Mineral metabolism.pdf

 Minerals are inorganic elements
 The minerals required in human nutrition can be
grouped into macrominerals and microminerals (trace
elements).
 The macrominerals are required in excess of 100
mg/day.
 The microminerals or trace elements are required in
amounts less than 100 mg/day.
 Minerals are inorganic elements
 The minerals required in human nutrition can be
grouped into macrominerals and microminerals (trace
elements).
 The macrominerals are required in excess of 100
mg/day.
 The microminerals or trace elements are required in
amounts less than 100 mg/day.

Metabolism Of Sodium, Potassium And Chloride

Sodium
 Sodium is the major cation of extracellular fluids.
 Sources: Table salt (NaCl), salty foods, animal foods,
milk and some vegetables.
 Recommended dietary allowance per day: 1–5 gm
Sodium
 Sodium is the major cation of extracellular fluids.
 Sources: Table salt (NaCl), salty foods, animal foods,
milk and some vegetables.
 Recommended dietary allowance per day: 1–5 gm

Metabolic functions
 It maintains the osmotic pressure and water balance.
 It is a constituent of buffer and involved in the
maintenance of acid-base balance.
 It maintains muscle and nerve irritability at the proper
level.
 Sodium is involved in cell membrane permeability.
 Sodium is required for intestinal absorption of glucose,
galactose and amino acids.
Metabolic functions
 It maintains the osmotic pressure and water balance.
 It is a constituent of buffer and involved in the
maintenance of acid-base balance.
 It maintains muscle and nerve irritability at the proper
level.
 Sodium is involved in cell membrane permeability.
 Sodium is required for intestinal absorption of glucose,
galactose and amino acids.

Plasma Sodium
 The plasma concentration of sodium is 135-145
mEq/L.
 Whereas blood cell (intracellular) contain only about
35 mEq/L.
Plasma Sodium
 The plasma concentration of sodium is 135-145
mEq/L.
 Whereas blood cell (intracellular) contain only about
35 mEq/L.

Clinical Conditions Related to Plasma Sodium Level
Hypernatremia
Hypernatremia is an increase in serum sodium
concentration above the normal range of 135– 145 mEq/L.
Hyponatremia
Fall in serum sodium concentration below the normal range
135 to 145 mEq/L.
.
Clinical Conditions Related to Plasma Sodium Level
Hypernatremia
Hypernatremia is an increase in serum sodium
concentration above the normal range of 135– 145 mEq/L.
Hyponatremia
Fall in serum sodium concentration below the normal range
135 to 145 mEq/L.
.

Causes of hypernatremia
 Water depletion, e.g. diabetes insipidus.
 Water and sodium depletion, e.g. diabetes mellitus,
excessive sweating or diarrhea in children
 Excessive sodium intake or retention due to excessive
aldosterone secretion, e.g. in Cushing’s syndrome
Symptoms of hypernatremia
Dehydration ,hypertension and edema.
Causes of hypernatremia
 Water depletion, e.g. diabetes insipidus.
 Water and sodium depletion, e.g. diabetes mellitus,
excessive sweating or diarrhea in children
 Excessive sodium intake or retention due to excessive
aldosterone secretion, e.g. in Cushing’s syndrome
Symptoms of hypernatremia
Dehydration ,hypertension and edema.

Causes of hyponatremia
 Retention of water: e.g. in heart failure, liver disease, nephrotic
syndrome, renal failure, syndrome of inappropriate ADH
secretion (SIADH).
 Loss of sodium: e.g. vomiting, diarrhea, or in urine. Urinary loss
may be due to aldosterone deficiency (Addison’s disease).
Symptoms of hyponatremia
Constant thirst, muscle cramps, nausea, vomiting, abdominal
cramps, weakness and lethargy.
Causes of hyponatremia
 Retention of water: e.g. in heart failure, liver disease, nephrotic
syndrome, renal failure, syndrome of inappropriate ADH
secretion (SIADH).
 Loss of sodium: e.g. vomiting, diarrhea, or in urine. Urinary loss
may be due to aldosterone deficiency (Addison’s disease).
Symptoms of hyponatremia
Constant thirst, muscle cramps, nausea, vomiting, abdominal
cramps, weakness and lethargy.

Potassium
 Potassium is the main intracellular cation.
 Dietary food sources: Vegetables, fruits, whole grain,
meat, milk, legumes and tender coconut water.
 Recommended dietary allowance per day: 2–5 gm.
 Serum potassium: 3.5–5 mEq/L.
Potassium
 Potassium is the main intracellular cation.
 Dietary food sources: Vegetables, fruits, whole grain,
meat, milk, legumes and tender coconut water.
 Recommended dietary allowance per day: 2–5 gm.
 Serum potassium: 3.5–5 mEq/L.

Metabolic functions
 Potassium maintains the intracellular osmotic pressure,
water balance and acid-base balance.
 It influences activity of cardiac and skeletal muscle.
 Several glycolytic enzymes need potassium for their
formation.
 Potassium is required for transmission of nerve impulses.
 Nuclear activity and protein synthesis are dependent on
potassium.
Metabolic functions
 Potassium maintains the intracellular osmotic pressure,
water balance and acid-base balance.
 It influences activity of cardiac and skeletal muscle.
 Several glycolytic enzymes need potassium for their
formation.
 Potassium is required for transmission of nerve impulses.
 Nuclear activity and protein synthesis are dependent on
potassium.

