MINERALS DEFECIENCY FUNCTIONS

1. M I N E R A L S
MICRO

2. Micro minerals are often referred to as trace
minerals, meaning they are present at low levels
in the body or required in smaller amounts in
the animals diet. Micro minerals include
chromium, cobalt, copper, fluorine, iodine, iron,
manganese, molybdenum, selenium, and zinc

3. • Iron was used in very early years as a medicine.
• In the Ebers papyrus of Egypt, rust was prescribed as an ointment
to prevent baldness.
• In early Greece, a solution of iron in wine was considered as a
means to restore male potency.
• In the 17th century the treatment of chlorosis included iron
supplementation.
• Later it was found that chlorosis is a iron deficiency.
• Even before the role was in nutrition of iron firmly established, the
first clinical description of iron overload disease was reported in
1871.
• The major aspects of iron metabolism were elucidated before
1960.

4. FUNCTION
Carrier of Oxygen and Carbon Dioxide:
The major role of iron is to permit the transfer of oxygen and carbon dioxide from one tissue
to another. It does this as a part of haemoglobin in blood and myoglobin in muscle but also as
a part of several tissue enzymes essential in cell respiration. The exchanges are involved
primarily in the release of energy within
the cell.
Blood Formation:
Haemoglobin is an essential component of the mature red blood cell. Erythrocytes begin in
the bone marrow as immature cell lnown as erythroblasts, which contain a nucleus. mature in
the bone marrow, they synthesize haem, an iron-containing protein from the amino acid
glycine and iron along with vitamin B and copper. Haem now unites with a protein called
globin, and forms haemoglobin.
The RBC has no nucleus and so cannot synthesize the enzymes essential for metabolism. As a
result it lives only as long as the enzymes present at its maturity remain functional--usually
about 4 months. As RBCs die, they are removed from the blood by the cells of the liver, bone
marrow and spleen. In the spleen, iron and amino acids of the haemoglobin molecule are
salvaged and recycled.

5. Anti-infective Agent
During iron deficiency, there is a decrease in the producion of
iron-containing cnzymes and other immune substances neeiler
to destroy infectious organisms, and iron-deficient people are
less able to fight infections. Lactoferrin in human milk is an
iron-containing substance that is effective against E. coli
organisms in the gastrointestinal tract of infants. Here
lactoferin binds iron and so it is not available for bacterial
growth.

6. Other Functions
Iron performs many other important functions including the following:
б
catalyses the conversion of B-carotene to vitamin A.
б
It is involved in the synthesis of purines which are required for formation of DNA and RNA.
б
It is involved in the synthesis of carnitine, which is needed for fatty acid transport.
Synthesis of collagen, the structural protein surrounding
the cell.
It is necessary for antibody production.
Other Functions
Iron performs many other important functions including the following:
catalyses the conversion of B-carotene to vitamin A.
It is involved in the synthesis of purines which are required for
formation of DNA and RNA.
It is involved in the synthesis of carnitine, which is needed for fatty acid
transport.
Synthesis of collagen, the structural protein surrounding
the cell.
It is necessary for antibody production.

7. IRON METABOLISM
• The metabolism of iron can be described as two loops, one internal and one external. The
internal loop is represented mainly by the formation and destruction of red cells.
• When a red cell dies, after about 120 days, it is usually taken care of by the macrophages of
the reticuloendothelial system of the body.
• The iron is released and delivered to the transferrin molecules in the plasma. Transferrin, a
protein specially designated for iron transport in plasma, brings the iron back to the red-cell
precursors in the bone marrow, or to other cells in different tissues under growth and
development.
• There is thus a continuous reutilization of the iron from haemoglobin in the red cells back to
new red cells or other tissues.

