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MINERAL METABOLISM
IODINE & ZINC
MARYAM JAMILAH BINTI ABDUL HAMID
082013100002
IMS BANGALORE
INTRODUCTION
What is minerals metabolism?
Chemical processes undergo by minerals that occur
within a living organism in order to maintain life
IODINE
Sources:
Sea water, fish, cereals, vegetables and iodize
salt
ZINC
Sources: legumes, potato, cabbage
IODINE
 Biochemical function:
 Formation of thyroid hormones
 Thyroxine (T4)
 Tri-iodothyronine (T3)
 Total body contains: 25-30 mg of iodine
 Normal level in blood: 5-10 mg/dL
 80 % stored in the thyroid gland
 Daily requirement: 150-200 µg/day
IODINE METABOLISM
GOITROGENS
- Ingredients in foodstuffs, which prevent
utilization of iodine
- Cassava, maize, millet, bamboo shoots,
sweet potatoes and beans
THIOCYANATE
- Inhibits iodine uptake by thyroid
- Cabbage and tapioca
THIOUREA
- Inhibits iodination of thyroglobulin
Step 1: Uptake of Iodine
Step 2: Oxidation of Iodine
Step 3: Iodination
Step 4: Coupling
Step 5: Storage
Step 6: Utilization
Step 7: Hydrolysis
Step 8: Release
Step 9: Salvaging of iodine
Step 10:Transport of thyroid hormones
Step 11:Catabolism of thyroid hormones
Step 1: Uptake of iodine
-thyroid gland takes up
and concentrates iodine
Inhibition:
thiocyanate & perchlorate
Stimulate:TSH
Congenital defectiodine
trapping,maybe treated
by large doses of iodine
Step 2: Oxidation of iodine
-oxidized to active form
(I-  I+) *can only be performed in a
thyroid
-catalyzed by thyroperoxidase
-NADPH-dependent reaction
Inhibition:
Antithyroid drugs; thiourea, thiouracil
and methimazole
Stimulate:TSH
Congenital defectiodide oxidation
defect, treatment withT4 is
administered
Step 3: Iodination
-Thyroglobulin (Tgb) is
iodinated
-Tgb secreted by the
thyroid follicular cells
-So 3,5-di-iodotyrosin
(DIT) and 3-
monoiodotyrosine (MIT)
are produced
Step 4: Coupling
 Location: in the border of the follicular cells
 Some of the tyrosine residues in the thyroglobulin are aligned opposite to
each other and are coupled.
 When two DIT molecules couple, one molecule of tetraiodothyronine (T4) is
formed.
 Tri-iodo-tyronine (T3) may be formed by de-ionization of outer ring ofT4 by
5’-deiodinase.
 Under normal condition,99% is produced byT4.
 Iodotyrosyl coupling defect will be treated by giving T4
DEFICIENCY of IODINE
Children
 Cretinism
Adults
 Goiter
 Hypothyroidism
 Myxedema
ZINC
 As a cofactor:-
 Carboxypeptidase A
 DNA polymerase & RNA polymerase
 Superoxide dismutase
 Carbonic anhydrase
 Total zinc content of body: 2g (60% in skeletal
muscle, 30 % in bones)
 Daily intake for adults and children: 10 mg/day
 Daily intake for lactation and pregnancy: 15-20
mg/day
 Highest concentration of zinc: hippocampus
area of brain and prostatic secretion
 Rich dietary sources:
beans,nuts,cheese,meat and shellfish
 Copper,calcium,cadmiun,iron and phytate
will interfere with absorption of zinc.
 Zinc can be used to reduce copper absorption
inWilson’s disease
 In liver, zinc is stored in combination with a
specific protein, metallothionein.
 Zinc is excreted through pancreatic juice and to a
lesser extent through sweat.
 Zinc stabilize insulin molecules in pancreas
 Zinc containing protein (Gusten) in saliva is for
taste sensation
 Zinc dependent enzymes: carboxypeptidase,
carbonic anhydrase, alkaline phosphatase,
lactate dehydrogenase, ethanol
dehydrogenase, glutamate dehydrogenase
and superoxide dismutase.
Zinc toxicity
 intake > 1000 mg/day
 Inhalation of zinc oxide fumes
 Rat poisons
 Chronic toxicity can lead to gastric ulcer,
pancreatitis, anemia, nausea, vomiting and
pulmonary fibrosis.
 Acute toxicity is manifested as fever, excessive
salivation, headache and anemia
DEFICIENCY of ZINC
 Poor growth
 Hypogonadism
 Impaired wound healing
 Reduction in number ofT and B lymphocytes
 Depression, dementia and other psychiatric
disorders
 Impotence in male
REFERENCES
 Vasudevan, D., S, S., &Vaidyanathan, K.
(2013).Textbook of biochemistry for medical
students.New Delhi: Jaypee Brothers Medical
Publishers (P) Ltd.