Clinical Conditions Related to Plasma Potassium
 Hyperkalemia: elevated plasma potassium above the
normal range 3.5–5 mEq/L.
 Hypokalemia : Low Plasma Concentration
Clinical Conditions Related to Plasma Potassium
 Hyperkalemia: elevated plasma potassium above the
normal range 3.5–5 mEq/L.
 Hypokalemia : Low Plasma Concentration

Causes of hyperkalemia
 Renal failure
 Mineralocorticoid deficiency: For example, in
Addison’s disease.
 Cell damage: For example, in trauma and malignancy.
Symptoms of hyperkalemia
cardiac arrest, changes in electro- cardiogram, cardiac
arrhythmia, muscle weakness ,abnormal tingling
sensation
Causes of hyperkalemia
 Renal failure
 Mineralocorticoid deficiency: For example, in
Addison’s disease.
 Cell damage: For example, in trauma and malignancy.
Symptoms of hyperkalemia
cardiac arrest, changes in electro- cardiogram, cardiac
arrhythmia, muscle weakness ,abnormal tingling
sensation

Causes of hypokalemia
Gastrointestinal losses: due to vomiting, diarrhea.
Renal losses: Due to renal disease, administration of
diuretics.
Symptoms of hypokalemia
Muscular weakness, tachycardia, electrocardiographic
(ECG) changes (flattering of ECG waves), lethargy, and
confusion.
Causes of hypokalemia
Gastrointestinal losses: due to vomiting, diarrhea.
Renal losses: Due to renal disease, administration of
diuretics.
Symptoms of hypokalemia
Muscular weakness, tachycardia, electrocardiographic
(ECG) changes (flattering of ECG waves), lethargy, and
confusion.

Chloride
 Major anion in the extracellular fluid.
 Dietary food sources: Table salt, leafy vegetables, eggs
and milk.
 Recommended dietary allowance (RDA) per day: 2–5 gm.
 Plasma chloride: 95–105 mEq/L.
Chloride
 Major anion in the extracellular fluid.
 Dietary food sources: Table salt, leafy vegetables, eggs
and milk.
 Recommended dietary allowance (RDA) per day: 2–5 gm.
 Plasma chloride: 95–105 mEq/L.

Functions
 As a part of sodium chloride, chloride is essential for water balance,
regulation of osmotic pressure, and acid-base balance.
 Chloride is necessary for the formation of HCl.
Clinical Conditions
Hyperchloremia
An increased chloride concentration occurs in dehydration, metabolic
acidosis and Cushing's syndrome.
Hypochloremia
A decreased chloride concentration is seen in severe vomiting, metabolic
alkalosis, excessive sweating and Addison's disease
Functions
 As a part of sodium chloride, chloride is essential for water balance,
regulation of osmotic pressure, and acid-base balance.
 Chloride is necessary for the formation of HCl.
Clinical Conditions
Hyperchloremia
An increased chloride concentration occurs in dehydration, metabolic
acidosis and Cushing's syndrome.
Hypochloremia
A decreased chloride concentration is seen in severe vomiting, metabolic
alkalosis, excessive sweating and Addison's disease

Metabolism Of Calcium, Phosphorus,
And Magnesium

Calcium
 Calcium is the most abundant mineral in the body.
 The adult human body contains about 1 kg of calcium.
 About 99% the body’s calcium is present in bone
together with phosphate as the mineral hydroxyapatite
[Ca10 (PO4)6 (OH)2], with small amounts in soft tissue
and extracellular fluid.
Calcium
 Calcium is the most abundant mineral in the body.
 The adult human body contains about 1 kg of calcium.
 About 99% the body’s calcium is present in bone
together with phosphate as the mineral hydroxyapatite
[Ca10 (PO4)6 (OH)2], with small amounts in soft tissue
and extracellular fluid.

Functions
1.Formation of bone and teeth: 99% of the body’s calcium
is located in bone in the form of hydroxyapatite crystal
[3Ca3 (PO4)2 Ca (OH)2]. The hardness and rigidity of
bone and teeth are due to hydroxyapatite.
2.Blood coagulations: Calcium present in platelets involved
in blood coagulation, the conversion of an inactive protein
prothrombin into an active thrombin requires calcium ions.
Functions
1.Formation of bone and teeth: 99% of the body’s calcium
is located in bone in the form of hydroxyapatite crystal
[3Ca3 (PO4)2 Ca (OH)2]. The hardness and rigidity of
bone and teeth are due to hydroxyapatite.
2.Blood coagulations: Calcium present in platelets involved
in blood coagulation, the conversion of an inactive protein
prothrombin into an active thrombin requires calcium ions.

3. Muscle contraction: Muscle contraction is initiated
by the binding of calcium to troponin.
4. Release of hormones: The release of certain
hormones like parathyroid hormone, calcitonin,
etc. requires calcium ions.
5. Release of neurotransmitter: Influx of Ca2+ from
extracellular space into neurons causes release of
neurotransmitter.
3. Muscle contraction: Muscle contraction is initiated
by the binding of calcium to troponin.
4. Release of hormones: The release of certain
hormones like parathyroid hormone, calcitonin,
etc. requires calcium ions.
5. Release of neurotransmitter: Influx of Ca2+ from
extracellular space into neurons causes release of
neurotransmitter.

6. Regulation of enzyme activity: Activation of number of
enzymes requires Ca2+ as a specific cofactor.
7. Second messenger: For epinephrine or glucagon. Ca
also functions as a third messenger for some
hormones such as antidiuretic hormone (ADH).
8. Membrane excitability
.
6. Regulation of enzyme activity: Activation of number of
enzymes requires Ca2+ as a specific cofactor.
7. Second messenger: For epinephrine or glucagon. Ca
also functions as a third messenger for some
hormones such as antidiuretic hormone (ADH).
8. Membrane excitability
.

9. Cardiac activity:. Myocardial contractility increases
with increased Ca 2+ concentration and
decreases with decreased calcium concentration.
10. Maintenance of Membrane integrity and
permeability
.
9. Cardiac activity:. Myocardial contractility increases
with increased Ca 2+ concentration and
decreases with decreased calcium concentration.
10. Maintenance of Membrane integrity and
permeability
.

