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 RETINAo 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 DEFICIENCYCREATININURIAMUSCULAR WEAKNESSRBCs FRAGILITY

BIOCHEMICAL ROLE OF VITAMIN- E NATURE'S MOST POTENT FAT SOLUBLE

ANTIOXIDANT SELENIUM METABOLISM1. 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 STERILITYo 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 DIETCAUSES 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

FUNCTIONS1. 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-K1. CAUSES MOST COMMON FAT MALABSORPTION SYNDROMEo PANCREATIC DYSFUNCTIONo 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