minerals
TRANSCRIPT
Seminar on
MINERALS
CONTENTS
Introduction
Mineral:Sources,Dailyrequirement,Metabolism,
Functions and their clinical manifestations.
-Sodium
- Potassium
-Chlorine
-Calcium
-Phosphorus
-Magnesium
-Sulphur
-Iron
-Iodine
-Zinc
-Copper
-Molybdenum
-Fluorine
-Selenium
-Cobalt
-Chromium
-Manganese
Minerals and periodontium
Minerals are inorganic substances that play an important role in a variety of
metabolic reactions, as cofactors. They form one of the essential components
of the diet. They are essentially divided into two major groups:
macronutrients which are required in large amounts such as calcium,
magnesium, sulphur, sodium, potassium and chloride; and micronutrients or
trace elements which are required in very small quantities in the diet.
The micronutrients in the diet.
- Those recognized as essential for human nutrition and for which
sufficient information is available to justify the recommended dietary
allowances (RDA) such as zinc, iodine and iron.
- Those probably essential for human nutrition (known to be essential in
animals, but insufficient information is available regarding humans).
Copper, molybdenum, fluorine, selenium, cobalt, chromium and
manganese are examples of this type.
- Those present in human tissues, but have not yet been proved to be
essential, for example, nickel, silicon, tin and vanadium.
Specialized instruments tike flame photometer and absorption
spectrophotometer need to be used for the detection of minerals.
This seminar describes the sources, recommended daily allowances,
factors affecting the absorption and excretion, transportation, metabolism and
deficiency manifestations of the macro-and microminerals.
I. Sodium :
Sodium is the electrolyte which is found in large amount in
extracellular fluid compartments.
Sources:
Sodium is widely distributed in natural foods.
It is present in table salt.
Large amounts are found in cheese and butter.
Daily requirement:
Adult : 0.5 g
Children : 1g .Serum level 136-146mmol/L
Absorption:
Sodium is absorbed with the help of the sodium pump, involving Na+,
K+- ATPase.
Active absorption of Na+ is often coupled with energy generated by
metabolism of glucose or amino acids.
Functions:
Fluid balance: Maintains osmotic equilibrium.
Acid-base balance. Na+ and H+ exchange occurs in the kidney and is
involved in the maintenance of acid-base balance.
Neurotransmission: Sodium is involved in the maintenance of the
resting membrane potential and also in the propagation of the action
potential.
Role in muscular excitability. Along with other cations such as
potassium, neuromuscular irritability.
Maintenance of viscosity of blood. Sodium and potassium regulate the
degree of hydration of the plasma proteins and maintains the viscosity
of blood.
Excretion:
Sodium is excreted via the kidneys and skin.
Regulation:
Aldosterone, renin-angiotensin system, kinins and prostaglandins
regulate sodium homeostasis.
Clinical manifestations:
Hypernatraemia:
It occurs due to the presence of high amounts of sodium.
It is less common than hyponatraemia.
It could be due to hyperactivity of adrenal cortex (Cushing’s
syndrome), or prolonged administration of corticosteroids.
Hypernatraemia may also be due to an overenthusiastic, intravenous
administration of saline.
Water can be retained along with sodium and the patient may show
puffiness of the face.
Hyponatraemia:
It occurs in the following conditions :
- Gastroenteritis with diarrhoea and vomiting
- Severe burns
- Small gut obstruction
- Addison’s disease
- Use of mercurial diuretics.
II. POTASSIUM :
Potassium is the major intracellular cation. It is widely present in the
body fluids and tissues.
Sources:
It is most widely distributed in vegetables.
Daily requirement:
Adult : 2-4 gms
children : 1-3 gms .Serum level 3.5-5.1mmol/L
Absorption:
Potassium is easily absorbed.
Potassium exhibits a tendency to diffuse against concentration gradient
from the intracellular to the extracellular fluid. The sodium pump
transports potassium into the cells.
Excretion:
It is excreted in the urine. The amount excreted is dependent on the
sodium intake.
It is excreted via the gastrointestinal tract, saliva, pancreatic and
intestinal juices and faeces.
Small amounts are lost via skin as sweat.
Function:
Some of the functions of potassium are same as those of sodium.
Serum potassium concentration does not vary appreciably in response
to water loss or retention.
Cellular uptake of potassium is stimulated by insulin.
Helps in maintaining Acid-base balance. A reciprocal relationship
exists between potassium and hydrogen ions. As acidosis develops,
potassium ions are disposed from the cells in order to maintain
electroneutrality. Thus potassium is involved in acid-base balance.
It is important in cardiac and muscular functions. Too high or too low
concentration of potassium may have life-threatening consequences.
Helps in enzyme action. An enzyme such as pyruvate kinase requires
K+ as a cofactor.
Like sodium, it is also involved in neurotransmitter.
Applied aspects:
Extracellular levels of potassium are measured in serum.
Hemolysis and allowing the serum sample to stand for very long,
produces changes in the potassium values So, the sample should be
analyzed as soon as possible.
Clinical manifestations:
Hyperkalemia:
Causes
-The kidneys may not be able to excrete a potassium load when glomerular
filtrate is low. Acidosis aggravates the problem.
- In addison’s disease and adrenalectomy, high levels of potassium are
observed.
- Potassium is released from damaged cells.
Clinical symptoms :
Muscle weakness
Hyperkalaemia can cause sudden death as cardiac arrest is the first
manifestation. It lowers the resting membrane potential, shortens
cardiac action potential and increases the velocity of repolarization. It is
therefore necessary to be alert.
