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TRACE ELEMENT-I
Binaya Tamang
UCMS-Bhairahawa
Minerals
any of a class of substances occurring in natu
re, usually comprising inorganic substances
• Only small portion of body weight with
wide variation.
• Normal growth and maintainance of the
body and various functions.
General function
• Minerals perform several vital functions
which
• are absolutely essential for the very
existence of the organism.
• calcification of bone,
• blood coagulation,
• Neuromuscular irritability, acid-base
equilibrium, fluid balance
• and osmotic regulation
integral components
• hemoglobin (Fe), thyroxin (l), insulin (Zn)
and vitamin B12 (Co).
• Sulfur is present in thiamine, biotin, lipoic
acid and coenzyme A.
• Several minerals participate as cofactors for
enzymes in metabolism (e.g. Mg, Mn, Cu, Zn,
K).
• Some elements are essential constituents of
certain enzymes (e.g. Co, Mo, Se).
Two types :- macro and trace
minerals
• If the daily requirement
is more than 100mg/day
they are called major
elements. Which
constitute 60-80% of
body inorganic materials
• if the daily requirements
is less than 100mg/day
they are called minor
elements.
Trace or micro element
• Essential trace elements : lron , copper,
iodine, manganese/zinc, molybdenum,
cobalt, fluorine, selenium and chromium.
• Possibly essential trace elements: Nickel,
vanadium, cadmium and barium.
• Non-essential trace elements: Aluminium,
lead, mercury, boron, silver, bismuth etc.
IRON (Fe)
Distribution of iron
• Total body iron content is 3 to 5 gm
• 75% in blood, the rest is in liver, bone marrow
and muscles.
• Iron is present in almost all cells
• Blood contains 14.5 g of Hb per 100 ml
• About 75% of total iron is in hemoglobin, and 5%
is in myoglobin and 15% in ferritin.
Iron-containing proteins
Sources of Iron
• Leafy vegetables
• Pulses and cereals
• Liver and meat
• Cooking in iron utensils will
improve the iron content of the
diet.
• Milk is a very poor source of
iron, containing less than 0.1
mg/100 ml.
Requirement of Iron
• Adult man - 10 mg, 10 % is only absorbed.
• Mensturatin women- 18 mg/day
• Children between 13-15 yrs - 20-30 mg/day.
• Pregnant and lactating women need 40 mg/day.
Transfer of iron and calcium from mother to fetus
occurs mainly in the last trimester of pregnancy.
Therefore, during this period mother's food should
contain surplus quantities of iron and calcium.
• In the first 3 months of life,
• iron intake is negligible because milk is a poor
source of iron.
• During this time, child is dependent on the iron
reserve received from mother during
pregnancy.
• In premature babies, the transplacental transfer
of iron might not have taken place.
• Hence such babies are at a risk of iron
deficiency. After 3 months of life, diet
supplementation with cereals is essential for
supplying the iron requirement.
Iron Toxicity
• Iron can damage tissues
• Catalyzes the conversion of hydrogen
peroxide to free-radical ions
• Free-radicals can attack:
– Cellular membranes
– Proteins
– DNA
• Iron excess possibly related to cancers, cardiac
toxicity and other factors
Factors Influencing Absorption of
Iron
• Iron is absorbed by upper part of duodenum.
Reduced form of iron Only Fe++ (ferrous) form
(reduced form) is absorbed. Fe+++ (ferric) form is
not absorbed.
Ascorbic acid
• Ferric ions are reduced with the help of gastric
HCl, ascorbic acid, cysteine and -SH groups of
proteins.
• Therefore, these will favor iron absorption.
Interfering substances
• Interfering substances
• Iron absorption is decreased by phytic acid (in cereals)
and oxalic acid (in leafy vegetables) by forming
insoluble iron salts.
• Other minerals
• Calcium, copper, lead and phosphates will inhibit iron
absorption.
• One atom of lead will inhibit absorption of 1000 atoms
of iron.
• A glass of milk, which contains calcium will appreciably
reduce iron absorption.
Mucosal Block Theory
• Duodenum and jejunum are the sites of absorption.
