Iron
, Iron
* Haem iron: is present in
D!t r"#i$ of Ir$ haemoglobin, myoglobin, cytochrome
oxidase,
Cytochrome b ,c1, C, oxidase (a, a3),
Total body iron content is 3 to 5g; 75% of b5, P450; catalase, peroxidase,
which is in blood, the rest is in liver, bone tryptophan pyrrolase and nitric oxide
marrow and muscles. synthase.
Blood contains 14.5g of Hb per 100 mL. About
75% of total iron is in hemoglobin, and 5% is * Non-haem iron: present in ferritin,
in myoglobin and 15% in ferritin. transferrin, haemosiderin, aconitase,
succinctness dehydrogenase, xanthine
oxidase, Fe-S in ETC.
Requ%eme& of Ir$ (ICMR)
I. Daily allowance for adult is 10mg/day of iron,
out of which about 1-2mg is absorbed.
ii. Pregnant & lactating - 25-40mg/day
iii. Children between 13–15 years need 20–30mg/
day.
iv. Menstruating women - 18-20mg/day
So'c( of Ir$ i. Leafy vegetables (20 mg/100 g) are good sources. Pulses (10 mg/100 g) and
cereals (5 mg/100 g).
ii. Liver (5 mg/100 g) and meat (2 mg/100 g)
iii. Jaggery is a good source for iron.
iv. Cooking in iron utensils will improve the iron content of the diet.
v. Milk is a very poor source of iron, containing less than 0.1 mg/100 mL.
Iron is absorbed by upper part of duodenum & jejunum.
Fact)s Influenc+g The following factors affect absorption of iron:
Abs)pti$ of Ir$ 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. About 50–
75 mg of ascorbic acid per day will be sufficient for normal iron absorption.
, Interfering Substances
Iron absorption is decreased by phytic acid (in cereals) and oxalic acid (in
leafy vegetables) by forming insoluble iron salts.. phytates and oxalates
reduce the absorption, and only about 1 mg of iron is absorbed.
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
i. 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.
ii. 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.
iii. Only ferrous (and not ferric) form of
iron is absorbed. Ferric iron is reduced to
ferrous iron by ferric reductase, an enzyme
present on the surface of enterocytes.
Ferrous iron in the intestinal lumen binds to
mucosal cell protein, called divalent metal
transporter-1 (DMT-1). This bound iron is
then transported into the mucosal cell. The
rest of the unabsorbed iron is excreted.
iv. Inside the mucosal cell,iron is oxidized to
ferric state, and is complexed with
apoferritin to form ferritin. It is kept
temporarily in the mucosal cell. If there is
anemia, the iron is further absorbed into
the blood- stream.
When iron is in excess, absorption is
reduced; this is the basis of “mucosal
block”.
v. iron release from intestinal cell to the bloodstream
Iron in the ferritin is released, then crosses the mucosal cell with the help of a transport protein
called, ferroportin. But this can happen only when there is free transferrin in plasma to bind the iron.
Iron crosses cell membrane in ferrous form. In blood it is re-oxidized to ferric state, and
transported by transferrin.
vi. Intestinal uptake of heme iron occurs with the help of heme carrier protein (HCP1).The iron is
released from heme in enterocytes by the action of microsomal heme oxygenase.
, Iron
* Haem iron: is present in
D!t r"#i$ of Ir$ haemoglobin, myoglobin, cytochrome
oxidase,
Cytochrome b ,c1, C, oxidase (a, a3),
Total body iron content is 3 to 5g; 75% of b5, P450; catalase, peroxidase,
which is in blood, the rest is in liver, bone tryptophan pyrrolase and nitric oxide
marrow and muscles. synthase.
Blood contains 14.5g of Hb per 100 mL. About
75% of total iron is in hemoglobin, and 5% is * Non-haem iron: present in ferritin,
in myoglobin and 15% in ferritin. transferrin, haemosiderin, aconitase,
succinctness dehydrogenase, xanthine
oxidase, Fe-S in ETC.
Requ%eme& of Ir$ (ICMR)
I. Daily allowance for adult is 10mg/day of iron,
out of which about 1-2mg is absorbed.
ii. Pregnant & lactating - 25-40mg/day
iii. Children between 13–15 years need 20–30mg/
day.
iv. Menstruating women - 18-20mg/day
So'c( of Ir$ i. Leafy vegetables (20 mg/100 g) are good sources. Pulses (10 mg/100 g) and
cereals (5 mg/100 g).
ii. Liver (5 mg/100 g) and meat (2 mg/100 g)
iii. Jaggery is a good source for iron.
iv. Cooking in iron utensils will improve the iron content of the diet.
v. Milk is a very poor source of iron, containing less than 0.1 mg/100 mL.
Iron is absorbed by upper part of duodenum & jejunum.
Fact)s Influenc+g The following factors affect absorption of iron:
Abs)pti$ of Ir$ 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. About 50–
75 mg of ascorbic acid per day will be sufficient for normal iron absorption.
, Interfering Substances
Iron absorption is decreased by phytic acid (in cereals) and oxalic acid (in
leafy vegetables) by forming insoluble iron salts.. phytates and oxalates
reduce the absorption, and only about 1 mg of iron is absorbed.
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
i. 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.
ii. 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.
iii. Only ferrous (and not ferric) form of
iron is absorbed. Ferric iron is reduced to
ferrous iron by ferric reductase, an enzyme
present on the surface of enterocytes.
Ferrous iron in the intestinal lumen binds to
mucosal cell protein, called divalent metal
transporter-1 (DMT-1). This bound iron is
then transported into the mucosal cell. The
rest of the unabsorbed iron is excreted.
iv. Inside the mucosal cell,iron is oxidized to
ferric state, and is complexed with
apoferritin to form ferritin. It is kept
temporarily in the mucosal cell. If there is
anemia, the iron is further absorbed into
the blood- stream.
When iron is in excess, absorption is
reduced; this is the basis of “mucosal
block”.
v. iron release from intestinal cell to the bloodstream
Iron in the ferritin is released, then crosses the mucosal cell with the help of a transport protein
called, ferroportin. But this can happen only when there is free transferrin in plasma to bind the iron.
Iron crosses cell membrane in ferrous form. In blood it is re-oxidized to ferric state, and
transported by transferrin.
vi. Intestinal uptake of heme iron occurs with the help of heme carrier protein (HCP1).The iron is
released from heme in enterocytes by the action of microsomal heme oxygenase.