(a) Management :
Infusion of insulin and glucose.
Infusion of calcium gluconate may also counteract the effect of
hyperkalemia.
Dialysis is sometimes necessary.
Hypokalaemia :
Causes
Gastrointestinal losses, diarrhoea, vomiting or surgical fistula.
Renal diseases, administration of diuretics and increased aldosterone
production.
Administration of diuretics and corticosteroids.
Alkalosis which shifts potassium from the extracellular fluid to the
intracellular fluid
Clinical symptoms :
Neuromuscular weakness and hypotonia
Cardiac arrhythmias, digoxin toxicity and changes in ECG.
Impaired concentrating ability of the kidneys leading to polyuria and
polydypsia.
Metabolic alkalosis
Management :
Oral administration of salts is given in an enteric coating because
potassium salts are unpleasant.
Intravenous potassium can be given.
Applied aspect:
Intravenous potassium should be given slowly and under ECG
monitoring except in extreme cases.
III. CHLORINE :
Chlorine is the principle extracellular anion. Its plasma concentration
tends to follow that of sodium.
Sources:
Chlorine is present in table salt.
Many vegetables and meats contain chloride
Water is also “chlorinated”.
Daily requirements:
Adults : 2-5 gms
Children : 0.5 – 2 gms .Serum level 98-106mmol/L
Absorption:
Occurs in small intestines.
High renal threshold.
Excretion:
Through sweat, faeces and urine.
Regulation:
Chloride levels in plasma are directly proportional to sodium ions,
whereas they are inversely related to the bicarbonate concentrations.
Functions:
Important in gastric juice as part of the gastric hydrochloride.
Involved in the chloride shift. It is involved in the maintenance of
intracellular homeostasis in the RBCs.
Clinical manifestations:
Hyperchloraemia:
It can be caused by chloride gain and vomiting.
- It may be associated with hypematraemia, metabolic alkalosis and
repiratory acidosis.
Hypochloremia:
Metabolic alkalosis which is saline responsive occurs. It occurs during
vomiting, diuretic therapy, injection of alkali and diarrhoea.
Metabolic alkalosis can also be saline nonresponsive. It occurs during
mineralocorticoid excess and severe K+ deficiency.
IV. CALCIUM :
About half of calcium present in blood is in ionized from and the rest,
in unionized from. Some of unionized calcium is bound to protein, and a
small amount is bound to citrate.
Calcium taken in the diet is in the form of calcium phosphate or
carbonate.
Sources:
Milk , eggs, fish, and vegetables,
Cereals (wheat and rice) contain only small amounts of calcium.
Daily requirement:
Adult : 0.5 gms
Pregnancy : 1.5 gms
Children: 1.0 gm .Serum level 2.1-2.6mmol/L.
Absorption:
Takes placed in the first and second part of duodenum against electric
and concentration gradients.
Two mechanisms have been proposed for absorption of calcium. They
are simple diffusion and active transport process involving energy and
the Ca2+pump.
The factor which increases the calcium absorption are vitamin D,
parathyroid hormone, acidity and amino acids such as lysine and
arginine.
The factors which decrease the calcium absorption are phytic acids or
hexaphosphates of inositol present in cereals, oxalates from leafy
vegetables, malabsorption syndrome, and high phosphate content in
foodstuff.
Functions:
Intracellular concentration of calmodulin modulates the intracellular
calcium levels to maintain the various calcium-dependent reactions.
Any excess calcium ions are removed out of the cell via protein.
Calcification of bones and teeth
In addition, it helps in the following biochemical and physiological
activities.
- Blood coagulation. Ionic calcium helps in the production of
thromboplastin and in the conversion of prothrombin into thrombin.
Thus, calcium plays a role in blood coagulation.
- Action of enzymes. Several enzymes including lipase, succinic
dehydrogenase, adenosine triphosphatase and certain proteolytic
enzymes are activated by calcium.
- Muscle contraction. Calcium ions neutralize the negative charge of
myosin which then combines with action, to help contraction. Ca2+ ions
also activate the myosin ATPase which in turn hydrolyzes the ATP to
supply energy required for contraction.
- Neuromuscular excitability. Calcium is essential for excitation of
nerves.
- Hormone action. Ca2+ serves as an intracellular secondary messenger of
different hormones.
- Membrane permeability. Membrane permeability generally is increased
by calcium. This effect balances the opposite action of sodium and
potassium capillary permeability.
Clinical manifestations:
Deficiency of calcium leads to rickets, osteoporosis, and
hyperexcitability.
Hypercalcaemia:
It may occur in the following conditions:
- Hyperparathyroidism
- Multiple myeloma
- Metastatic carcinoma of bone
- Milk-alkali syndrome
- Treatment with drugs such as diuretics
- Hypervitaminosis D
Hypocalcaemia:
It is observed in:
- Tetany
- Hypoparathyroidism
- Fanconi’s syndrome (disorder of tubular reabsorption)
- Acute pancreatitis
- Vitamin D deficiency
- Chronic renal failure.
Applied aspects:
If the level of ionic calcium falls, the nervous system becomes
hyperirritable.
This could lead to tetany. On the other hand, high calcium content
depresses nervous irritability. Thus, the administration of calcium salts is
indicated in the alleviation of tetany.
PHOSPHORUS
Total body phosphate weighs about 1 kg, 80% of which is present in
bone and teeth while 10% is in muscles.
Sources:
Cheese, milk, nuts, eggs, etc.
