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RDA
• Males = 10mg/day
• Females = 8 mg/day
• Pregnancy = 10mg/day
• The pharmacological dose of the vitamin is
200–400 IU per day.
• There are eight naturally occurring tocopherols
out of alpha tocopherol is most active form .
• Absorption :- absorbed along with other fats
and needs the help of bile salts occur in small
intestine.
• Packed in chylomicrons & transported in
plasma.
• It is stored in adipose tissue.
Role In lipid Peroxidation
• Vitamin E is the most powerful anti-oxidant.
It protects lipid peroxidation and also protects the
plasma membranes from the attack of free radicals.
Vitamin E protects RBC from hemolysis . By
preventing the peroxidation , it keeps the structural
and functional integrity of all cells.
• The aging process is due to the cumulative effects of
attack of the free radicals. Vitamin E also boosts
immune response. The vitamin reduces the risk of
atherosclerosis by reducing the oxidation of LDL.
Sparing action of selenium
• Lipid peroxides produced by oxidation of lipids
are neutralized by glutahione peroxidase as
second line of defence .
• This enzyme contains selenium as cofactor
• Selenium is present in glutathione peroxidase;
an important enzyme that oxidizes and destroys
the free radicals.
• Selenium has been found to decrease the
requirement of vitamin E and vice versa.
Anti atherogenic effect
• Oxidation of LDL is an critical event in
development of atherosclerosis .
• Vitamin E is known to prevent this oxidation in
the initial stage .
• But once the atherosclerosis process has started
by oxidized LDL & other cells. It is no longer
depend on the oxidation of LDL . Cytokines
released by the cells & other factors perpetrate
atherosclerosis .
• So, it play anti atherogenic role in the initial stage
Other function
• Prevention of hemolysis by maintaining RBCs
membrane integrity
• Maintaining the structural and functional
integrity of cells and organs-----antiaging factor.
• Beneficial in alzheimer’s disease , skin disease,
cancers etc.
• Anti-sterility role .
• Occur in malabsorption syndromes.
• Deficiency can also cause anemia , due to oxidative
damage to red blood cells.
• Delayed milestones in premature infants.
• Neurological deficiency :- neuropathy,
demyelization of nerves , cerebellar ataxia
• Retinal pigment degeneration, retinopathy,
peripheral neuropathy and myopathies.
• A betalipoproteniemia ( defect in chylomicron or
VLDL)
Deficiency manifestation
VITAMIN K ( coagulation factor)
• Exits in two form K1,K2
RDA & Sources
• 50-100 microgram /day
• Easily available in diet.
sources :- green leafy vegetables .
Synthesized by intestinal bacteria.
• Absorption :- require bile salt.
• Transported in blood in chylomicrons &
VLDL.
• Stored in liver.( less amount)
• The vitamin K may be derived from the diet or
intestinal bacterial synthesis
Biochemical function of vitamin K
• Vitamin K is required for the synthesis of blood
clotting factors are factor II (prothrombin);
factor VII ; factor IX , factor X .
• All these factors are synthesized by the liver as
inactive zymogens. They undergo post-
translational modification; gamma carboxylation
of glutamic acid residues. These are the binding
sites for calcium ions. The gamma
carboxyglutamic acid (GCG) synthesis requires
vitamin K as a cofactor.
• Occur activation of clotting factors.
Carboxylation at gamma carbon
Role of γ-carboxylate glutamate in
clotting factors
• γ-carboxyl group of clotting factors such as
prothrombin chelates Ca++ ions & so
helps in binding of blood clotting factors to
platelet cell membrane through –ve
charged phospholipids .
• In vitamin K deficiency , this carboxylation
does not occur & leads to coagulation
failure .
Role of warfarin as anticoagulant
Contd.
• Warfarin is dicumerol type of synthetic
anticoagulant that inhibit vitamin K2 by
competitive inhibition .
• It is then excreted leading vitamin K deficiency.
• It is used as a rat poison .
• High doses of vitamin K act as antidote for
warfarin toxicity.
Causes
• Premature infants & new born babies
- Unable to store vitamin K
- chronic liver diseases
- malabsorption from intestine
- Prolonged use of antibotics
- Prolonged use of warfarin ( anticoagulant drug)
Diagonsis
• Increased prothrombin time ( PT)
• to rule out liver disease , PT is measured
before and after giving viatmin K
• PT is between 11-14 sec.
• Clotting time is usually 6-8 min.
• Chronic use of aspirin ( MI patients) :-
increase PT .
• Hypervitaminosis K : - hemolysis , jaundice,
symptoms of brain damage
• Q1. Name vitamin E and describe its function
and deficiency manifestation??
• Q2. Name vitamin K and describe its function
and deficiency state and test used to evaluate
the deficiency ?

