Vitamin E & K (fat Soluble Vitamin)

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