Daily requirement:
Adults : 500 mg
Pregnant women : 1 gm
Children: 400 –600 mg. Serum level 0.8-5.1mmol/L.
Absorption:
Absorption of phosphate is stimulated by parathormone (PTH) and
vitamin D3. The absorption is mainly from jejunum.
Functions:
Phosphate is an important constituent of bones and teeth.
It is needed for the production of high-energy phosphates such as ATP,
CTP, GTP and creatinine phosphate.
DNA and RNA have phosphate diester linkages that form the backbone
of the structure.
Certain enzymes are activated by phosphorylation
Phospholipids, phosphoproteins, lipoproteins, nucleotides contain
phosphate as one of their components.
Regulation of calcium and phosphorus:
Regulation depends on:
Vitamin D. Intestinal absorption of calcium and phosphorus is
increased by vitamin D. It promotes mineral deposition in bones and
phosphate reabsorption in kidneys.
Calcitonin. It lowers serum calcium and phosphorus. It reduces
mobilization from bones.
PTH increases serum calcium and lowers phosphorus.
Calcium: Phosphorus ratio is important. There is reciprocal relationship
between serum calcium and phosphorus. Rise in calcium or phosphorus
is accompanied by fall in the other ion.
Estrogens and testosterone promote retention and deposition of calcium
in bones.
In women, osteoporosis in which, delayed recovery from fractures are
observed after menopause.
Serum level of phosphate required by adults is 3-4 mg/day, while
normal children require 5-6 mg/day.
Clinical manifestations:
Deficiency of phosphorus results in osteomalacia, renal rickets and
cardiac arrhythmia.
Hyperphosphataemia:
It is observed in:
- Diabetes mellitus, starvation
- Renal insufficiency
- Hypothyroidism
- Hypervitaminosis D
Hypophosphataemia:
It is seen in:
- Rickets
- Fanconi’s syndrome
- Intake of drugs such as antacids
Applied aspects:
The whole blood phosphate is about 40 mg / dl.
RBCs and WBCs contain a lot of phosphate.
Hemolysis should be prevented when blood is taken for phosphate
estimation.
V. MAGNESIUM :
Magnesium is found both in intracellular and extracellular fluids. Total
body magnesium is about 20 g, 75% of which is complexed with calcium in
bone.
Source:
Green vegetables, potatoes, almond, cheese, cereals, beans and almost
all animal tissues.
Daily requirement:
Adults : 350 mg
Pregnant women : 450 mg
Children: 150 mg. Serum level 0.7-1.0mmol/L.
Absorption:
Absorption of magnesium takes place primarily in the small bowel by a
specific carrier mechanism.
Factors which increase the absorption of magnesium are vitamin D,
PTH, high-protein intake, neomycin therapy.
Factors which decrease the absorption are increased calcium intake,
fatty acids, phytates and phosphate.
Functions:
Involved in enzyme action. Magnesium is the cofactor of many
enzymes requiring ATP. Alkaline phosphatase, hexokinase,
fructokinase, adenylate cyclase, cAMP-dependent kinase need
magnesium. Magnesium forms ATP-Mg2+ complexes and binds to the
enzymes.
Required in neuromuscular activity.
An important constituent of bone and teeth
Normal serum blood level is 2-3 mg/ dl (1-1.5mmol/l).
Clinical manifestations:
Deficiency of magnesium causes muscular tremor, confusion,
vasodilation and hyperirritability.
Hypermagnesaemia is observed in:
- Hypothyroidism
- Diabetic mellitus
- Acute renal failure
Hypomagnesaemia is seen in:
- Hyperthyroidism
- Chronic alcoholism
- Malnutrition
- Prolonged use of diuretics
- Portal cirrhosis
Toxicity due to the increased use of magnesium-containing laxatives
and antacids has been reported in the elderly. The chief symptoms are
drowsiness, lethargy and weakness.
VI. SULPHUR
Proteins contain about 1% sulphur by weight. This forms the organic
sources of sulphur in the diet. Sulphates of sodium , potassium and
magnesium are also found in the diet.
Source:
Meal, fish legums, eggs, cereals and cauliflower.
Daily requirement:
Adequate intake of protein fulfills the sulphur requirements.
Absorption:
Sulphur –containing amino acids produce inorganic sulphur.
A part of it is conjugated with phenolic and heterocyclic compounds in
liver to produce ethereal sulphates.
It is secreted in urine as:
- Inorganic sulphur
- Neutral sulphur
- Ethereal sulphur
Intestinal putrefaction causes increased ethereal sulphates.
Excretion:
Sulphate excretion increases when catabolism of tissues protein is increased.
Functions:
Detoxication. Compounds possessing phenolic groups (e.g., phenol,
skatoles, indole) may be detoxicated in liver by conjugation with sulphate
from amino acids. Hydrocarbons are detoxicated by conjugation with
esters of acetylated cysteine.
Enzymes such as papain, urease, cathepsin depend on free sulphahydryl
groups for their catalytic sites.
Nonhaem iron enzymes such as mitochondrial NADH dehydrogenase, Fe-
S proteins contain sulphur.
SAM acts as a coenzyme for methyltransferases
-SH group of glutathione acts as donor of reducing equivalents and enables
it to function as a reducing agent.
-SH group of CoA and acyl carrier protein (ACP) form fatty acid
thioesters. They participate in the transfer of fatty acyl groups.
Methionine + ATP Methyladenosyl Transferase (liver) PPi +Pi + SAM
Adenosine 3’-P-5’ sulphate (PAPS) is formed in the liver from ATP and
sulphate with the help of ATP sulphurase and adenosine 5’ –sulphate-
3’kinase. The sulphate group of “active” sulphate is transferred to other
substrates like chondroitin.