Dietary sources
Milk and dairy products, (half a liter of milk contains
approximately 1,000 mg of calcium) cheese, cereal grains,
legumes, nuts and vegetables.
Recommended dietary allowance (RDA) per day
 Adults: 800 mg/day
 Pregnancy , lactation and for teenagers: 1200 mg/day
 Infants: 300–500 mg/day.
Dietary sources
Milk and dairy products, (half a liter of milk contains
approximately 1,000 mg of calcium) cheese, cereal grains,
legumes, nuts and vegetables.
Recommended dietary allowance (RDA) per day
 Adults: 800 mg/day
 Pregnancy , lactation and for teenagers: 1200 mg/day
 Infants: 300–500 mg/day.

Absorption
Calcium is absorbed from small intestine and the degree
of absorption is affected by different factors.

Factors affecting absorption
Factors that stimulate calcium absorption
1. Vitamin D stimulates absorption of calcium from
intestine by inducing the synthesis of calcium
binding protein, necessary for the absorption
of calcium from intestine.
2. Parathyroid hormone (PTH) stimulates calcium
absorption indirectly via activating vitamin D.
Factors affecting absorption
Factors that stimulate calcium absorption
1. Vitamin D stimulates absorption of calcium from
intestine by inducing the synthesis of calcium
binding protein, necessary for the absorption
of calcium from intestine.
2. Parathyroid hormone (PTH) stimulates calcium
absorption indirectly via activating vitamin D.

3. Acidic pH: Since, calcium salts are more soluble in
acidic pH, the acidic foods and organic acids (citric
acid, lactic acid, pyruvic acid, etc.) favour the
absorption of calcium from intestine.
4. High protein diet favours absorption of calcium.
Basic amino acids, lysine and arginine derived from
hydrolysis of the dietary proteins increase calcium
absorption.
5. Lactose increase Ca absorption
3. Acidic pH: Since, calcium salts are more soluble in
acidic pH, the acidic foods and organic acids (citric
acid, lactic acid, pyruvic acid, etc.) favour the
absorption of calcium from intestine.
4. High protein diet favours absorption of calcium.
Basic amino acids, lysine and arginine derived from
hydrolysis of the dietary proteins increase calcium
absorption.
5. Lactose increase Ca absorption

Factors that inhibit calcium absorption
 Phytates and Oxalates. Phytates present in many cereals
and oxalates present in green leafy vegetables.
 High fat diet decreases the absorption of calcium. High
phosphate content in diet
 The Ca: P ratio should be 1:2–2:1 for optimum
absorption of calcium..
 High fiber diet decreases the absorption of calcium from
intestine.
Factors that inhibit calcium absorption
 Phytates and Oxalates. Phytates present in many cereals
and oxalates present in green leafy vegetables.
 High fat diet decreases the absorption of calcium. High
phosphate content in diet
 The Ca: P ratio should be 1:2–2:1 for optimum
absorption of calcium..
 High fiber diet decreases the absorption of calcium from
intestine.

Excretion
The excretion of calcium is partly through the kidneys
but mostly by way of the small intestine through feces.
Small amount of calcium may also be lost in sweat.
Excretion
The excretion of calcium is partly through the kidneys
but mostly by way of the small intestine through feces.
Small amount of calcium may also be lost in sweat.

Plasma Calcium
The plasma calcium concentration in normal individual is
approximately 9–11 mg% (2–3 mEq/L).

Calcium is present in plasma in three forms:
1. Free or unbound or ionic calcium, Ca2+
: In blood
50% of the plasma calcium is free, unbound, ionic
form which is functionally most active.
2. Bound calcium: 40% of the plasma calcium is bound
to protein mostly to albumin.
3. Complex calcium: 10% of the plasma calcium is in
complex with anions including bicarbonate HCO3
-),
phosphate (H2PO4
– ), lactate and citrate
Calcium is present in plasma in three forms:
1. Free or unbound or ionic calcium, Ca2+
: In blood
50% of the plasma calcium is free, unbound, ionic
form which is functionally most active.
2. Bound calcium: 40% of the plasma calcium is bound
to protein mostly to albumin.
3. Complex calcium: 10% of the plasma calcium is in
complex with anions including bicarbonate HCO3
-),
phosphate (H2PO4
– ), lactate and citrate

Equilibrium between physiochemical states of calcium in plasma.

Regulation of Plasma Calcium Level
 Function of three main organs:
1. Bone
2. Kidney
3. Intestine.
 Function of three main hormones:
1. Parathyroid hormone (PTH)
2. Vitamin D or cholecalciferol or calcitriol
3. Calcitonin.
Regulation of Plasma Calcium Level
 Function of three main organs:
1. Bone
2. Kidney
3. Intestine.
 Function of three main hormones:
1. Parathyroid hormone (PTH)
2. Vitamin D or cholecalciferol or calcitriol
3. Calcitonin.

The four major processes are
1. Absorption of calcium from the intestine, mainly
through the action of vitamin D.
2. Reabsorption of calcium from the kidney, mainly
through action of parathyroid hormone and vitamin D.
3. Demineralization of bone mainly through action of
parathyroid hormone, but facilitated by vitamin D.
4. Mineralization (calcification) of bone through the action
of calcitonin.
The four major processes are
1. Absorption of calcium from the intestine, mainly
through the action of vitamin D.
2. Reabsorption of calcium from the kidney, mainly
through action of parathyroid hormone and vitamin D.
3. Demineralization of bone mainly through action of
parathyroid hormone, but facilitated by vitamin D.
4. Mineralization (calcification) of bone through the action
of calcitonin.

Clinical Conditions
Hypocalcemia
 Hypoparathyroidism: Due to neck surgery, or due to magnesium
deficiency
 Vitamin D deficiency: due to dietary deficiency, malabsorption or
little exposure to sunlight. It may lead to bone disorders,
osteomalacia in adults and rickets in children.
 Renal disease: The diseased kidneys fail to synthesize calcitriol
due to impaired hydroxylation.
Clinical Conditions
Hypocalcemia
 Hypoparathyroidism: Due to neck surgery, or due to magnesium
deficiency
 Vitamin D deficiency: due to dietary deficiency, malabsorption or
little exposure to sunlight. It may lead to bone disorders,
osteomalacia in adults and rickets in children.
 Renal disease: The diseased kidneys fail to synthesize calcitriol
due to impaired hydroxylation.

