VITAMIN - E

 ALPHA TOCOPHEROL (VIT-E) 5, 7, 8

TRIMETHYLTOCOPHEROL α, β, γ, DELTA, ETA.
ZETA AND EPSILON TYPES
 SOURCE/OCCURRENCE - (WHEAT GERM OIL)
 ABSORPTION, STORAGE AND EXCRETION
 METABOLIC ROLE/BIOCHEMICAL FUNCTION
– POTENT FAT SOLUBLE ANTIOXIDANT
– SELENIUM METABOLISM & VIT-E ACT IN
COORDINATION WITH EACH OTHER
STORED IN ADIPOSE TISSUE
 VIT-E IS A MOST IMPORTANT NATURAL ANTI
OXIDANT VIT-E APPEARS TO BE THE FIRST
LINE OF DEFENSE AGAINST PEROXIDATION
OF POLY UNSATURATED FATTY ACIDS IN
MEMBRANE IN LDL PARTICLES TO BE
MODIFIED
• CONTAINED IN CELLULAR AND SUB
CELLULAR MEMBRANE PHOSPHOLIPIDS
 α-TOCOPHEROL IS CONCENTRATED IN PHOSPHOLIPID OF
MITOCHONDRIAL, E.R. AND PL MEMBRANES
 THIS ACTION IS EFFECTIVE AT INCREASED CONC. SO IT
TENDS TO CONC IN LIPID STRUCTURES e.g. ERYTHROCYTE
MEMBRANE AND MEMBRANES OF RESPIRATORY TREE AND
RETINA
o VIT E AND SELENIUM ACT SYNERGISTICALLY AND
REDUCE THE BODY REQUIREMENT FOR EACH OTHER
o DEFICIENCY OF VIT E MAY GIVE RISE TO ANEMIA OF THE
NEWBORN DECREASED Hb AND SHORTENED LIFE OF
RBCs
SIGNS OF DEFICIENCY
 CREATININURIA
 MUSCULAR WEAKNESS
 RBCs FRAGILITY
 BIOCHEMICAL ROLE OF VITAMIN- E
 NATURE'S MOST POTENT FAT SOLUBLE
ANTIOXIDANT
 SELENIUM METABOLISM
1. ANTIOXIDANT ROLE
 FIRST LINE DEFENSE AGAINST PEROXIDATION OF
CELLULAR/ SUBCELLULAR MEMBRANE PL. THEIR
P.U.F.A CONTENT
 GLUTATHIONE PEROXIDASE ENZYME ALONG WITH
SELENIUM IS SECOND LINE DEFENSE TO DESTROY THE
PEROXIDES
 SO BY THIS MECHANISM BOTH PROTECT THE CELLULAR
AND SUBCELLULAR ELEMENTS AND THEREBY DEFEND
AGAINST THE PHYSICAL AND CHEMICAL INSULT TO
BODY
2. SELENIUM METABOLISM
 PANCREATIC FUNCTION
 RETENTION OF VIT E IN BLOOD PLASMA PROTEIN
 COMPONENT OF GLUTATHION AND THEREFORE
INDIRECTLY IT SPARES VIT E.
3. VITMIN – C, ASCORBIC ACID
REGENERATE (TOCOH) & TOCOPHEROL (VIT-E)
FROM FREE RADICAL OF TOCOPHEROL (TOCO)
 ANTIOXIDANT NUTRIENTS MAY
PREVENT DISEASE

• FREE RADICALS AND OTHER REACTIVE

MOLECULES ARE INVOLVED IN DISEASE
PROCESS.
• INCIDENCE OF DISEASE DUE TO DECREASED
ANTIOXIDANT NUTRIENTS IN BLOOD AND
DIET
• CANCER PRONE DUE TO DECREASED LEVEL
OF, SELENIUM, VIT A, ( CAROTENE, VITAMIN
C AND VITAMIN E
• INVERSE RELATIONSHIP BETWEEN
CARDIOVASCULAR DISEASE AND STATUS OF
VITAMIN E (OXIDISED-LDL ARE INCREASED)
AND VITAMIN –C- (PREVENT
ATHEROSCEROSIS)
• TOPICAL VIT E PROTECTS AGAINST
DAMAGE BY UV RAYS
RECOMMENDATION
• DUE TO ABOVE EVIDENCE CONSUMPTION
OF CEREALS, NUTS, FRUITS AND
VEGETABLES SHOULD BE INCREASED
 EFFECT OF DEFICIENCY