“Active sulphates” viz., PAPS, SAM, CoA CAP – are high-energy sulphur
compounds.
Sulphur-containing vitamins are biotin and thiamine (coenzymes).
Protein-structure. SH of cysteine forms intrachain and interchain S-S
linkages contributing to secondary, tertiary and quaternary structures.
Sulphate mucopolysaccharides and sulphalipids. Hexosamine gets
sulphated endowing the molecules with negative charges.
Applied aspects:
Role of sulphur :
- Curing skin disorders
- As a component of sulphur drugs
VII. IRON :
Iron is present in all organisms and in all cells. It is a transient metal
capable of being present in Fe2+ (ferrous) and Fe3+ (ferric) forms. Iron is
essential for the formation of haemoglobin in RBCs, transport of oxygen and
oxido-reduction reactions of the electron transport chain.
Sources:
Food iron can be classified as haem iron and nonhaem iron (iron-
porphyrin complexes are referred to haem compounds while nonhaem iron
refers to substances which have iron in the prosthetic group but no porphyrin).
Haeme iron in the body is constituted by Hb (85%), Mb (5%) and
heame enzymes (10%) such as cytochromes, cytochrome oxidase and
peroxidase. 40% of total food iron is heame iron. It is obtained from
organ meats, fish etc.
Nonhaeme iron is present in Fe-S proteins such as ferredoxin,
adrenodoxin, flavoproteins, succinate dehydrogenase transferrin,
ferritin, haemosiderin. The food sources of nonhaeme protein are
vegetables, fruits, legumes and nuts 60% of total food iron is
nonhaeme iron.
Daily requirement:
- Adult man and postmenopausal women : 10 mg.
- Premenopausal women : 15-20 mg.
- Pregnant women: 30-60 mg.Serum level 11-32umol/L.
- 1 g of haemoglobin contains –3.4 mg iron.
- - 30 mg iron loss occurs in menstruation.
Absorption:
Mainly occurs in gastrointestinal mucosal cells.
Vit.C, calcium, gastric HCL, tissue needs have positive influence.
Tissue saturation, high pH, high phosphates, phytates and oxalates have
negative influence.
Haem iron:
- Generally, haeme iron is in combination with globin.
- Proteolytic enzymes release the globin part.
- Haeme iron enters the mucosal cells. it is transferred via transferrin.
Nonhaeme iron:
- Haeme uptake is enhanced by vitamin C, succinic acid, sugars, sulphur
containing amino acids and increased calcium levels. Calcium chelates
with phytates.
- Phosphates, phytates, tannic acid found in tea and antacid preparations
inhibit absorption.
Absorption of iron takes place largely in the upper part of the small
intestine.
- Most foods contain iron in the ferric state.
- The acid medium frees the bound iron.
- Reducing substances such as vitamin C, glutathione help to convert
ferric iron to ferrous iron, this is then absorbed.
- Ferrous iron forms chelates with vitamin C, amino acids and sugars.
- These chelates remain soluble in the jejunum and duodenum.
- Absorption occurs by passive diffusion.
- The iron combines with apoferritin of form ferritin.
Conservation of iron:
- Body reutilizes iron to compensate for the low capability of iron
absorption.
- Iron is called a “one way” substance. Only 10% is absorbed but once
absorbed, little is excreted.
Applied aspects:
- In pregnancy, more iron is needed. Milk contains low amounts of iron.
- Foetus uses maternal iron. Approximately 600 mg is transferred to the
foetus.
- Foetal Hb levels are 22-23 mg/dl.
Storage and transport forms of iron:
- Ferritin is made up of a protein part (apoferritin) and iron. 4300 iron
atoms are present in one molecule of apoferritin.
- Haemosiderin is the form of brownish granules, which are large
aggregates of ferritin molecules. Iron content is high. Increased levels
cause haemosiderosis.
- Both these molecules are storage forms of iron.
- The following are transport forms of iron.
Lactoferrin is present in milk, tears, cervical mucous, seminal plasma,
bile, saliva.
- Transferrin binds two atoms of Fe3+ iron.
Transferring plays a dual role-
Accepts iron from Delivers iron to
a) Intestinal tract a) Bone for synthesis of Hb
b) Sites of storage b) Reticulo-endothelial system for storage
c) Hb destruction c) Placenta
b) Cells containing enzymes.
Excretion of iron:
- Faeces.
- Desquamation of skin increases iron loss with sweating.
- Urinary loss is negligible.
- Menstrual loss is large.
- In pregnancy, iron is transferred to the foetus.
- In lactation, 1.5 mg/day of iron is lost.
Clinical manifestations:
- Increased amounts of iron are excreted in haematuria and
haemoglobinuria.
- Iron deficiency leads to low plasma bound protein, increase in total iron
binding capacity (TIBC) and decrease in iron and Hb levels.
- In women, there is poor intake and absorption of iron. There is loss
during menstruation, sometimes due to multiple pregnancies.
Anaemia:
It can be classified as follows:
- Dyshaemopoietic. Insufficient blood formed due to inadequate intake,
absorption and utilization of iron. Factors required in adequate amounts
are:
Minerals – iron, traces of cobalt and copper.
Proteins.
Vitamin, B12, vitamin C and folic acid.
- Haemorrhagic. Occurs due to blood loss caused by piles, ulcers,
bleeding and anti-inflammatory drugs.
