either as ferric hydroxide or as ferric organic compounds. Acidic pH of the gastrointestinal tract favours the absorption whereas alkaline pH decreases it. In an acid medium, these compounds are broken down into free ferric ions or loosely bound organic iron, reducing substances such as —SH groups ex. cysteine and ascorbic acid which convert ferric iron into the reduced (ferrous) state, in this form iron is more soluble and should therefore be more readily absorbed.
(b) A diet high in phosphate, phytic acid and oxalic acid decreases iron absorption since these substances form the insoluble compounds with iron. Conversely, a diet very low in phosphate markedly increases iron absorption.
(c) The extent of absorption depends on the degree of saturation of the tissue, ex. anemic individuals absorb more than normal individuals.
(d) Iron absorption is enhanced by protein, possibly as a result of the formation of low molecular weight digestive products (peptides, amino acids) which can form soluble iron chelates.
(e) It is also increased in pernicious anaemia and in hypo plastic anaemia.
(f) Impaired absorption takes place in patients who have total removal of stomach or a removal of considerable amount of the intestine.
(g) Achlorhydria, administration of alkali, copper deficiency decrease iron absorption.
(h) Alcohol ingestion favours iron absorption.
Mechanism of Iron Absorption:
Ferrous ion on entering the mucosal cells is oxidized to ferric state and then combines with apoferritin forming ferritin which contains 23% of iron by weight. When apoferritin gets saturated with iron no further iron can be taken up by the mucosal cells to store it in the form of ferritin. Heme enters the mucosal cells without being released from the porphyrin ring. Heme is broken down in the mucosa and iron appears in the plasma transferrin.
Transport:
In the plasma, the iron is bound to transferrin which is only partially saturated. Plasma iron is also in exchange with interstitial and intra-cellular compartments. The iron in these compartments is generally referred to as ‘labile iron pool’ and is estimated to be in the order of 80 to 90 mg. Here the iron may stay briefly on the cell membrane before its incorporation into haem or storage compounds. Nearly all the iron released from the mucosal cell enter the portal blood mostly in the ferrous state (Fe2+). In the plasma, Fe2+ is oxidized rapidly to the ferric state (Fe3+) and then incorporated into a specific protein.
Storage:
Stores of iron are maintained chiefly in the liver, spleen and bone marrow in the form of ferritin and haemosiderin. Women have lower stores than men and therefore, develop anaemia much more frequently than men. Iron stores are increased in haemochromatosis, severe haemolytic anaemias, aplastic anaemia and in persons receiving multiple blood transfusions, prolonged oral or parenteral iron therapy.
The normal content of protein bound iron (FBI) in plasma of males is 120-140 jig/100 ml; in females it is 90-120 pg/100ml. However, the total iron binding capacity (TIBC) is about the same in both sexes i.e. 300-360 pg/100 ml.
Excretion:
Physiological excretion of iron is minimal. The normal routes of excretion are urine, bile, faeces, cellular desquamation, and sweat. Daily excretion in an adult male is estimated to be about 1 mg. In women of reproductive age, additional loss through menstruation averages to 1 mg per day.
Abnormal iron metabolism:
Ferritin and hemosiderin, the storage forms of iron act as internal iron reserve to protect against sudden loss of iron by bleeding. Ferritin is present not only in the intestine but also in liver (about 700 mg) spleen and bone marrow. If excess iron is administered parenterally exceeding the capacity of the body to store it as ferritin, it accumulates in the liver as hemosiderin, a form of colloidal iron oxide in association with protein.
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-combining pigments in the tissues.
Physiological functions:
1. Iron functions mainly in the transport of oxygen to the tissues.
2. Involved in the process of cellular respiration.
3. Essential component of hemoglobin, myoglobin, cytochromes and the respiratory enzyme systems (cytochrome oxidase, catalase and peroxidase).
4. Non-heme iron is completely protein-bound (storage and transport).
5. Non-heme iron is utilized in the structure of xanthine dehydrogenase (xanthine oxidase) and succinate dehydrogenase and also in the iron sulphur proteins of the respiratory chain.