 IN RATS
 IN HUMAN BEING
 IN RATS
 DAMAGE TO GERMINAL EPITHELIUM
o PERMANENT MALE STERILITY
o FEMALE, LOSS OF FETUS (REVERSIBLE)
 MUSCLES (SK MUSCLE) CARDIAC MUSCLE
 HEPATIC NECROSIS
 SPINAL CORD (PARESIS)
 IN HUMAN
 FRAGILITY OF R.B.C INCREASED HEMOLYSIS
 MUSCULAR WEAKNESS C.P.K ACTIVITY
INCREASED
 CREATINURIA
 INCREASED REQ IN POLYUNSATURATED FATTY ACIDS
IN DIET
 CAUSES OF DEFICIENCY
 LIPID MALAABSORPTION
 STEATORRHOEA
 LIVER DISORDER
 RESECTED INTESTINES
 ABETALIPOPROTEINEMIA
 VITAMIN K+
SOURCE:
1. VEGETABLE OIL, LEAFY GREEN VEG. WHEAT BRAN
VIT K1 (PHILOQUINONES)
2. BY THE INTESTINAL BACTERIAL FLORA VIT-K2
[MENAQUIONE]
3. SYNTHETIC = MENADIONE VIT- K3
• ABSORPTION OF VIT K REQUIRES NORMAL FAT
ABSORPTION
• PHYLLOQUINONES AND MENAQUINONE ARE
ABSORBED AND FOLLOW THE ROUTE OF FAT
ABSORPTION
• MENADIONE BEING WATER SOL PASS DIRECTLY TO
HEPATIC PORTAL VEIN
 VITAMIN K+
• STORAGE OF VIT K IS LIMITED IN LIVER
FUNCTIONS
1. VIT K IS REQUIRED FOR THE BIOSYNTHESIS OF
BLOOD CLOTTING FACTORS, ACT AS COENZYME
FOR CARBOXYLATION OF, II, VII, IX AND X ALL OF
WHICH ARE SYNTHESIZED IN LIVER INITIALLY AS
INACTIVE PRECURSOR PROTEINS
• VIT K ACTS AS A COFACTOR OF THE CARBOXYLASE
THAT FORMS “2-CARBOXY GLUTAMATE RESIDUES”
IN PRECURSOR PROTIENS
• PROTHROMBIN (FACTOR-II) WHICH CONTAINS 10 OF
THESE RESIDUES WHICH ALLOW CHELATION OF
Ca++ IN A SPECIFIC PROTEIN PHOSPHOLIPID
INTERACTION
2. IN MAY ACT LIKE COENZYME – Q IN
RESPIRATORY CHAIN
3. SYNTHESIS OF OSTEOCALCIN, GLA
RESIDUES FOR Ca2+ BINDING FETAL
WARFARINE SYNDROME CAN RESULT
PREGNANT WOMEN
4. HYDROXYPROLINE IS ALSO PRESENT IN
OSTEOCALCIN
 THE VITAMIN K CYCLE ALLOWS
REDUCED VIT K TO BE REGENERATED
 THE VIT K RELATED METABOLIC ACTIVBITIES IN LIVER
 THE LOCUS OF ACTION OF DICUMAROL TYPE
ANTICOAGULANT IS SHOWN. THE DETAILS OF SOME
REACTIONS STILL NOT KNOWN
HEMORRHAGIC DISEASE OF THE NEW BORN IS CAUSED BY DEF
OF VIT K
 PLACENTA CAN NOT PASS VIT K. EFF. TO FETUS & GUT IS
STERILE IMMEDIATELY AFTER BIRTH
 DEFICIENCY IN ADULTS CAN RESULT DUE TO
 ANTIBIOTIC THERAPY FOR PROLONGED PERIOD
 PANCREATIC DYSFUNCTION
 BILIARY DISEASES
 ATROPHY OF MUCOSA OF GIT
 STEATORHOEA
 DEFICIENCY OF VIT-K
1. CAUSES
 MOST COMMON FAT MALABSORPTION SYNDROME
o PANCREATIC DYSFUNCTION
o BILLIARY DISEASE (BILE SALT DECREASED)
o INTESTINAL MUCOSAL ATROPHY DUE TO COELIC
DISEASE, CROHN’S DISEASE, GLUTEN
ENTEROPATHY
o ANY CAUSE OF STEATORRHOEA
 DIARRHOEA DUE TO SPRUE AND ULCERATIVE
COLITIS
 BROAD SPECTRUM ANTIBIOTIC FOR PROLONGED
PERIODS
 NEW BORN BABIES (PREMATURE)
2. EFFECTS OF DEFICIENCY
 BIOLOGICALLY ACTIVE FORMS OF CLOTTING FACTOR, II,
VII, IX AND X NOT AVAILABLE
 INCREASED PROTHROMBIN TIME (P.T)
 INCREASED CLOTTING TIME (C.T)
 TENDENCY TO BLEED PROFUSELY FROM MINOR WOUNDS
OR EVEN SPONTANEOUS BLEEDING FROM MUCOUS
MEMBRANES
 BLEEDING FROM RESPIRATOR TRACT, G.I.T URINARY
TRACT AND UTERUS
 PROLONGED USE OF ANTICOAGULANTS
 DECREASED OSTEOCALCIN AND BONE MATRIX GLA
PROTEIN
 TOXICITY
 MEGADOSE OF VIT K
 HEMOLYSIS IN INFANTS
 AGGRAVATE HYPERBILIRUBINEMIA