- Haemolytic. Occurs due to excessive intravascular blood destruction
caused by red cell destruction and sensitizing of glucose 6-phosphate
dehydrogenase.
- Iron deficiency anaemia. In its severest form, it is characterized by
hypochromic, microcytic red cells. defective synthesis of haem-
complex and iron-containing metalloenzymes is responsible for fatigue
and epithelial changes. It is a public health problem resulting in
substandard performance of millions of people. Causes include :
Poor intake, absorption, loss of iron during menstruation, repeated
pregnancies, prolonged lactation, parasitic infection. Blood donors
may develop iron deficiency.
Diseases of bone marrow diminish RBC production, e.g., ionizing
radiation, “crowding out” of red cell precursors. This condition
occurs in leukemia, multiple myeloma and Hodgkin’s disease.
- Treatment of iron deficiency anemia includes fortified food, doses of
ferrous sulphate, Fe2+ gluconate and rarely intramuscular injections.
Iron excess or overload:
- Idiopathic hemochromatosis, a genetically determined disease, is
caused by increased iron absorption over years.
- In Bantu tribes, haemosiderosis occurs.
- Thalassemia patients receiving repeated blood transfusion and have
defective Hb show accumulation of iron.
- Refractory anaemia occurs due to high-iron diet intake. Interestingly,
patients with iron overload can trigger and alarm at the airport when
they go through metal detector.
- In treatment, iron chelating agent, viz., desferrioxamine is used.
Bronze diabetes:
- It is a disease that leads to :
Increased deposits of haemosiderin.
Degeneration of cardiac muscle, congestive heart failure and
hepatic fibrosis. Pancreatic damage results in diabetes mellitus.
Iron toxicity:
- Results in hepatic failure, diabetes, testicular atrophy, arthritis,
cardiomyopathy, peripheral neuropathy and hyperpigmentation.
- The following are the laboratory tests for assessing patients with iron
disorders :
RBC count and estimation of Hb.
Determination of plasma iron, TIBC and percentage of transferrin.
Ferritin by RIA.
Prussian blue stain of tissue.
Amount of iron (mg/dl) in tissue biopsy.
VIII. Iodine :
It is an essential component of thyroid hormones (T3 and T4).
Sources:
- Iodized table salts, flesh and oil of marine fish, onion, iodate-enriched
bread.
Daily requirement:
- Adult man: 140mg; adult women: 100mg.
- Adolescent boy: 150mg; adolescent girl: mg.
- Pregnant woman: 125mg; lactating woman: 150mg.
- Children: 60-100mg.
Incorporation of iodine:
- Concentration of iodine occurs in the thyroid follicle actively, with the
help of a NA + K+- ATPase pump.
- This iodide (I-) is then oxidized to iodine (I+) with the help of
peroxidase.
- Iodination of the tyrosine residues of the protein thyroglobulin now
occurs.
- Thyroglobulin, a glycoprotein, contains approximately 5000 amino
acids. 115 tyrosine residues present.
Absorption and metabolism:
- Free iodine and inorganic iodate are first converted to iodide which are
easily absorbed from gastrointestinal tract.
- Iodides can also be absorbed from mucous membrane, lungs and skin.
- Thyroid hormones, i.e., triiodothyronine (T3) and tetraiodothyronine
(T4) are iodinated derivatives of the amino acid, thyronine.
- In the thyroid gland, iodine is taken up by the active transport and
oxidized to active iodine.
- The active iodine is then utilized to iodinate tyrosine to form
iodotyrosine.
- Iodotyrosine residues are then coupled to form T3 and T4.
Functions of iodine:
- Iodine is required for the synthesis of hormones, T3 and T4. Iodine acts
only when it is synthesized and it carries out the following functions :
Increases metabolism and oxygen consumption of tissues. Increases
basal metabolic rate.
Increases conversion of glycogen to glucose leading to increase in
blood sugar level.
Increases heart rate.
Depletes calcium and phosphorus of bones and increases urinary
calcium excretion.
Excretion:
- Liver, kidneys, muscles and heart deaminate iodothyronine to
iodothyropyruvate. This is then decarboxylated to iodothyroacetate.
Deiodination occurs in peripheral tissues.
- Detoxication is carried out by methylation or conjugation with
glucuronic and sulphuric acids excreted in bile and urine.
Circulation of T3 and T4:
Iodine deficiency:
- It leads to still births, abortions, congenital heart anomalies, endemic
cretinism, mental retardation and neurological defects. Treatment of
iodine deficiency before pregnancy prevents disorders in children.
Applied aspects:
- Goitre is the enlargement of thyroid gland. There are normal, hypo and
hyperthyroid states. Simple goitre results in decreased thyroxine
production. It occurs due to defect in the steps for production of thyroid
hormones.
- Simple endemic goitre occurs due to inadequate supply of iodine,
hypothyroidism and myxoedema in adults.
- Myxoedema is due to hypothyrodisim in adults. Basal metabolic rate
and body temperature are lowered and memory is poor in this disease.
- Cretinism is due to incomplete development or congenital absence of
thyroid gland. It is evident in children. Children are dwarfed, mentally
retarded and have protruding tongue and pot bellies.
Hyperthyroidism:
- Expoththalmus, enlarged and hyperactive thyroid.
- Grave’s disease results from increased production of thyroid
stimulating immunoglobin (TSI) that activates TSH receptor, LATS
(long-acting thyroid stimulating factor).
- Hahimoto’s disease. Occurs due to destruction of thyroid tissues,
effects of antithyroid antibiotics, overproduction of TSH and
hyperthyroidism.