Clinical features of hypocalcemia
 Neuromuscular irritability
 Neurologic features such as tingling, tetany,
numbness ,Muscle cramps
 Cardiovascular signs such as an abnormal ECG.
 Cataracts.
Clinical features of hypocalcemia
 Neuromuscular irritability
 Neurologic features such as tingling, tetany,
numbness ,Muscle cramps
 Cardiovascular signs such as an abnormal ECG.
 Cataracts.

Hypercalcemia
Causes of hypercalcemia
 Hyperparathyroidism
 Malignant disease.
Hypercalcemia
Causes of hypercalcemia
 Hyperparathyroidism
 Malignant disease.

Clinical features of hypercalcemia
 Neurological symptoms such as depression, confusion,
inability to concentrate.
 Muscle weakness
 Gastrointestinal problems such as anorexia, abdominal
pain, nausea and vomiting and constipation.
 Renal features such as polyuria and polydypsia.
 Cardiac arrhythmias.
Clinical features of hypercalcemia
 Neurological symptoms such as depression, confusion,
inability to concentrate.
 Muscle weakness
 Gastrointestinal problems such as anorexia, abdominal
pain, nausea and vomiting and constipation.
 Renal features such as polyuria and polydypsia.
 Cardiac arrhythmias.

Phosphorus
Adults contain about 400–700 gm of phosphorus, about
80% of which is combined with calcium in bones and
teeth..
Phosphorus
Adults contain about 400–700 gm of phosphorus, about
80% of which is combined with calcium in bones and
teeth..

Functions
 Constituent of bone and teeth
 Acid-base regulation
 Energy storage and transfer reactions
 Essential constituent of phospholipid of cell membrane,
nucleic acids (RNA and DNA), nucleotides (NAD,
NADP, c-AMP, c-GMP
 Regulation of enzyme activity
Functions
 Constituent of bone and teeth
 Acid-base regulation
 Energy storage and transfer reactions
 Essential constituent of phospholipid of cell membrane,
nucleic acids (RNA and DNA), nucleotides (NAD,
NADP, c-AMP, c-GMP
 Regulation of enzyme activity

Dietary sources
The foods rich in calcium are also rich in phosphorus, i.e. milk,
cheese, beans, eggs, cereals, fish and meat.
Recommended dietary allowance per day
 Both men and women is 800 mg/day.
 During pregnancy and lactation is 1200 mg/day.
Dietary sources
The foods rich in calcium are also rich in phosphorus, i.e. milk,
cheese, beans, eggs, cereals, fish and meat.
 Both men and women is 800 mg/day.
 During pregnancy and lactation is 1200 mg/day.

Absorption
 Like calcium, absorption of phosphorus is similarly affected by
different factors as that of calcium.
 Vitamin D stimulates the absorption of phosphate along with
calcium.
 Acidic pH favours the absorption of phosphorus.
 Phytates and oxalates decrease absorption of phosphate from
intestine.
 Optimum absorption of calcium and phosphate occurs when
dietary Ca: P ratio is 1:2 – 2:1.
Absorption
 Like calcium, absorption of phosphorus is similarly affected by
different factors as that of calcium.
 Vitamin D stimulates the absorption of phosphate along with
calcium.
 Acidic pH favours the absorption of phosphorus.
 Phytates and oxalates decrease absorption of phosphate from
intestine.
 Optimum absorption of calcium and phosphate occurs when
dietary Ca: P ratio is 1:2 – 2:1.

Plasma phosphorus
 Plasma contains 2.5–4.5 mg/dL of inorganic phosphate.
 Plasma phosphate concentration is controlled by the
kidney, where tubular reabsorption is reduced by PTH.
 The phosphate which is not reabsorbed in the renal
tubule acts as an important urinary buffer.
Plasma phosphorus
 Plasma contains 2.5–4.5 mg/dL of inorganic phosphate.
 Plasma phosphate concentration is controlled by the
kidney, where tubular reabsorption is reduced by PTH.
 The phosphate which is not reabsorbed in the renal
tubule acts as an important urinary buffer.

Clinical Conditions
Hypophosphatemia
In hypophosphatemia serum inorganic phosphate concentration is
less than 2.5 mg/dL.
Causes of hypophosphatemia
 Hyperparathyroidism: High PTH increases phosphate excretion
by the kidneys and this leads to low serum concentration of
phosphate.
 Congenital defects of tubular phosphate reabsorption, e.g.
Fanconi’s syndrome, in which phosphate is lost from body.
Clinical Conditions
Hypophosphatemia
In hypophosphatemia serum inorganic phosphate concentration is
less than 2.5 mg/dL.
Causes of hypophosphatemia
 Hyperparathyroidism: High PTH increases phosphate excretion
by the kidneys and this leads to low serum concentration of
phosphate.
 Congenital defects of tubular phosphate reabsorption, e.g.
Fanconi’s syndrome, in which phosphate is lost from body.

Clinical symptoms of hypophosphatemia
 Muscle pain and weakness and decreased myocardial
output.
 If hypophosphatemia is chronic; rickets in children or
osteomalacia in adults may develop.
Clinical symptoms of hypophosphatemia
 Muscle pain and weakness and decreased myocardial
output.
 If hypophosphatemia is chronic; rickets in children or
osteomalacia in adults may develop.

