This document discusses iron absorption, transport, storage, excretion, functions, deficiency, and toxicity in the human body. It notes that iron is an essential nutrient that is vital for oxygen transport and many enzyme systems. It is absorbed in the duodenum and jejunum and transported by transferrin in the bloodstream. Iron is stored in the liver bound to ferritin and hemosiderin. Deficiency can cause fatigue and anemia while toxicity is caused by excessive absorption leading to organ damage.

1. NAME : AABIDA
ROLL NUMBER:20051110007
STREAM: DCLN
TOPIC: IRON ABSORPTION,
TRANSPORT, STORAGE, EXCRETION,
FUNCTIONS, DEFICIENCY AND TOXICITY.

2. INTRODUCTION
• IRON IS ONE OF THE ESSENTIAL HEAVY METALS FOR HUMAN NUTRITION, AND IT
IS A VITAL ELEMENT FOR HUMAN LIFE.
• IT PLAYS CRITICAL ROLES IN OXYGEN AND ELECTRON TRANSPORT, CELL
DIVISION, DIFFERENTIATION, AND REGULATION OF GENE EXPRESSION.
• 70% OF THE IRON IN THE HUMAN BODY BINDS TO THE HEMOGLOBIN, THE
PIGMENT OF RED BLOOD CELLS (RBCS) THAT GIVES THE BLOOD ITS RED COLOR,
AND THE REST BINDS TO OTHER PROTEINS, SUCH AS MYOGLOBIN,
TRANSFERRIN, AND FERRITIN, OR IS STORED IN THE CELLS.
• TWO TYPES OF IRON CAN BE FOUND IN FOODS, INCLUDING HEME AND NONHEME. HEME IRON
IS PRESENT ONLY IN ANIMAL PRODUCTS SUCH AS MEAT, FISH, AND POULTRY, WHEREAS NON
HEME IRON IS FOUND IN FRUITS, VEGETABLES, DRIED BEANS, NUTS, GRAIN PRODUCTS
• . HEME IRON IS ABSORBED WITH BETTER EFFICIENCY FROM THE INTESTINE THAN NONHEME
IRON.

3. TOTAL IRON CONTENT
• In humans, the total quantity of iron in the body varies with
haemoglobin concentration, body weight, gender and the
amount of iron stored in various tissues.

4. SOURCES OF IRON

5. IRON ABSORPTION
• Iron absorption occurs predominantly in
the duodenum and upper jejunum
• A transporter protein called divalent
metal transporter 1 (DMT1) facilitates
transfer of iron across the intestinal
epithelial cells.
• Iron within the enterocyte is released via
ferroportin into the bloodstream. Iron is
then bound in the bloodstream by the
transport glycoprotein named transferrin.
Both DMT-1 and ferroportin are found in
a wide variety of cells involved in iron
transport, such as macrophages.

6. ABSORPTION OF NON-HAEM IRON
Uptake of iron by enterocytes: Ferrous iron
transverse the brush border of the intestine
better than ferric ions.
. After Tansversing the brush border, iron
binds to the receptor on the luminal surface of
enterocyte and is transported inside the cell.
Intra enterocyte transport:iron is transported
through the enterocyte to the basal lateral
membrane by iron binding protein-
mobilferrin.
.The iron which is not transport across cell for
release is stored as ferritin in mucosal cells.
Extra enterocyte transfer: After crossing
baso-lateral membrane, it binds to plasma
protein transferrin(iron is oxidized before it
binds to transferrin brought by ceruplasmin).
ABSORPTION OF HAEM IRON

7. FACTORS AFFECTING IRON ABSORPTION

8. TRANSPORT AND STORAGE
• Transferrin is a glycoprotein and has two binding sites for Fe3+. It
acts as an iron transport protein. Normally, in plasma it is one-third
saturated with ferric ions.
• Transferrin distributes iron to those tissues which have a demand for
its utilization. The transferrin–iron complex enters the cell through
specific receptors and the iron ions are released for metabolic
functions. The affinity of transferrin for Fe is extremely high, but
decreases progressively with decreasing pH below neutrality. When
not bound to iron, transferrin is known as “apotransferrin.
• In iron deficiency, transfenin saturation is reduced while in iron
overload, tansferrin saturation gets increased.

9. • Any absorbed iron in excess
of body needs is stored in the
liver, in two forms, as ferritin
and hnemosiderin.
• Ferritin and haemosiderin are
the two major iron storage
proteins.

10. EXCRETION
• People lose a small but steady amount
by gastrointestinal blood loss, sweating
and by shedding cells of the skin and
the mucosal lining of the gastrointestinal
tract.
• Daily losses in adult man are between
0.9 -1.05mg . About 0.08mg lost via
urine, 0.2mg via skin, and remaining in
the faeces.
• Women in the reproductive age lose
more iron Owing to menstrual cycle,
almost 1-2 mg.

11. FUNCTIONS OF IRON
• Iron plays a central role in many
biochemical processes in the body.
These include oxygen transport and
storage, assisting with immunity and
contributing to enzyme systems
• The key function of iron is to facilitate
oxygen transport by haemoglobin, the
oxygen-carrying pigment of the
erythrocytes (red blood cells).
• Our bodies need iron to convert blood sugar to
energy. It helps boost haemoglobin production and
thus increases the transport of oxygen to help
alleviate fatigue and tiredness.

12. DEFICIENCY OF IRON
• Iron deficiency is one of the most prevalent in
nutritional deficiency in the world today.
• It is estimated that two billion people worldwide
suffer from different degrees of iron deficiency
about half of them, manifesting iron deficiency
anaemia.
• The first stage is depletion of storage iron with
serum ferritin levels starting to decline. ,
• As iron stores get increasingly depleted, iron
deficiency develops which is the second stage.
During this stage, in addition to low serum ferritin
levels, transfenin saturation is also reduced and
erythrocyte protoporphyrin is elevated.
• when iron deficiency progresses to
anaemia, haemoglobin levels start declining;
this is the third and final stage of iron
deficiency.
• The functional effects of iron deficiency
anaemia result from both a reduction in
circulating haemoglobin and a reduction in
iron-containing enzymes and myoglobin.
• These include:
• fatigue, restlessness and impaired work
performance,
• disturbance in thermoregulation,
• impairment of certain key steps in immune
response,
• adverse effects on psychomotor and mental
development particularly in children, and
• increased maternal and perinatal mortality
and morbidity .

14. IRON TOXICITY
• An excessive body burden of iron can
be produced by greater-than-normal
absorption from the alimentary canal,
by parenteral injection or by a
combination of both.
• people with genetic defects develop
iron overload as it occurs in idiopathic
haemochromatosis. It is a hereditary
disorder of iron metabolism
characterized by abnormally high iron
absorption owing to a failure of iron
absorption control mechanism at the
intestinal level. High deposits of iron in
the liver and the heart can lead to
cirrhosis, hepatocellular cancer,
congestive heart failure and eventual
death.

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