Applied aspects:
- Antithyroid substances such as cabbages, turnip, soyabean cause
simple goitre. Goitrogenic substances contain L-5-viny-2-
thiooxazolidone.
- Radioiodine studies. radioiodine uptake studies are undertaken to
determine the overall activity of the gland, particularly in
hyperthyroidism. Trace doses of I125 or I131 are administered orally and
percentage of iodine taken up by thyroid gland is measured by counting
a-rays at standard time intervals.
- In patients with Grave’s disease, thyroid uptake is measured before and
after an 8-day course of iodinated T3 administration. No decline in
uptake is observed.
IX. Zinc :
The total content of zinc in the body is about 2.3 g of which 80-110
mg/dl is found in the plasma. High concentrations of zinc are found in
choroid of eyes, prostate, kidneys, liver and muscles.
Daily requirement:
- Pregnancy: 5mg.
- Lactation: 10mg.Serumlevel 11-24umol/L.
Sources:
- Meat, liver, seafood, eggs, vegetable and whole gram (less available
due to phytates).
Absorption:
- Zinc absorption is proportional to the protein (metallothionein) level in
intestinal muscosal cells. metallothionenin serves as a carrier for zinc
also.
- This absorption is interfered by copper, phosphate, phytate and
calcium.
Excretion:
- Occurs through faeces and urine (in traces) and some amount in sweat.
Functions:
- Over three hundred zinc-containing enzymes have been identified, e.g.,
LD, carbonic anyhydrase, alkaline phosphatase, carboxypeptidase.
- Zinc is also present in cytosolic superoxide dismutase. It also contains
copper. The mitochondrial superoxide dismutase contains manganese.
- It is involved in the synthesis of DNA and proteins.
- Zinc forms an essential and integral part of insulin during storage in b-
islet cells. Once released, it need not bind to zinc. Long-acting insulin
preparations are in the form of protamine-zinc-insulin.
- Zinc stimulates vitamin A release from liver and blood.
- Zinc protein, “gustin” is present in saliva and it plays an important role
in the sense of taste.
- Zinc is involved in wound healing.
Clinical manifestations:
- Decreased levels are seen in acute and chronic infection, myocardial
infarction, malignancies, patients with alcoholism liver disease and
malabsorption.
- Acrodermatitis enterohepatica is a rare inherited disorder due to a
defect in zinc absorption.
- Inherited zinc deficiency is associated with dermatologic,
ophthalmologic and intestine disturbances, hypogonadism, growth
retaradation and decreased size of male gonads.
- Zinc supplements can cure the deficiency.
- Zinc is relatively nontoxic.
- Inhalation of zinc oxide (ZnO) leads to acute illness and headache.
Poisoning due to ingestion from containers causes nausea and fever.
X. Copper :
The normal concentration of copper in serum is 90mg/dl. Copper is
transported in the bound form as ceruloplasmin. It is stored in liver, muscles
and bones of the body. Copper is present in a number of metalloenymes.
Daily requirement:
- Adults : 2mg.Serum level 11-20umol/L
Sources:
- Nuts, dried fruits, pulses, meats, fruits’ oysters and fish.
Functions:
- Copper is present in oxidases. Eleven such enzymes are identified, e.g.,
cytochrome oxidases, superoxide dismutase.
- Required for biosynthesis of haemoglobin. Utilization of iron for
haemoglobin synthesis is enhanced by ceruloplasmin which is a blue
copper protein complex that catalyzes Fe2+®Fe3+.
- Deficiency of copper leads to microcytic anaemia.
- Required for bone formation and maintenance of myelin.
- Plays role in lipid and amino acid metabolism.
- Copper-containing proteins are:
Ceruloplasmin.
Erythrocuprin.
Cytochrome oxidase.
Monoamine oxidase.
Melanin.
Absorption:
- Cu2+ is insoluble at intestinal pH.
- It gets bound to a protein (metallothionein) and gets absorbed from
intestional mucosal cells and stomach.
- Leucine enhances absorption of copper.
- Once absorbed, copper gets bound to albumin.
Excretion:
- It is excreted in bile, urine and sweat.
Clinical manifestations:
Wilson’s disease or hepatocellular degeneration:
- Caused by a defect in transporting the absorbed copper across the
serosal membrane of intestinal mucosal cells.
- Pathological changes include demyelination, degeneration and
cavitation of the basal ganglion in the brain and cirrhosis of the liver.
Personality changes, tremors and hepatic failure occur.
- Low plasma and high urinary levels, high deposition of copper and low
ceruloplasmin.
- Abnormal muscular movements, diabetes mellitus, renal tubular
damage, visible brown rings (Kayser-Fleischer ring) at the margin of
cornea, dementia and jaundice.
- The patient dies of hepatic failure.
- Copper-chelating agents are used to treat the disease, e.g.,
pencillamine.
Menke’s kinky hair syndrome:
- It is a genetic disorder.
- Occurs due to deficiency in copper absorption.
- Symptoms are kinky hair, pale skin, depigmented hair, low body
temperature and demineralization of the bone. Mental retardation
occurs.
Toxicity:
- Toxicity of copper results in nausea, vomiting, headache, dizziness,
hypertension and death. Copper toxicity also hepatic cirrhosis, tremor,
mental deterioration, Kayser-Fleischer rings, heaemolytic anaemia and
renal dysfunction (Fanconi-like syndrome).
XI. Molybdenum :
Though a deficiency of molybdenum has not been observed in man, it
is an essential constituent of many enzymes.