Hyperphosphatemia
 Causes of hyperphosphatemia
Renal failure:
Hypoparathyroidism
 Clinical symptoms
Decrease in serum calcium concentration leads to
tetany and seizures
Hyperphosphatemia
 Causes of hyperphosphatemia
Renal failure:
Hypoparathyroidism
 Clinical symptoms
Decrease in serum calcium concentration leads to
tetany and seizures

METABOLISM OF TRACE ELEMENTS (MICROMINERALS)

Copper (Cu)
Dietary food sources
Shellfish, liver, kidneys, egg yolk and some legumes
2–3 mg.
Functions
 Copper is required for the synthesis of hemoglobin.
Copper is a constituent of ALA synthase enzyme
required for heme synthesis.
Copper (Cu)
Shellfish, liver, kidneys, egg yolk and some legumes
2–3 mg.
Functions
 Copper is required for the synthesis of hemoglobin.
Copper is a constituent of ALA synthase enzyme
required for heme synthesis.

 Copper is an essential constituent of many - enzymes including:
– Ceruloplasmin (ferroxidase)
– Cytochrome oxidase
– Superoxide dismutase
– Dopamine b-hydroxylase
– Tyrosinase
– Tryptophan dioxygenase
– Lysyl oxidase.
 Copper is an essential constituent of many - enzymes including:
– Ceruloplasmin (ferroxidase)
– Cytochrome oxidase
– Superoxide dismutase
– Dopamine b-hydroxylase
– Tyrosinase
– Tryptophan dioxygenase
– Lysyl oxidase.

 Being a constituent of enzyme tyrosinase, copper is required
for synthesis of melanin pigment.
 Copper plays an important role in iron absorption.
Ceruloplasmin, the major copper containing protein in
plasma has ferroxidase activity that oxidizes ferrous ion to
ferric state before its binding to transferrin (transport form of
iron).
 Copper is required for the synthesis of collagen and elastin.
Lysyl oxidase, a copper containing enzyme converts certain
lysine residues to allysine needed in the formation of
collagen and elastin.
 Being a constituent of enzyme tyrosinase, copper is required
for synthesis of melanin pigment.
 Copper plays an important role in iron absorption.
Ceruloplasmin, the major copper containing protein in
plasma has ferroxidase activity that oxidizes ferrous ion to
ferric state before its binding to transferrin (transport form of
iron).
 Copper is required for the synthesis of collagen and elastin.
Lysyl oxidase, a copper containing enzyme converts certain
lysine residues to allysine needed in the formation of
collagen and elastin.

Plasma copper
Normal plasma concentration 100 to 200 mg/dl of which
90% is bound to ceruloplasmin.
Deficiency manifestation
 Neutropenia (decreased number of neutrophils) and
hypochromic anemia in the early stages.
 Osteoporosis and various bone and joint abnormalities,
due to impairment in copper-dependent cross-linking of
bone collagen and connective tissue.
Plasma copper
Normal plasma concentration 100 to 200 mg/dl of which
90% is bound to ceruloplasmin.
 Neutropenia (decreased number of neutrophils) and
hypochromic anemia in the early stages.
 Osteoporosis and various bone and joint abnormalities,
due to impairment in copper-dependent cross-linking of
bone collagen and connective tissue.

 Decreased pigmentation of skin due to depressed copper
dependent tyrosinase activity, which is required in the
biosynthesis of skin pigment melanin.
 Neurological abnormalities probably caused by
depressed cytochrome oxidase activity.
Inborn errors of copper metabolism
1. Menkes syndrome
2. Wilson’s disease
 Decreased pigmentation of skin due to depressed copper
dependent tyrosinase activity, which is required in the
biosynthesis of skin pigment melanin.
 Neurological abnormalities probably caused by
depressed cytochrome oxidase activity.
Inborn errors of copper metabolism
1. Menkes syndrome
2. Wilson’s disease

Menkes syndrome or Kinky-hair disease
 X-linked recessive disorder. The genetic defect is in
absorption of copper from intestine.
 Both serum copper and ceruloplasmin and liver copper
content are low.
 Clinical manifestations occur early in life and include:
 Kinky or twisted brittle hair (steely) due to loss of
copper catalyzed disulphide bond formation.
 Depigmentation of the skin and hair.
 Mental retardation.
Menkes syndrome or Kinky-hair disease
 X-linked recessive disorder. The genetic defect is in
absorption of copper from intestine.
 Both serum copper and ceruloplasmin and liver copper
content are low.
 Clinical manifestations occur early in life and include:
 Kinky or twisted brittle hair (steely) due to loss of
copper catalyzed disulphide bond formation.
 Depigmentation of the skin and hair.
 Mental retardation.

Wilson’s disease
 Wilson's disease is an inborn error of copper metabolism.
 It is an autosomal recessive disorder in which excessive
accumulation of copper occurs in tissues.
The possible causes are:
 An impairment in binding capacity of copper to
ceruloplasmin or inability of liver to synthesize
ceruloplasmin or both.
 An impairment in excretion of copper in bile.
Wilson’s disease
 Wilson's disease is an inborn error of copper metabolism.
 It is an autosomal recessive disorder in which excessive
accumulation of copper occurs in tissues.
The possible causes are:
 An impairment in binding capacity of copper to
ceruloplasmin or inability of liver to synthesize
ceruloplasmin or both.
 An impairment in excretion of copper in bile.

Symptoms
 Accumulation of copper in liver, brain, kidney and eyes leading to
copper toxicosis.
 Excessive deposition of copper in brain and liver leads to neurological
symptoms and liver damage leading to cirrhosis.
 Copper deposition in kidney leads to renal tubular damage and those
in cornea form yellow or brown ring around the cornea, known as
Kayser-Fleisher (KF) rings.
 The disease is also characterized by low levels of copper and
ceruloplasmin in plasma with increased excretion of copper in urine.
Symptoms
 Accumulation of copper in liver, brain, kidney and eyes leading to
copper toxicosis.
 Excessive deposition of copper in brain and liver leads to neurological
symptoms and liver damage leading to cirrhosis.
 Copper deposition in kidney leads to renal tubular damage and those
in cornea form yellow or brown ring around the cornea, known as
Kayser-Fleisher (KF) rings.
 The disease is also characterized by low levels of copper and
ceruloplasmin in plasma with increased excretion of copper in urine.