Iron metabolism is unique because homeostasis is
maintained by regulation at the level of absorption
and not by excretion
• No other nutrient is regulated in this manner.
• In other words, iron is a one-way element.
• When iron stores in the body are depleted,
absorption is enhanced.
• When adequate quantity of iron is stored,
absorption is decreased. This is referred to as
mucosal block of regulation of absorption of iron.
Storage Iron
 Ferritin
Free iron is toxic and catalyses the conversion of
H2O2 to hydroxy OH–radicals.
Iron bound to ferritin is nontoxic.
It is the storage protein of iron and found in blood,
liver, spleen, bone marrow and intestine (mucosal
cells).
Hemosiderin
hemosiderin is derived from ferritin and is ferritin
with partially stripped shell.
exists as microscopically visible Fe-staining particles
TRANSFERRIN
• Transferrin is a non-haem iron binding glycoproteins.
• Apotransferrin is the apoenzyme and Fe is its
prosthetic group.
• it can bind with two atoms of iron in the ferric state
(Fe+++) synergistically in presence of HCO3- ion.
• It exists in plasma as β1-globulin and is the true carrier
of iron.
• In plasma, transferrin is saturated only to the extent of
30 per cent to 33 per cent with iron.
• Prior to binding to transferrin, Fe++ (ous) iron has to be
oxidised to Fe+++(ic) form.
• Ceruloplasmin and ferroxidase are required for this
conversion.
Total iron binding capacity
It is the measurement of the maximum
concentration of iron that transferrin can bind.
(TIBC) in plasma is 400 mg/100 ml; this is provided
by the transferrin.
One-third of this capacity is saturated with iron.
This protein bound iron(serum iron) is about 120
mg/dl.
% saturation= serum iron/TIBC x 100.
BODY IRON CYCLING
IRON ABSORPTION
• Iron kept soluble and in ferrous state by gastric
acid.
• Absorbed mainly in duodenum.
• Quantity absorbed regulated by enterocyte
• Multiple proteins involved in control of iron
transport .
• Haem iron enters the enterocyte through
different process than inorganic iron.
EFFECTS OF IRON OVERLOAD
Non-transferrin-bound iron
(NTBI) circulates in the plasma
Excess iron promotes
the generation of free
hydroxyl radicals,
propagators of oxygen-
related tissue damage
Liver cirrhosis/
fibrosis/cancer
Insoluble iron complexes
are deposited in body
tissues and end-organ
toxicity occurs
Diabetes
mellitus
Growth
failure
Capacity of serum transferrin
to bind iron is exceeded
Iron overload
Cardiac
failure
Infertility
(Fenton Reaction)
O2- + H2O2 O2 + OH- + HO
Causes of Iron Deficiency
Nutritional deficiency of iron
Lack of absorption
Hookworm infection: 1hookworm > 0.3 ml blood
per day
Repeated pregnancies
Chronic blood loss
Nephrosis
Lead poisoning
CLINICAL ASPECT
Iron Deficiency Anemia: Iron deficiency anemia is
manifested as hypochromic microcytic anemia.
Hemochromatosis: When iron overload is
associated with injury to cells.
 Haemosiderosis: Iron overload without cell
damage is called haemosiderosis.
• Classic “triad” for diagnosis
1. Micro nodular cirrhosis with marked brown
pigmentation.
2. Diabetes mellitus and
3. Skin pigmentation called as “Bronze diabetes”.
Parameter Normal Iron deficient
erythropoiesis
Iron deficiency
anemia
Serum
ferritin(µg/dl)
50-200 Decreased<15 Decreased<15
TIBC (µg/dl) 300-360 Increased>380 Increased>400
Serum iron (µg/dl) 50-150 Decreased<50 Decreased<30
Transferrin
saturation (%)
30-50 Decreased<20 Decreased<10
RBC
protoporphyrin
(µg/dl)
30-50 Increased Increased
Soluble transferrin
receptor (µg/L)
4-9 Increased Increased
RBC morphology Normal Normal Microcytic
hypochromic
Table. Changes in various laboratory tests used to assess iron deficiency
anemia
If you have a "magnetic"
personality and yet people don't
get attracted to you - it's not
your fault. Just suggest them
iron diet.