Sources:
- Milk, beans, breads, cereals, liver and kidney.
Daily requirement:
- Adults: 0.15-0.5 mg.
Absorption:
- Readily absorbed. Excreted in urine and bile.
Functions:
- Involved in uric acid metabolism.
- Involved in enzymatic action.
Occurs in several metalloflavoproteins containing nonhaeme iron, e.g.,
aldhehyde dehydrogenase, xanthine oxidase.
Molybdenum-containing enzymes participate in electron transfer.
Traces of molybdenum help in utilization of copper while larger
amount diminish the same.
Toxicity:
- Increased molybdenum may produce microcytic anaemia, and low
levels of tissue copper.
II. Fluorine :
10-20 mg of fluorine in its ionized form is present in the blood.
Although not strictly essential, fluoride enhances well being. Fluoride is
found in the bones and teeth.
Sources:
- Drinking water, tea, salmon and sardine.
Requirement:
- 1-2ppm (since fluorine is absorbed through water it is expressed as
ppm).
Absorption and excretion:
- Easily absorbed from small intestine.
- More than half of the ingested fluoride is excreted through urine and
the rest is deposited in bones, where there is accumulation with age.
Functions:
- Tooth development and dental health.
Fluorine is required in traces for development of teeth.
Helps in prevention of dental caries.
Large amounts causes fluorosis involving mottling of the enamel. In
these conditions, enamel is stratified and it has dull white patches.
Tooth shows brown stains and pits.
- Bone development
Promotes bone development.
Increases calcium and phosphate retention and prevents old-age
osteoporosis.
Increased uptake enhances osteoblastic activity, calcium deposition
and density of bones.
Fluoride is an inhibitor of enolase, blocking this enzyme inhibits
glycolysis.
III. Selenium :
About 5-15mg of selenium is found in the body. Selenium serves to
protect cells against destruction.
Sources:
- Present in liver, kidney, seafood, meats and grains.
Daily requirement:
- Adult man/woman: 0.2 mg.
- Infants and children: 0.02-0.1 mg.
Functions:
- It is an integral part of enzymes, glutathione peroxidase, which has the
following functions :
Protects vital cell components, such as cell membranes from dangers
of hydrogen peroxide and other peroxides.
Supplements the action of superoxide dismutase in protecting cells
against superoxide (O2-) and other free radicals.
- Selenium spares vitamin E requirement in three ways :
Normal pancreatic function and thereby digestion and absorption of
lipids including vitamin E.
Component of glutathione peroxidase.
Aids retention of vitamin E in blood.
Toxicity:
- Humans living in selenium-rich soil zones are prone to its toxicity.
- Excess of selenium in cattle causes alkali disease, liver necrosis and
muscular dystrophy.
Deficiency symptoms:
- Cardiac dilation, abnormal ECG, congestive heart failure.
- An endemic disease, seen in children due to low selenium content is
called Keshan disease.
XVI. Cobalt:
Cobalt is a constituent of vitamin B12. The total body content of cobalt
is 1.1 mg. It is readily absorbed from the small intestine.
Daily requirement:
- Though the average intake of cobalt is 0.3 mg per day, the daily
requirement has not yet been established.
Sources:
Figs, cabbage, lettuce, spinach and animal products such as liver and
kidneys.
Functions:
- It is a component of vitamin B12 which contains 4% of the element. It is
necessary for Hb formation. It plays an analogous role to copper in
ferroxidase and iron in Hb.
- Cobalt may substitute for manganese as an activator of enzymes. It is a
specific activator of the enzyme, glycylglycine dipeptidase. It also
activates enzymes such as phosphotransferases and lyases.
- It causes an increase in the number of RBCs.
- Cobalt induces polycythemia by increasing formation or inhibiting
destruction of erythropoietin, the stimulating hormone secreted by
kidney. This leads to the development of macrocytic anaemia.
Excretion:
- 0.26 mg/day is excreted in urine.
Toxicity:
- Cobalt it added during processing of beer as a foam stabilizer.
Congestive heart failure from cardiomyopathy has been reported in
individuals who have consumed large quantities of beer.
XVII. Chromium:
Chromium exists in two forms, viz, the trivalent and the hexavalent.
The trivalent form is biologically active.
Sources:
- Yeast, milk, meat and cereals.
Daily requirement:
- Adults : 0.05-0.15mg
Absorption:
- It is absorbed by the small intestine.
Excretion:
- Traces are excreted in urine.
Functions:
- Acts as cofactor for insulin.
- Helps to increase not only glucose utilization but also transport of
amino acids.
- Important in lipoprotein metabolism. Small amounts play an important
role in carboydrate and lipid metabolism apparently as a cofactor for
insulin.
- Further classifications of the precise biochemical functions are needed.
Toxicity:
- Excess of chromium (Cr3+) is toxic.
- The hexavalent element is more toxic. Occupational exposure to
chromium dust causes lung cancer. Appreciable amount of chromium
are contributed by cooking in stainless steel containers.
XVIII. Manganese:
The total body content of manganese is about 30 mg.
Daily requirement:
- Adults: 2-5 mg.
- Children: 0.5-2.0 mg.
Sources:
- Cereals, vegetables, liver, kidney, muscle and tea.
Functions:
- Acts as a cofactor for enzymes such as arginase, isocitrate
dehydrogenase, leucine aminopeptidase. Manganese-containing
enzymes are hydrolases, kinases, decarboxylases and transferases. It is
a cofactor for mitochondrial superoxide dismutase.