Treatment
The excess copper is removed from the body by treatment
with penicillamine.
Treatment
The excess copper is removed from the body by treatment
with penicillamine.

Fluorine (F)
The body receives fluorine mainly from drinking water.
Some sea fish and tea also contain small amount of
fluoride.
1.5–4 mg per day or 1–2 ppm
Fluorine (F)
The body receives fluorine mainly from drinking water.
Some sea fish and tea also contain small amount of
fluoride.
1.5–4 mg per day or 1–2 ppm

Functions
 Fluoride is required for the proper formation of bone
and teeth.
 Fluoride becomes incorporated into hydroxyapatite, to
form fluoroapatite.
 Fluoroapatite increases hardness of bone and teeth and
provides protection against dental caries and attack by
acids.
Functions
 Fluoride is required for the proper formation of bone
and teeth.
 Fluoride becomes incorporated into hydroxyapatite, to
form fluoroapatite.
 Fluoroapatite increases hardness of bone and teeth and
provides protection against dental caries and attack by
acids.

Deficiency symptoms
Deficiency of fluoride leads to dental caries and
osteoporosis.
Toxicity
Excessive amounts of fluoride can result in dental fluorosis.
This condition results in teeth with a patch, dull white, even
chalk looking appearance. A brown mottled appearance can
also occur.
Deficiency symptoms
Deficiency of fluoride leads to dental caries and
osteoporosis.
Toxicity
Excessive amounts of fluoride can result in dental fluorosis.
This condition results in teeth with a patch, dull white, even
chalk looking appearance. A brown mottled appearance can
also occur.

Iodine (I2)
The adult human body contains about 50 mg of iodine.
The blood plasma contains 4–8 mg of protein bound
iodine (PBI) per 100 ml.
Seafood, drinking water, iodized table salt, onions,
vegetables, etc.
100–150 micro gm for adults
Iodine (I2)
The adult human body contains about 50 mg of iodine.
The blood plasma contains 4–8 mg of protein bound
iodine (PBI) per 100 ml.
Seafood, drinking water, iodized table salt, onions,
vegetables, etc.
100–150 micro gm for adults

Functions
Synthesis of thyroid hormones, triiodothyronine (T3) and
tetraiodothyronine (T4),
A deficiency of iodine in children leads to cretinism and in
adults endemic goiter.
Functions
Synthesis of thyroid hormones, triiodothyronine (T3) and
tetraiodothyronine (T4),
A deficiency of iodine in children leads to cretinism and in
adults endemic goiter.

Cretinism
 Severe iodine deficiency in mothers leads to
intrauterine or neonatal hypothyroidism results
in cretinism in their children.
 Cretinism is characterized by mental retardation,
slow body development, dwarfism and
characteristic facial structure.
Cretinism
 Severe iodine deficiency in mothers leads to
intrauterine or neonatal hypothyroidism results
in cretinism in their children.
 Cretinism is characterized by mental retardation,
slow body development, dwarfism and
characteristic facial structure.

Goiter
 A goiter is an enlarged thyroid with decreased thyroid
hormone production.
 An iodine deficiency in adults stimulates the proliferation of
thyroid epithelial cells, resulting in enlargement of the thyroid
gland.
 The thyroid gland collects iodine from the blood and uses it to
make thyroid hormones.
 In iodine deficiency, the thyroid gland undergoes
compensatory enlargement in order to extract iodine from
blood more efficiently.
Goiter
 A goiter is an enlarged thyroid with decreased thyroid
hormone production.
 An iodine deficiency in adults stimulates the proliferation of
thyroid epithelial cells, resulting in enlargement of the thyroid
gland.
 The thyroid gland collects iodine from the blood and uses it to
make thyroid hormones.
 In iodine deficiency, the thyroid gland undergoes
compensatory enlargement in order to extract iodine from
blood more efficiently.

Iron (Fe)
 A normal adult possesses 3–5 gm of iron.
 This small amount is used again and again in the body.
 Iron is called a one way substance, because very little of
it is excreted.
 Iron is not like vitamins or most other organic or even
inorganic substances which are either inactivated or
excreted in course of their physiological function.
.
Iron (Fe)
 A normal adult possesses 3–5 gm of iron.
 This small amount is used again and again in the body.
 Iron is called a one way substance, because very little of
it is excreted.
 Iron is not like vitamins or most other organic or even
inorganic substances which are either inactivated or
excreted in course of their physiological function.
.

 The best sources of food iron include liver, meat, egg
yolk, green leafy vegetables, whole grains and cereals.
 There are two types of food iron:
– In animal foods, iron is often attached to proteins called heme
proteins and referred to as heme iron and is found in meat,
poultry and fish.
– In plant foods, iron is not attached to heme proteins and is
classified as non-heme iron, found in green leafy vegetables.
 The best sources of food iron include liver, meat, egg
yolk, green leafy vegetables, whole grains and cereals.
 There are two types of food iron:
– In animal foods, iron is often attached to proteins called heme
proteins and referred to as heme iron and is found in meat,
poultry and fish.
– In plant foods, iron is not attached to heme proteins and is
classified as non-heme iron, found in green leafy vegetables.

 Adult men and post menopausal women: 10 mg
 Premenopausal women: 15–20 mg
 Pregnant women: 30–60 mg.
Women require greater amount than men due to the
physiological loss during menstruation.
 Adult men and post menopausal women: 10 mg
 Premenopausal women: 15–20 mg
 Pregnant women: 30–60 mg.
Women require greater amount than men due to the
physiological loss during menstruation.

Functions
Iron is required for:
 Synthesis of heme compound like hemoglobin,
myo- globin, cytochromes, catalase andperoxidase.
Thus iron helps mainly in the transport, storage and
utilization of oxygen.
 Synthesis of non-heme iron (NHI) compounds, e.g.
iron-sulfur proteins of ETC.
Functions
Iron is required for:
 Synthesis of heme compound like hemoglobin,
myo- globin, cytochromes, catalase andperoxidase.
Thus iron helps mainly in the transport, storage and
utilization of oxygen.
 Synthesis of non-heme iron (NHI) compounds, e.g.
iron-sulfur proteins of ETC.