Iron deficiency:
Iron deficiency is the commonest cause of nutritional anaemia and is prevalent all over the world. Causes of iron deficiency:
(1) Dietary deficiency:
The iron content in the diet is sufficient to meet the daily requirements, but excessive amount of phytates in cereals, is responsible for non-absorbability of this iron. Hence higher daily intake of iron is recommended for vegetarians.
(2) Lack of absorption:
This may be seen in malabsorptive syndromes.
(3) Increased demand:
This occurs during rapid growth in infancy and pregnancy.
(4) Poor stores at birth:
These are found in premature birth and twin pregnancy.
(5) Pathological blood loss:
With loss of 1g of haemoglobin 3.4 mg of iron is lost. Hook-worm infestation is the most important factor responsible for blood loss. Other sources of blood loss are bleeding piles, peptic ulcer, hiatus hernia, cancer of gastrointestinal tract, chronic aspirin ingestion, and oesophageal varies.
(6) Iron deficiency anemia:
Iron deficiency anemia is widely prevalent among children, adolescent girls and nursing mothers. The hemoglobin content of the blood during iron deficiency anemia is 5 to 9 g/100 ml.
(a) Women of child bearing age:
The clinical symptoms are breathlessness on exertion, giddiness and pallor of the skin. In severe cases, there may be edema of the ankles.
(b) Weaned infants and young children:
The hemoglobin level is 5 to 9 g/100 ml of blood. The children are dull and inactive and show pallor of the skin. The appetite is poor and growth and development are retarded.
Treatment of iron deficiency anaemia:
Anaemia responds to oral iron therapy. The commonly used preparations are ferrous sulphate, ferrous fumarate and ferrous gluconate. Iron dextran can be administered both intramuscularly and intravenously, iron sorbitex is given intramuscularly, and saccharide iron oxide is given intravenously.
Anemic women should take ferrous sulphate tablet. For a child 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 for curing.
Iron overload:
Hypersiderosis may occur as a primary disorder (Idiopathic haemochromatosis) or secondary with excessive entry of exogenous, iron into the body.
1. 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 various tissues, mainly in the liver. This may occur due to repeated blood transfusions, excessive breakdown of erythrocytes in hemolytic types of anemia and inadequate synthesis of hemoglobin as in pernicious anemia.
2. Nutritional siderosis:
This 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.
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 pigment respectively.
Copper:
Source:
Richest sources:
Liver, kidney, other meats, shell fish, nuts and dried legumes.
Poor sources:
Milk and milk products. The concentration of copper in the fetal liver is 5-10 times higher than that in liver of an adult.
Daily requirements:
Infants and children – 0.05 mg/kg body weight
Adults – 2.5 mg
A nutritional deficiency of copper has never been demonstrated in man, although it has been suspected in case of nephrosis.
Absorption:
About 30% of the normal daily diet of copper is absorbed in the duodenum.
Blood copper:
The normal concentration of copper in serum is 90 µg/100 ml. Both RBC and serum contain copper. 80% of RBC copper is present as superoxide dismutase (erythrocuperin), Plasma copper occurs as firmly bound form and loosely bound forms. The firmly bound copper consists of ceruloplas-min. Loosely bound copper is called ‘directly reacting copper’ and is bound to serum albumin. The plasma copper levels increase in pregnancy because of their estrogen content. Oral contraceptives have a similar effect.
Physiological functions:
1. It has important role in hemoglobin synthesis.
2. It is required for melanin formation, phospholipids synthesis and collagen synthesis.
3. It has a role in bone formation and in maintenance of the integrity of myelin sheath.
4. It is a constituent of several enzymes such as tyrosinase, cytochrome oxidase, ascorbic acid oxidase, uricase, ferroxidase I (ceruloplasmin), ferroxidase II, superoxide dismutase, amino oxidase and dopamine hydroxylase.
5. Three copper containing proteins namely cerebrocuperin, erythrocuperin and hepatocuperin are present in brain, RBC and liver respectively.
Excretion:
Only 10 to 60 mg of copper is excreted in the urine. 0.5 to 1.3 mg is excreted through bile and 0.1 to 0.3 mg is excreted by intestinal mucosa into the bowel lumen.
Effects of copper deficiency:
1. Although iron absorption is not disturbed but the release of iron into the plasma is prevented due to the decreased synthesis of ceruloplasmin. As a result, hypoferremia occurs which leads to the depressed synthesis of heme developing anemia in severe deficiency of copper.
