2. Iron metabolism
• Introduction
• Sources & RDA
• Biochemical functions
• Factors affecting iron absorption
• Absorption, transport & storage
• Disorders of iron metabolism
• Case report
• RGUHS questions
3. • Most essential trace element
• Total body iron - 3 to 5 g.
• 75% present in blood & also in liver, bone
marrow & muscles.
• Iron is present in almost all cells.
• Iron containing compounds include-heme
or non-heme compounds.
4. • Heme iron containing molecules:
• Hemoglobin, myoglobin, cytochrome b, c &
cytochrome oxidase, catalase, peroxidase.
• Non-heme iron containing molecules:
• SDH, xathine oxidase, Transferrin, ferritin,
hemosiderin, iron sulfur proteins
5. • Sources:
• Rich sources - liver, eggs, fruits & yeast
• Moderate sources – meat, fish, green leafy
vegetables & cereals.
• Jaggery - good source of iron
• Milk - poor source of iron.
6. RDA
• Adult man & postmenopausal women:10 mg/day
• Premenopausal women: 15 to 20 mg/day
• Pregnant & lactating women: 30 to 60 mg/day
• Women require greater amount than men due
to physiological loss during menstruation.
7. Biochemical functions
1. Required for synthesis of
– Hemoglobin,
– Myoglobin,
– Cytochromes (ETC),
– Catalase
– Peroxidase (phagocytosis).
8. 2. Essential for synthesis of non heme iron
(NHI) compounds like,
• Succinate dehydrogenase.
• Iron-sulfur proteins.
3. Iron is associated with effective immuno-
competence of body.
9. Factors affecting iron absorption
• Factors increasing the iron absorption:
• Iron is mainly absorbed in the ferrous form.
• Ascorbic acid, cysteine & HCL favors the
reduction of ferric form of iron to ferrous form
• Small peptides & amino acids favour iron
uptake
10. Factors decreasing iron absorption
• Phytates & oxalates in the food.
• Calcium, copper, lead & phosphate content.
• Gastrointestinal diseases.
• Achlorohydria, malabsorption syndromes.
• Surgical removal of stomach or intestine.
11. Absorption, transport & storage
• Absorption:
• Upper small intestine & in ferrous form
• Iron is called as one way substance, because it
is absorbed & excreted from small intestine.
12. Transport of Iron
• Iron in the mucosal cells:
• The iron (Fe2+) entering the mucosal cells by
absorption is oxidized to ferric form (Fe3+) by
the enzyme ferroxidase (ferroxidase activity
of ceruloplasmin)
• Major sources of iron in the plasma is from
degraded erythrocytes.
• Fe3+ combines with apoferritin to form ferritin.
13. • From the mucosal cells, iron may enter the
blood stream.
• Transport of iron in the plasma:
• Iron enters plasma in ferrous state.
• It is oxidized to ferric form by ceruloplasmin -
ferroxidase activity.
• Ferric iron binds with a specific iron binding
protein-transferrin or siderophilin.
• Transport form of iron is transferrin.
• It is a glycoprotein, synthesized in liver.
14. • Normal plasma level of transferrin: 250 mg/dl.
• Normal plasma iron: 50-150 μg/dl.
• Serum iron and serum iron binding capacity:
• Total iron binding capacity (TIBC) of transferrin
is 250-450 µg/dl;
• In iron deficiency anemia, serum iron level is
decreased and TIBC is increased.
15. Storage
• Ferritin is the storage form.
• Stored in intestinal mucosal cells, liver, spleen &
bone marrow.
• In the mucosal cells, ferritin is the temporary
storage form of iron.
• Ferritin level in plasma (males: 25-380 ηg/ml,
females: 15-150 ηg/ml) is elevated in iron over
load.
16. • Ferritin level in blood is an index of body iron
stores.
• Ferritin is an acute phase protein/reactant,
elevated in inflammatory diseases.
• Hemosiderin:
• It is formed by partial degradation of ferritin.
• Present in liver, spleen & bone marrow.
• Hemosiderin accumulates when iron levels are
increased.
18. Excretion
• The normal Iron excretion is about 1mg/day.
• The major excretory pathway is through
intestine.
• Iron is not excreted in urine, but in nephrotic
syndrome loss of transferrin may lead to
increased loss of iron in urine.
19. Disorders of iron metabolism
• Iron deficiency & iron overload.
• Iron deficiency
• Iron deficiency causes a reduction in the rate
of hemoglobin synthesis & erythropoiesis.
• It can result in iron deficiency anemia
(microcytic hypochromic anemia).
20. • Causes:
• Caused by inadequate intake, impaired
absorption, chronic blood loss & increased
demand.
• Iron deficiency anemia mostly occurs in
growing children, adolescent girls, pregnant
& lactating women.
21. Clinical features
• Microcytic hypochromic anemia.
• Weakness, fatigue, dizziness and palpitation,
• Laboratory findings:
• Serum iron level is decreased & TIBC level is
increased.
• Treatment: 100 mg of iron & 500 mg of folic acid
to pregnant women.
• 20 mg of iron & 100 mg of folic acid to children.
22. Iron over load
• Hemosiderosis and hemochromatosis are
conditions associated with iron over load.
• Hemosiderosis:
• Accumulation of hemosiderin in liver & other
reticulo-endothelial system.
• There is no significant tissue destruction.
• Hemosiderosis is an initial stage of iron over
load.
23. Hemochromatosis
• Hemochromatosis: In liver, hemosiderin
deposit leads to death of cell & cirrhosis.
• Pancreatic cell death leads to diabetes.
• Deposits under skin cause yellow-brown
discoloration, called hemochromatosis.
• Hemochromatosis & diabetes are referred to
as bronze diabetes.
24. Case report - 25
• A 34 year old women visited general practitioner
because of dizziness & excessive tiredness. She was
out of breath with little walking. She always stuck to
a strict vegetarian diet. On examination, she had
pallor and spooning of nails (koilonychia). Interpret
the following laboratory findings.
Investigations Report
Hemoglobin 8.7 g%
Random blood sugar 106 mg/dl
Serum total protein 7 g/dl
Blood smear Microcytic & hypochromic RBCs
25. RGUHS Questions
1. Write in detail about iron metabolism.
2. Iron - absorption, transport & storage.
3. Disorders of Iron metabolism.