- Role in animal reproduction. Deficiency causes sterility in animals and
disturbance in citric acid cycle.
- Proteoglycan synthesis. Promotes synthesis and deposition of
proteoglycan in many tissues including bones due to
glycosyltransferase activity.
- Porphyrin synthesis. Some porphyrins of erythrocytes contain
manganese.
- Bone growth and cholesterol synthesis require manganese.
Absorption, transport and excretion:
- Absorbed from gut.
- Miners absorb manganese dust through lungs.
- Transported in combination with b-globulin called transmanganin.
- Stored in liver.
- Little is excreted in urine.
- Excreted mainly through bile and faeces.
Clinical manifestations:
- Deficiency results in the following symptoms :
Defective growth in mammals and birds.
Respiratory dysfunction.
Disturbance in lipid metabolism.
Hypoglycemia, poor bone growth and lactation problems.
Toxicity:
- Miners show encephalitis.
- Impotence, psychosis and extra pyramidal syndrome (EPS) seen.
Minerals and periodontium
Calcium and periodontium
Rats placed on calcium-deficient diet showed osteoporotic changes in
alveolar bone, reduction in the number and diameter of PDL fibers and
reduction in amount of secondary cementum (Fergusson and Oliver, 1969).It
also showed to stimulate osteoclastic activity (Roberts,1975).Patients with
osteoporosis are at increased risk for attachment loss (Rondoros et al 2000).
Krall et al., (2001) studies suggested that low dietary intake of calcium may
result in severe progression of periodontal diseases.
Its content is increased on the exposed part of the root surface wall of
the pocket. Calcium channel blockers ex.Diltiazem,Verapamil,Nifedipine etc.
are known to induce gingival enlargement. Calcium (39%) is one of the main
content present in calculus.
Magnesium and periodontium
Widening of PDL has been observed with magnesium deficiency
(Klein et al 1935).the eruption rate of rat incisors has been reported to
decrease in animals fed with Mg deficient diet.Thse effects may be related to
the role of Mg ions in several enzyme systems.Animal as well as clinical
studies suggested that Mg supplementation may prevent or retard
periodontitis (Meyle et al 1987).
High Mg concentrations inhibit free-radical generation; activation of
neutrophils is an early effect of hypomagnesaemia (Bussiere et al 2002).Mg
deficiency is also associated with low bone mass, which is manifested in the
oral cavity as loss of alveolar crestal bone height and tooth loss, accompanied
by stimulation of pro-inflammatory cytokines(Wactawski-Wende 2001).Daily
oral supplementation may have beneficial effects in reducing bone loss
(Dimai et al 1998).
Fluoride and periodontium
.it was observed that there fewer areas of PDL hyalinization in fluoride
treated animals than in controls.Hellsing and Hammarstrom (1991)found a
significant reduction in pressure side osteoclast numbers in orthodontically
moved teeth in rats treated with sodium fluoride.
Iron and periodontium
Severe iron deficiency has been related to periodontal destruction in
dogs (hall and robinson, 1937).Laison et al (1968) gained the impression that
patients with moderate to severe periodontitis sometimes had subnormal
levels of iron. Iron deficiency is also associated with decreased lymphocyte
proliferation, neutrophil chemotactic activity and antibody response.
Zinc and periodontium
Zinc helps in stabilization of membranes, antioxidant activity, collagen
synthesis, inhibition of mast cell release of histamine. zinc deficiency is
associated with decreased antibody response, phagocytic function of
macrophages and B-cell and T-cell proliferation. Thus supplementation of
zinc may help in treatment of periodontal diseases as an adjuvant.
Metal intoxications
Bismuth intoxication:
Bismuth pigmentation in the oral cavity usually appears as a narrow,
bluish-black discoloration of the gingival margin in areas of preexistent
gingival inflammation. Such pigmentation results from the precipitation of
particles of bismuth sulfide associated with vascular changes in inflammation.
Lead intoxication:
The pigmentation of the gingiva is linear (burtonian line), steel gray and
associated with local irritation. Oral signs may occur without toxic symptoms.
Mercury intoxication:
Gingival pigmentation in linear form results from the deposition of mercuric
sulfide. The chemical also acts as an irritant, which accentuates the
preexistent inflammation and commonly leads to notable ulceration of the
gingiva and adjacent mucosa and destruction of the underlying bone.
Other chemicals, such as phosphorus, arsenic and chromium, may
cause necrosis of the alveolar bone with loosening and exfoliation of the
teeth.
Conclusion
Minerals are essential for good health. Evidence of mineral
malnutrition are various minor and serious health conditions such as
premature aging and degenerative diseases like osteoporosis etc.In many
cases these could be prevented with proper mineral supplementation .Thus
even though nutrition is not recognized as a risk factor for periodontal
diseases, nutrition is acknowledged to have a significant impact on optimal
functioning of the immune response. Dental professionals need to routinely
assess nutritional status and provide basic nutrition counseling to their
patients ensure optimal functioning of the immune system in combating
infection and to promote optimal periodontal health.
References:
A Textbook of Biochemistry by A.V.S.S Rama Rao.
Textbook of Physiology by Guyton and Hall.
Dent Clin N Am 47 (2003) 337-354.
J Dent Res (10):937-941, 2005.
Carranza’s clinical Periodontology 9th Ed.
The periodontal; ligament in health and disease by B K B Berkovitz, Moxham
Newman 2nd Ed.
Periodontics in the tradition of Orban and Gottlieb by Daniel Grant, Stern,
and Listgarten. 6th edition.