They maybe "iron deficient" 

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Trace element 1

  • 2. Minerals any of a class of substances occurring in natu re, usually comprising inorganic substances • Only small portion of body weight with wide variation. • Normal growth and maintainance of the body and various functions.
  • 3. General function • Minerals perform several vital functions which • are absolutely essential for the very existence of the organism. • calcification of bone, • blood coagulation, • Neuromuscular irritability, acid-base equilibrium, fluid balance • and osmotic regulation
  • 4. integral components • hemoglobin (Fe), thyroxin (l), insulin (Zn) and vitamin B12 (Co). • Sulfur is present in thiamine, biotin, lipoic acid and coenzyme A. • Several minerals participate as cofactors for enzymes in metabolism (e.g. Mg, Mn, Cu, Zn, K). • Some elements are essential constituents of certain enzymes (e.g. Co, Mo, Se).
  • 5. Two types :- macro and trace minerals • If the daily requirement is more than 100mg/day they are called major elements. Which constitute 60-80% of body inorganic materials • if the daily requirements is less than 100mg/day they are called minor elements.
  • 6. Trace or micro element • Essential trace elements : lron , copper, iodine, manganese/zinc, molybdenum, cobalt, fluorine, selenium and chromium. • Possibly essential trace elements: Nickel, vanadium, cadmium and barium. • Non-essential trace elements: Aluminium, lead, mercury, boron, silver, bismuth etc.
  • 7.
  • 8.
  • 10. Distribution of iron • Total body iron content is 3 to 5 gm • 75% in blood, the rest is in liver, bone marrow and muscles. • Iron is present in almost all cells • Blood contains 14.5 g of Hb per 100 ml • About 75% of total iron is in hemoglobin, and 5% is in myoglobin and 15% in ferritin.
  • 12. Sources of Iron • Leafy vegetables • Pulses and cereals • Liver and meat • Cooking in iron utensils will improve the iron content of the diet. • Milk is a very poor source of iron, containing less than 0.1 mg/100 ml.
  • 13. Requirement of Iron • Adult man - 10 mg, 10 % is only absorbed. • Mensturatin women- 18 mg/day • Children between 13-15 yrs - 20-30 mg/day. • Pregnant and lactating women need 40 mg/day. Transfer of iron and calcium from mother to fetus occurs mainly in the last trimester of pregnancy. Therefore, during this period mother's food should contain surplus quantities of iron and calcium.
  • 14. • In the first 3 months of life, • iron intake is negligible because milk is a poor source of iron. • During this time, child is dependent on the iron reserve received from mother during pregnancy. • In premature babies, the transplacental transfer of iron might not have taken place. • Hence such babies are at a risk of iron deficiency. After 3 months of life, diet supplementation with cereals is essential for supplying the iron requirement.
  • 15. Iron Toxicity • Iron can damage tissues • Catalyzes the conversion of hydrogen peroxide to free-radical ions • Free-radicals can attack: – Cellular membranes – Proteins – DNA • Iron excess possibly related to cancers, cardiac toxicity and other factors
  • 16. Factors Influencing Absorption of Iron • Iron is absorbed by upper part of duodenum. Reduced form of iron Only Fe++ (ferrous) form (reduced form) is absorbed. Fe+++ (ferric) form is not absorbed. Ascorbic acid • Ferric ions are reduced with the help of gastric HCl, ascorbic acid, cysteine and -SH groups of proteins. • Therefore, these will favor iron absorption.
  • 17. Interfering substances • Interfering substances • Iron absorption is decreased by phytic acid (in cereals) and oxalic acid (in leafy vegetables) by forming insoluble iron salts. • Other minerals • Calcium, copper, lead and phosphates will inhibit iron absorption. • One atom of lead will inhibit absorption of 1000 atoms of iron. • A glass of milk, which contains calcium will appreciably reduce iron absorption.