Absorption
 The normal intake of iron is about 10–20 mg/day.
 Normally, about 5–10% of dietary iron is absorbed.
 Non-heme iron bound to organic acids or proteins is
absorbed in the ferrous (Fe2+) state into the mucosal
cell .
 Heme of food is absorbed as such by the intestinal
mucosal cells. It is subsequently broken down and iron
is released.
Absorption
 The normal intake of iron is about 10–20 mg/day.
 Normally, about 5–10% of dietary iron is absorbed.
 Non-heme iron bound to organic acids or proteins is
absorbed in the ferrous (Fe2+) state into the mucosal
cell .
 Heme of food is absorbed as such by the intestinal
mucosal cells. It is subsequently broken down and iron
is released.

Absorption, storage, and
utilization of food iron.

Transport
 The transfer of iron from the storage ferritin (Fe3+ form)
to plasma involves reduction of Fe3+ to Fe2+ in the
mucosal cell with the help of ferroreductase.
 Fe2+ then enters the plasma where it is reoxidized to
Fe3+ by a copper protein, ceruloplasmin (ferroxidase).
 Fe3+ is then incorporated into transferrin by combin- ing
with apotransferrin.
 Apotransferrin is a specific iron binding - protein. Each
apotransferrin can bind with two Fe3+ ions.
Transport
 The transfer of iron from the storage ferritin (Fe3+ form)
to plasma involves reduction of Fe3+ to Fe2+ in the
mucosal cell with the help of ferroreductase.
 Fe2+ then enters the plasma where it is reoxidized to
Fe3+ by a copper protein, ceruloplasmin (ferroxidase).
 Fe3+ is then incorporated into transferrin by combin- ing
with apotransferrin.
 Apotransferrin is a specific iron binding - protein. Each
apotransferrin can bind with two Fe3+ ions.

Storage
 Iron in plasma is taken up by cells and either incorporated into
heme or stored as ferritin or hemosiderin. Storage of iron occurs in
most cells but predominantly in cells of liver, spleen and bone
marrow.
 Ferritin is the major iron storage compound and readily available
source of iron. Each apoferritin molecule can take up about 4500
iron atoms.
 In addition to storage as ferritin, iron can also be found in a form of
hemosiderin. Normally very little hemosiderin is to be found in the
liver, but the quantity increases during iron overload.
Storage
 Iron in plasma is taken up by cells and either incorporated into
heme or stored as ferritin or hemosiderin. Storage of iron occurs in
most cells but predominantly in cells of liver, spleen and bone
marrow.
 Ferritin is the major iron storage compound and readily available
source of iron. Each apoferritin molecule can take up about 4500
iron atoms.
 In addition to storage as ferritin, iron can also be found in a form of
hemosiderin. Normally very little hemosiderin is to be found in the
liver, but the quantity increases during iron overload.

Excretion
 Iron is not excreted in the urine, but is lost from the
body via the bile, feces and in menstrual blood.
 Iron excreted in the feces is exogenous, i.e. dietary iron
that has not been absorbed by the mucosal cells is
excreted in the feces.
 Females may have additional losses due to menstruation
or pregnancy.
Excretion
 Iron is not excreted in the urine, but is lost from the
body via the bile, feces and in menstrual blood.
 Iron excreted in the feces is exogenous, i.e. dietary iron
that has not been absorbed by the mucosal cells is
excreted in the feces.
 Females may have additional losses due to menstruation
or pregnancy.

Factors affecting iron absorption
 State of iron stores in the body
 Rate of erythropoiesis
 The contents of the diet
 Nature of gastrointestinal secretions and
chemical state of iron
Factors affecting iron absorption
 State of iron stores in the body
 Rate of erythropoiesis
 The contents of the diet
 Nature of gastrointestinal secretions and
chemical state of iron

Disorders of iron metabolism
Iron deficiency and iron overload are the major disorders of
iron metabolism.

Iron deficiency
A deficiency of iron result in iron deficiency anemia. The
main causes are:
 Deficient intake
 Impaired absorption
 Excessive loss
Iron deficiency
A deficiency of iron result in iron deficiency anemia. The
main causes are:
 Deficient intake
 Impaired absorption
 Excessive loss

Iron deficiency causes low hemoglobin resulting in
hypochromic microcytic anemia in which the size of the
red blood cells are much smaller than normal and have
much reduced hemoglobin content.
Iron deficiency causes low hemoglobin resulting in
hypochromic microcytic anemia in which the size of the
red blood cells are much smaller than normal and have
much reduced hemoglobin content.

Clinical features of anemia
 Weakness, fatigue, dizziness and palpitation.
 Nonspecific symptoms are nausea, anorexia,
constipation, and menstrual irregularities.
 Some individuals develop pica, a craving for
unnatural articles of food such as clay or chalk.
Clinical features of anemia
 Weakness, fatigue, dizziness and palpitation.
 Nonspecific symptoms are nausea, anorexia,
constipation, and menstrual irregularities.
 Some individuals develop pica, a craving for
unnatural articles of food such as clay or chalk.

Iron overload
Hemosiderosis and hemochromatosis are the conditions
associated with iron overload.
Iron overload
Hemosiderosis and hemochromatosis are the conditions
associated with iron overload.

Hemosiderosis
Hemosiderosis is a term that has been used to imply an
increase in iron stores as hemosiderin without
associated tissue injury. Hemosiderosis is an initial stage
of iron overload.
Hemosiderosis
Hemosiderosis is a term that has been used to imply an
increase in iron stores as hemosiderin without
associated tissue injury. Hemosiderosis is an initial stage
of iron overload.

