Vitamin E & K (Fat Soluble Vitamin)
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Transcript of 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 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