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Vitamin E and K Functions, Deficiency, and Testing

  • 1.
  • 2.
  • 3. RDA • Males = 10mg/day • Females = 8 mg/day • Pregnancy = 10mg/day • The pharmacological dose of the vitamin is 200–400 IU per day.
  • 4. • There are eight naturally occurring tocopherols out of alpha tocopherol is most active form . • Absorption :- absorbed along with other fats and needs the help of bile salts occur in small intestine. • Packed in chylomicrons & transported in plasma. • It is stored in adipose tissue.
  • 5.
  • 6. Role In lipid Peroxidation • Vitamin E is the most powerful anti-oxidant. It protects lipid peroxidation and also protects the plasma membranes from the attack of free radicals. Vitamin E protects RBC from hemolysis . By preventing the peroxidation , it keeps the structural and functional integrity of all cells. • The aging process is due to the cumulative effects of attack of the free radicals. Vitamin E also boosts immune response. The vitamin reduces the risk of atherosclerosis by reducing the oxidation of LDL.
  • 7. Sparing action of selenium • Lipid peroxides produced by oxidation of lipids are neutralized by glutahione peroxidase as second line of defence . • This enzyme contains selenium as cofactor • Selenium is present in glutathione peroxidase; an important enzyme that oxidizes and destroys the free radicals. • Selenium has been found to decrease the requirement of vitamin E and vice versa.
  • 8. Anti atherogenic effect • Oxidation of LDL is an critical event in development of atherosclerosis . • Vitamin E is known to prevent this oxidation in the initial stage . • But once the atherosclerosis process has started by oxidized LDL & other cells. It is no longer depend on the oxidation of LDL . Cytokines released by the cells & other factors perpetrate atherosclerosis . • So, it play anti atherogenic role in the initial stage
  • 9. Other function • Prevention of hemolysis by maintaining RBCs membrane integrity • Maintaining the structural and functional integrity of cells and organs-----antiaging factor. • Beneficial in alzheimer’s disease , skin disease, cancers etc. • Anti-sterility role .
  • 10. • Occur in malabsorption syndromes. • Deficiency can also cause anemia , due to oxidative damage to red blood cells. • Delayed milestones in premature infants. • Neurological deficiency :- neuropathy, demyelization of nerves , cerebellar ataxia • Retinal pigment degeneration, retinopathy, peripheral neuropathy and myopathies. • A betalipoproteniemia ( defect in chylomicron or VLDL) Deficiency manifestation
  • 11. VITAMIN K ( coagulation factor) • Exits in two form K1,K2
  • 12. RDA & Sources • 50-100 microgram /day • Easily available in diet. sources :- green leafy vegetables . Synthesized by intestinal bacteria.
  • 13. • Absorption :- require bile salt. • Transported in blood in chylomicrons & VLDL. • Stored in liver.( less amount) • The vitamin K may be derived from the diet or intestinal bacterial synthesis
  • 14. Biochemical function of vitamin K • Vitamin K is required for the synthesis of blood clotting factors are factor II (prothrombin); factor VII ; factor IX , factor X . • All these factors are synthesized by the liver as inactive zymogens. They undergo post- translational modification; gamma carboxylation of glutamic acid residues. These are the binding sites for calcium ions. The gamma carboxyglutamic acid (GCG) synthesis requires vitamin K as a cofactor. • Occur activation of clotting factors.
  • 16. Role of γ-carboxylate glutamate in clotting factors • γ-carboxyl group of clotting factors such as prothrombin chelates Ca++ ions & so helps in binding of blood clotting factors to platelet cell membrane through –ve charged phospholipids . • In vitamin K deficiency , this carboxylation does not occur & leads to coagulation failure .
  • 17. Role of warfarin as anticoagulant
  • 18. Contd. • Warfarin is dicumerol type of synthetic anticoagulant that inhibit vitamin K2 by competitive inhibition . • It is then excreted leading vitamin K deficiency. • It is used as a rat poison . • High doses of vitamin K act as antidote for warfarin toxicity.
  • 19.
  • 20. Causes • Premature infants & new born babies - Unable to store vitamin K - chronic liver diseases - malabsorption from intestine - Prolonged use of antibotics - Prolonged use of warfarin ( anticoagulant drug)
  • 21.
  • 22. Diagonsis • Increased prothrombin time ( PT) • to rule out liver disease , PT is measured before and after giving viatmin K • PT is between 11-14 sec. • Clotting time is usually 6-8 min. • Chronic use of aspirin ( MI patients) :- increase PT . • Hypervitaminosis K : - hemolysis , jaundice, symptoms of brain damage
  • 23.
  • 24. • Q1. Name vitamin E and describe its function and deficiency manifestation?? • Q2. Name vitamin K and describe its function and deficiency state and test used to evaluate the deficiency ?