Hemochromatosis
Hemochromatosis is a clinical condition in which excessive deposits
of iron in the form of hemosiderin are present in the tissues, with
injury to involved organs .
 Liver: Leading to cirrhosis
 Pancreas: Leading to diabetes mellitus
 Skin: Skin pigmentation, bronzed diabetes
 Endocrine organ: leading to hypothyroidism, testicular
atrophy
 Joints: Leading to arthritis
 Heart: Leading to arrhythmia and heart failure
Hemochromatosis
Hemochromatosis is a clinical condition in which excessive deposits
of iron in the form of hemosiderin are present in the tissues, with
injury to involved organs .
 Liver: Leading to cirrhosis
 Pancreas: Leading to diabetes mellitus
 Skin: Skin pigmentation, bronzed diabetes
 Endocrine organ: leading to hypothyroidism, testicular
atrophy
 Joints: Leading to arthritis
 Heart: Leading to arrhythmia and heart failure

Selenium (Se)
 Liver, kidney, sea-foods and meat are good sources of
selenium.
 Grains have a variable content depending on the
region where they are grown.
50–200 micro gm for normal adults.
Selenium (Se)
 Liver, kidney, sea-foods and meat are good sources of
selenium.
 Grains have a variable content depending on the
region where they are grown.
50–200 micro gm for normal adults.

Functions
 Selenium functions as an antioxidant along with vitamin E.
 Selenium is a constituent of glutathione peroxidase.
 Selenium, as a constituent of glutathione peroxidase is
important in preventing lipid peroxidation and protecting cells
against superoxide (O2-) and some other free radicals.
 Selenium also is a constituent of iodothyronine deiodinase,
the enzyme that converts thyroxine to triiodothyronine
Functions
 Selenium functions as an antioxidant along with vitamin E.
 Selenium is a constituent of glutathione peroxidase.
 Selenium, as a constituent of glutathione peroxidase is
important in preventing lipid peroxidation and protecting cells
against superoxide (O2-) and some other free radicals.
 Selenium also is a constituent of iodothyronine deiodinase,
the enzyme that converts thyroxine to triiodothyronine

Deficiency manifestations
 Selenium deficiency has been associated in some areas of
China with Keshan disease, a cardiomyopathy, that
primarily affects children and women of child bearing
age.
 Its most common symptoms include dizziness, loss of
appetite, nausea, abnormal electrocardiograms, and
congestive heart failure.
Deficiency manifestations
 Selenium deficiency has been associated in some areas of
China with Keshan disease, a cardiomyopathy, that
primarily affects children and women of child bearing
age.
 Its most common symptoms include dizziness, loss of
appetite, nausea, abnormal electrocardiograms, and
congestive heart failure.

Selenium toxicity (selenosis)
Excessive selenium intake results in alkali disease,
characterized by loss of hair and nails, skin lesions, liver
and neuromuscular disorders that are usually fatal.
Selenium toxicity (selenosis)
Excessive selenium intake results in alkali disease,
characterized by loss of hair and nails, skin lesions, liver
and neuromuscular disorders that are usually fatal.

Zinc (Zn)
Total zinc content of the adult body is about 2 gm. In blood,
RBCs contain very high concentration of zinc as compared to
plasma.
Meat, liver, sea-foods, and eggs are good sources. Milk including
breast milk also is a good source of zinc.
The colostrum is an especially rich source.
15 mg per day for adults with an additional 5 mg during
pregnancy and lactation.
Zinc (Zn)
Total zinc content of the adult body is about 2 gm. In blood,
RBCs contain very high concentration of zinc as compared to
plasma.
Meat, liver, sea-foods, and eggs are good sources. Milk including
breast milk also is a good source of zinc.
The colostrum is an especially rich source.
15 mg per day for adults with an additional 5 mg during
pregnancy and lactation.

Functions
 Zinc is a constituent of a number of enzymes. For example,
– Carbonic anhydrase
– Alkaline phosphatase
– DNA and RNA-polymerases
– Porphobilinogen (PBG) synthase
 Because it is required by many of the enzymes needed for DNA
and RNA synthesis, zinc is necessary for the growth and division
of cells.
Functions
 Zinc is a constituent of a number of enzymes. For example,
– Carbonic anhydrase
– Alkaline phosphatase
– DNA and RNA-polymerases
– Porphobilinogen (PBG) synthase
 Because it is required by many of the enzymes needed for DNA
and RNA synthesis, zinc is necessary for the growth and division
of cells.

 Zinc is an important element in wound healing as it is a
necessary factor in the biosynthesis and integrity of
connective tissue.
 Zinc stabilizes structure of protein and nucleic acids.
 Zinc is required for the secretion and storage of insulin from
the β-cells of pancreas.
 Gustin, a Zn containing protein present in saliva is required
for the development and functioning of taste buds.
Therefore, zinc deficiency leads to loss of taste acuity
 Zinc is an important element in wound healing as it is a
necessary factor in the biosynthesis and integrity of
connective tissue.
 Zinc stabilizes structure of protein and nucleic acids.
 Zinc is required for the secretion and storage of insulin from
the β-cells of pancreas.
 Gustin, a Zn containing protein present in saliva is required
for the development and functioning of taste buds.
Therefore, zinc deficiency leads to loss of taste acuity

 Clinical symptoms of zinc deficiency include:
 Growth failure
 Hair loss
 Anemia
 Loss of taste sensation
 Impaired spermatogenesis
 Neuropsychiatric symptoms.
 Clinical symptoms of zinc deficiency include:
 Growth failure
 Hair loss
 Anemia
 Loss of taste sensation
 Impaired spermatogenesis
 Neuropsychiatric symptoms.

Acrodermatitis enteropathica
A rare inherited disorder of zinc metabolism is due to an
inherited defect in zinc absorption that causes low plasma
zinc concentration and reduced total body content of zinc,
it is manifested in infancy as skin rash.
Acrodermatitis enteropathica
A rare inherited disorder of zinc metabolism is due to an
inherited defect in zinc absorption that causes low plasma
zinc concentration and reduced total body content of zinc,
it is manifested in infancy as skin rash.

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