Thank
you

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Mineral metabolism (iodine & zinc) -Biochemistry

  • 1. MINERAL METABOLISM IODINE & ZINC MARYAM JAMILAH BINTI ABDUL HAMID 082013100002 IMS BANGALORE
  • 2. INTRODUCTION What is minerals metabolism? Chemical processes undergo by minerals that occur within a living organism in order to maintain life IODINE Sources: Sea water, fish, cereals, vegetables and iodize salt ZINC Sources: legumes, potato, cabbage
  • 3. IODINE  Biochemical function:  Formation of thyroid hormones  Thyroxine (T4)  Tri-iodothyronine (T3)  Total body contains: 25-30 mg of iodine  Normal level in blood: 5-10 mg/dL  80 % stored in the thyroid gland  Daily requirement: 150-200 µg/day
  • 4. IODINE METABOLISM GOITROGENS - Ingredients in foodstuffs, which prevent utilization of iodine - Cassava, maize, millet, bamboo shoots, sweet potatoes and beans THIOCYANATE - Inhibits iodine uptake by thyroid - Cabbage and tapioca
  • 6. Step 1: Uptake of Iodine Step 2: Oxidation of Iodine Step 3: Iodination Step 4: Coupling Step 5: Storage Step 6: Utilization Step 7: Hydrolysis Step 8: Release Step 9: Salvaging of iodine Step 10:Transport of thyroid hormones Step 11:Catabolism of thyroid hormones
  • 7. Step 1: Uptake of iodine -thyroid gland takes up and concentrates iodine Inhibition: thiocyanate & perchlorate Stimulate:TSH Congenital defectiodine trapping,maybe treated by large doses of iodine
  • 8. Step 2: Oxidation of iodine -oxidized to active form (I-  I+) *can only be performed in a thyroid -catalyzed by thyroperoxidase -NADPH-dependent reaction Inhibition: Antithyroid drugs; thiourea, thiouracil and methimazole Stimulate:TSH Congenital defectiodide oxidation defect, treatment withT4 is administered
  • 9. Step 3: Iodination -Thyroglobulin (Tgb) is iodinated -Tgb secreted by the thyroid follicular cells -So 3,5-di-iodotyrosin (DIT) and 3- monoiodotyrosine (MIT) are produced
  • 10. Step 4: Coupling  Location: in the border of the follicular cells  Some of the tyrosine residues in the thyroglobulin are aligned opposite to each other and are coupled.  When two DIT molecules couple, one molecule of tetraiodothyronine (T4) is formed.  Tri-iodo-tyronine (T3) may be formed by de-ionization of outer ring ofT4 by 5’-deiodinase.  Under normal condition,99% is produced byT4.  Iodotyrosyl coupling defect will be treated by giving T4
  • 11. DEFICIENCY of IODINE Children  Cretinism Adults  Goiter  Hypothyroidism
  • 13. ZINC  As a cofactor:-  Carboxypeptidase A  DNA polymerase & RNA polymerase  Superoxide dismutase  Carbonic anhydrase  Total zinc content of body: 2g (60% in skeletal muscle, 30 % in bones)  Daily intake for adults and children: 10 mg/day  Daily intake for lactation and pregnancy: 15-20 mg/day
  • 14.  Highest concentration of zinc: hippocampus area of brain and prostatic secretion  Rich dietary sources: beans,nuts,cheese,meat and shellfish  Copper,calcium,cadmiun,iron and phytate will interfere with absorption of zinc.  Zinc can be used to reduce copper absorption inWilson’s disease
  • 15.  In liver, zinc is stored in combination with a specific protein, metallothionein.  Zinc is excreted through pancreatic juice and to a lesser extent through sweat.  Zinc stabilize insulin molecules in pancreas  Zinc containing protein (Gusten) in saliva is for taste sensation
  • 16.  Zinc dependent enzymes: carboxypeptidase, carbonic anhydrase, alkaline phosphatase, lactate dehydrogenase, ethanol dehydrogenase, glutamate dehydrogenase and superoxide dismutase.
  • 17. Zinc toxicity  intake > 1000 mg/day  Inhalation of zinc oxide fumes  Rat poisons  Chronic toxicity can lead to gastric ulcer, pancreatitis, anemia, nausea, vomiting and pulmonary fibrosis.  Acute toxicity is manifested as fever, excessive salivation, headache and anemia
  • 18. DEFICIENCY of ZINC  Poor growth  Hypogonadism  Impaired wound healing  Reduction in number ofT and B lymphocytes  Depression, dementia and other psychiatric disorders  Impotence in male
  • 19. REFERENCES  Vasudevan, D., S, S., &Vaidyanathan, K. (2013).Textbook of biochemistry for medical students.New Delhi: Jaypee Brothers Medical Publishers (P) Ltd.