  • 18. Mucosal Block Theory • Duodenum and jejunum are the sites of absorption. Iron metabolism is unique because homeostasis is maintained by regulation at the level of absorption and not by excretion • No other nutrient is regulated in this manner. • In other words, iron is a one-way element. • When iron stores in the body are depleted, absorption is enhanced. • When adequate quantity of iron is stored, absorption is decreased. This is referred to as mucosal block of regulation of absorption of iron.
  • 19. Storage Iron  Ferritin Free iron is toxic and catalyses the conversion of H2O2 to hydroxy OH–radicals. Iron bound to ferritin is nontoxic. It is the storage protein of iron and found in blood, liver, spleen, bone marrow and intestine (mucosal cells). Hemosiderin hemosiderin is derived from ferritin and is ferritin with partially stripped shell. exists as microscopically visible Fe-staining particles
  • 20. TRANSFERRIN • Transferrin is a non-haem iron binding glycoproteins. • Apotransferrin is the apoenzyme and Fe is its prosthetic group. • it can bind with two atoms of iron in the ferric state (Fe+++) synergistically in presence of HCO3- ion. • It exists in plasma as β1-globulin and is the true carrier of iron. • In plasma, transferrin is saturated only to the extent of 30 per cent to 33 per cent with iron. • Prior to binding to transferrin, Fe++ (ous) iron has to be oxidised to Fe+++(ic) form. • Ceruloplasmin and ferroxidase are required for this conversion.
  • 21. Total iron binding capacity It is the measurement of the maximum concentration of iron that transferrin can bind. (TIBC) in plasma is 400 mg/100 ml; this is provided by the transferrin. One-third of this capacity is saturated with iron. This protein bound iron(serum iron) is about 120 mg/dl. % saturation= serum iron/TIBC x 100.
  • 23. IRON ABSORPTION • Iron kept soluble and in ferrous state by gastric acid. • Absorbed mainly in duodenum. • Quantity absorbed regulated by enterocyte • Multiple proteins involved in control of iron transport . • Haem iron enters the enterocyte through different process than inorganic iron.
  • 24.
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  • 26.
  • 27. EFFECTS OF IRON OVERLOAD Non-transferrin-bound iron (NTBI) circulates in the plasma Excess iron promotes the generation of free hydroxyl radicals, propagators of oxygen- related tissue damage Liver cirrhosis/ fibrosis/cancer Insoluble iron complexes are deposited in body tissues and end-organ toxicity occurs Diabetes mellitus Growth failure Capacity of serum transferrin to bind iron is exceeded Iron overload Cardiac failure Infertility (Fenton Reaction) O2- + H2O2 O2 + OH- + HO
  • 28. Causes of Iron Deficiency Nutritional deficiency of iron Lack of absorption Hookworm infection: 1hookworm > 0.3 ml blood per day Repeated pregnancies Chronic blood loss Nephrosis Lead poisoning
  • 29. CLINICAL ASPECT Iron Deficiency Anemia: Iron deficiency anemia is manifested as hypochromic microcytic anemia. Hemochromatosis: When iron overload is associated with injury to cells.  Haemosiderosis: Iron overload without cell damage is called haemosiderosis. • Classic “triad” for diagnosis 1. Micro nodular cirrhosis with marked brown pigmentation. 2. Diabetes mellitus and 3. Skin pigmentation called as “Bronze diabetes”.
  • 30. Parameter Normal Iron deficient erythropoiesis Iron deficiency anemia Serum ferritin(µg/dl) 50-200 Decreased<15 Decreased<15 TIBC (µg/dl) 300-360 Increased>380 Increased>400 Serum iron (µg/dl) 50-150 Decreased<50 Decreased<30 Transferrin saturation (%) 30-50 Decreased<20 Decreased<10 RBC protoporphyrin (µg/dl) 30-50 Increased Increased Soluble transferrin receptor (µg/L) 4-9 Increased Increased RBC morphology Normal Normal Microcytic hypochromic Table. Changes in various laboratory tests used to assess iron deficiency anemia
  • 31. If you have a "magnetic" personality and yet people don't get attracted to you - it's not your fault. Just suggest them iron diet. They maybe "iron deficient" 