8. ABSORPTION:-
Ingested inorganic iron is solubilized and ionized by the
acid gastric juice, reduced to the ferrous(Fe++)form
Absorption occurs at small intestine, most edficiently
duodenum.
MIBP( membrane iron binding protien) which tranfers iron
into cell

9. IRON DEFICIENCY
When iron can no longer be mobilized from the iron stores, insufficient
amounts of iron will be delivered to transferrin, the circulating transport
protein for iron. The binding sites for iron on transferrin will thus contain
less and less of iron. This is called reduction of the transferrin saturation
(TS). When the transferrin saturation drops to about 16% which is
considered to be a critical level, the red-cell precursors get an insufficient
supply of iron.
Simultaneously the supply of iron to other tissues by transferrin will also
be impaired. Cells with a high turnover rate, e.g. intestinal mucosa cells
with a short lifespan are immediately affected.
Hence an iron deficiency can be seen in growing tissues.
The haemoglobin formation is also impaired. When the deficiency is
sufficiently severe and longstanding will lead to a microcytic hypochromic
anaemia.

10. IODINE
IODINE

11. lodine is an essential constituent of the thyroid hormone thyroxine. The major
role of iodine in nutrition arises from the importance of thyroid hormones to
growth and development.
Todine was discovered by Courtois in 1811 during the course of making
gunpowder. Some seaweed ash was being used from which the iodine
vaporized as a violet vapour. The element was discovered in the thyroid gland
by Baumann in 1895.
The relation of iodine deficiency to the enlargement of the thyroid gland or
goitre was first shown by David Marine, who found that hyperplastic changes
occurred regularly in the thyroid when iodine concentration fell below 0.1%.
Subsequently Marine and Kimball (1922) demonstrated that endemic goitre
could be prevented and substantially reduced by the administration of small
amounts of iodine.
Mass prophylaxis of goitre with iodized salt was first introduced in
Switzerland and in Michigan.

12. IODINE DEFICIENCY DISORDERS
The effects of deficiency are evident at all stages, the foetal stage, neonatal stage and infancy
which are periods of rapid growth

13. FUNCTIONS OF COPPER
1. Copper plays a part in preventing anaemia by
i. aiding in iron absorption
ii. stimulating the synthesis of haem or globin
releasing stored Fe from ferritin
Micro Minerals
iv. ferroxidase 1 and It or ceruloplasmin are involved in the oxidation of ferrous to ferric ion.
1. Required for synthesis of phospholipids wlich are esential in the formation of myelin
surrounding nerve fibres.
FUNCTIONS OF COPPER
1. Copper plays a part in preventing anaemia by
i. aiding in iron absorption
ii. stimulating the synthesis of haem or globin
releasing stored Fe from ferritin
Micro Minerals
iv. ferroxidase 1 and It or ceruloplasmin are involved in the oxidation of ferrous to ferric ion.
1. Required for synthesis of phospholipids wlich are esential in the formation of myelin
surrounding nerve fibres.

14. COPPER
The adult body contains about 100-180 mg of copper. It is present in all tissues but liver,
brain, heart and kidney contain the highest arnounts.
In blood, copper is present in equal amounts in plasma
(0.115 Mg/100 ml) and erythrocytes (0.11 ug/100 g).
About 90% of plasm a copper is present in ceruloplasmin while 60% of RBC copper is
present in a protein called erythrocuprein.
0.3% copper is present in a protein called cerebrocuprein which is present in the brain. Adult
liver contains about
10-15 mg copper, kidney contains 10 mg and brain also contain
10 mg.

16. COPPER TOXICITY OR WILSON'S DISEASE
It is a rare hereditary disorder of copper metabolism. In Wilson's disease about 50% of ingested copper is
absorbed as compared to the normal 2-10%.
Copper is toxic when it exists as the unbound copper ion as it acts as an inhibitor to many enzyme systems.
There is an accumulation of copper in the liver, brain and kidney and cornea of the eye where it is identified
by brown or green rings.
If intake of copper salts is 10% higher than normal it can lead to nausea and vomiting.
Clinical Features of Wilson's Disease
The biochemical abnormality in Wilson's disease is present from birth but clinical signs do not appear until
adolescence.
1. Hepatic type-_-liver cirrhosis eventually leading to liver failure.
2. Cerebral type--progressive dementia and loss of emotional control and Parkinsonism.
3. Eye lesions- -Causes a golden brown yellow or green ring around the cornea. This lesion is called Kayser
Fleischer ring.