2. The experimental animals on a copper deficient diet lose weight and die.
3. In copper deficient lambs, low cytochrome oxidase activity results in neonatal ataxia.
4. Copper deficiency produces marked skeletal changes, osteoporosis and spontaneous fractures.
5. 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.
6. Copper deficiency results in 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 (hepatoreticular 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 percent); whereas 2 to 5 percent 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 transported 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.
Iodine:
Source:
Rich sources are sea water, marine vegetation and vegetables as well as fruits grown on the sea board. Plants 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 concentrations of 1:5000 to 1:200000.
Daily requirement:
Adults – 100 to 150 μg
In adolescence and in pregnancy – 200 μg
Distribution:
Normal iodine content of body is 10 to 20 mg. 70 to 80% of this is present in thyroid gland. Muscles contain large amount of iodine. The concentration of iodine in the salivary glands, ovaries, pituitary gland, brain and bile is greater than that in muscle. Iodine in saliva is inorganic iodide, while most of the iodine present in tissue is in the organic form.
Blood Iodine:
Practically all the iodine in the blood is in the plasma. The normal concentration in plasma or serum is 4 to 10 μg/100 ml. 0.06 to 0.08 μg/100 ml is in inorganic form, 4 to 8 μg/100 ml is in the organic form bound to protein, precipitated by protein precipitating agents. 90% of the organic form consists of thyroxine and the remainder tri and di-iodothyronine. About 0.05% of thyroxine is in the free state. RBC contains no organic iodine.
Absorption:
Iodine and iodide are absorbed most readily from the small intestine. Organic iodide compounds (di-iodothyronine and thyroxine) are partly absorbed as such and a part is broken down in the stomach and intestines with the formation of iodides. Absorption also takes place from outer mucus membrane and skin.
Storage:
90% of the iodine of the thyroid gland is in organic combination and stored in the follicular colloid as ‘thyroglobulin’ a glycoprotein containing thyroxine, di-iodothyronine and smaller amounts of triiodothyronine.
On demand these substances are mobilized and thyroxine as well as triiodothyronine is passed into the systemic circulation. They undergo metabolic degradation in the liver.
Excretion:
1. Inorganic iodine is mostly excreted by the kidney, liver, skin, lungs and intestine and in milk.
2. About 10% of circulating organic iodine is excreted in feces. This is entirely unabsorbed food iodine.
3. 40 to 80 % is usually excreted in the urine, 20 to 70 μg daily in adults, 20 to 35 μg in children. The urinary elimination is largest when the intake is lowest.
4. Urinary iodine is increased by exercise and other metabolic factors.
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.
Iodine deficiency:
1. In adults the thyroid gland is enlarged producing goiter. If treatment is started very early, the thyroid becomes normal. If treatment is delayed, the enlargement persists.
ADVERTISEMENTS:
2. In children, severe iodine deficiency results in the extreme retardation of growth causing cretinism.
Prevention of goiter:
Goiter can be prevented by the regular use of iodized salt or iodine added to the drinking water.
Goitrogenic substances in foods:
Cabbage, cauliflower and radish contain substance like vinyl-2- thiooxazolidone which makes iodide present in the food unavailable by reacting with it. Such substances are called ‘goitrogenic’ substances.
Selenium:
i. Good dietary sources are kidney cortex, pancreas, pituitary and liver.
ii. It is rapidly absorbed mainly in duodenum.
iii. It is distributed in liver 0.44 μg/gm in skin 0.27 μg/gm and in muscle 0.37 μg/gm.
iv. In the cells it is present as selenocystine nad selenomethionine.
v. Selenium along with Vitamin E plays an important role in tissue respiration.
vi. Selenium is involved in biosynthesis of coenzyme Q (ubiquinone), which is involved in respiratory chain.
vii. Selenium acts as an antioxidant providing protection against peroxidation in tissues and membrane.
viii. It is an essential component of glutathione peroxidase, an enzyme which catalyzes the conversion of reduced glutathione to its oxidized form.
ix. Selenium is excreted in faeces, urine and via exhalation.
x. It causes toxic effect called selenosis.
