Water Soluble Vitamins PDF

Lippincott’s illustrated reviews Chapter 28 – Page 373 Lecture 40 Water Soluble Vitamins 1  Specific Objectives By the end of this lecture students can be able to: Understand the biochemical functions of vitamin C. Discuss symptoms of vitamin C defi...

Lippincott’s illustrated reviews Chapter 28 – Page 373 Lecture 40 Water Soluble Vitamins 1  Specific Objectives By the end of this lecture students can be able to: Understand the biochemical functions of vitamin C. Discuss symptoms of vitamin C deficiency. Understand the functions vitamin B complex. Explain diseases resulted from deficiency of different types vitamin B complex. 2  Vitamins are chemically unrelated organic compounds that cannot be synthesized in adequate quantities by humans and, therefore, must be supplied by the diet. 3 4  Properties Water soluble vitamins Fat soluble vitamins Solubility in fat Not soluble Soluble Water solubility Soluble Not soluble Absorption Absorption simple (except Along with lipids vitamin B12) Requires bile salts Carrier proteins No carrier proteins (except Present vitamin B12) Storage No storage (except vitamin Stored in liver B12) Deficiency Manifests rapidly as there is Manifests only when stores no storage (except vitamin are depleted B12) Toxicity Unlikely, since excess is Hypervitaminosis may result excreted 5 Major vitamins C and B complex A, D, E and K  Ascorbic acid (vitamin C) Only L-ascorbic acid and dehydroascorbic acid have antiscorbutic activity. Requirement of Vitamin C Recommended daily allowance (RDA) is 75 mg/day (equal to 50 ml orange juice). During pregnancy, lactation, and in aged people requirement may be 100 mg/day. 6 Biochemical Functions of Vitamin C i. Hydroxylation of proline and lysine: This process is absolutely necessary for the normal production of supporting tissues such as osteoid, collagen and intercellular cement substance of capillaries. 7  ii. Iron metabolism: Ascorbic acid enhances the iron absorption from the intestine. Ascorbic acid reduces ferric iron to ferrous state, which is preferentially absorbed. iii. Hemoglobin metabolism: It is useful for reconversion of met-hemoglobin to hemoglobin. iv. Antioxidant property: As an antioxidant, it may prevent cancer formation. v. Therapeutic Use of Vitamin C Vitamin C has been recommended for treatment of ulcer, trauma, and burns. 8 Deficiency Manifestations of Vitamin C i. Scurvy: Gross deficiency of vitamin C results in scurvy. In severe cases of scurvy, the gum becomes painful, swollen, and spongy. The pulp is separated from the dentine and finally teeth are lost. Wound healing may be delayed. ii. Anemia: In vitamin C deficiency, microcytic, hypochromic anemia is seen 9 iii. Hemorrhagic tendency: In ascorbic acid deficiency, collagen is abnormal and the intercellular cement substance is brittle. So capillaries are fragile, leading to the tendency to bleed even under minor pressure. iv. Internal hemorrhage: Internal bleeding may be seen as epistaxis, hematuria or malena. In severe cases. hemorrhage may occur in the conjunctiva and retina. V. Bones: In the bones, the deficiency results in the failure of the osteoblasts to form the intercellular substance, osteoid. There may be hemorrhage into joint cavities. 10  THIAMINE (VITAMIN B1) Thiamine pyrophosphate is the biologically active form of the vitamin. Thiamine pyrophosphate serves as a coenzyme in the oxidative decarboxylation of α -keto acids. 11 Beriberi: This is a severe thiamine-deficiency syndrome found in areas where polished rice is the major component of the diet. Signs of infantile beriberi include tachycardia, vomiting, convulsions, and, if not treated, death. Adult beriberi is characterized by dry skin, irritability, disordered thinking, and progressive paralysis. 12  RIBOFLAVIN (VITAMIN B2) The two biologically active forms are flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD). FMN and FAD are bound tightly—sometimes covalently— to flavoenzymes that catalyze the oxidation or reduction of a substrate. 13 Riboflavin deficiency Deficiency symptoms include dermatitis Cheilosis (fissuring at the corners of the mouth), glossitis (the tongue appearing smooth and purplish). 14  NIACIN (Vitamin B3) The biologically active coenzyme forms are nicotinamide adenine dinucleotide (NAD+) and nicotinamide adenine dinucleotide phosphate (NADP+). NAD+ and NADP+ serve as coenzymes in oxidation- reduction reactions. 15 Deficiency of niacin: A deficiency of niacin causes pellagra, a disease involving the skin, gastrointestinal tract, and CNS. The symptoms of pellagra progress through the three Ds: dermatitis, diarrhea, dementia—and, if untreated, death. 16  PANTOTHENIC ACID (Vitamin B5) Pantothenic acid is a component of coenzyme A (CoA), which functions in the transfer of acyl groups. Pantothenic acid deficiency is not well characterized in humans. 17  PYRIDOXINE (VITAMIN B6) Vitamin B6 is a collective term for pyridoxine, pyridoxal, and pyridoxamine, all derivatives of pyridine. All three compounds can serve as precursors of the biologically active coenzyme, pyridoxal phosphate. Pyridoxal phosphate functions as a coenzyme for a large number of enzymes, particularly those that catalyze reactions involving amino acids. 18  Dietary deficiencies in pyridoxine are rare but have been observed in newborn infants fed formulas low in B6, in women taking oral contraceptives, and in alcoholics. Toxicity of pyridoxine Pyridoxine is the only water-soluble vitamin with significant toxicity. Neurologic symptoms (sensory neuropathy) occur at intakes above 200 mg/day, an amount more than 100 times the RDA. 19  BIOTIN (Vitamin B7) Biotin is a coenzyme in carboxylation reactions, in which it serves as a carrier of activated carbon dioxide. Biotin deficiency does not occur naturally because the vitamin is widely distributed in food. Also, a large percentage of the biotin requirement in humans is supplied by intestinal bacteria. 20  FOLIC ACID (B9) Function of folic acid Tetra hydro folate (reduced folate) enter in the synthesis of amino acids, purines, and thymidine mono phosphate (TMP) (a pyrimidine found in DNA). 21 Deficiency in folic acid Inadequate serum levels of folate appear in case of: increased demand (for example, pregnancy and lactation), poor absorption caused by pathology of the small intestine, alcoholism. treatment with drugs that are dihydrofolate reductase inhibitors, for example, methotrexate. 22 1. Folate and anemia: Cause macrocytic anemias [Note: These macrocytic anemias are commonly called megaloblastic because a deficiency of folic acid or vitamin B12 causes accumulation of large, immature red cell precursors, known as megaloblasts, in the bone marrow and the blood.] 23 2. Folate and neural tube defects in the fetus: Spina bifida and anencephaly, the most common neural tube defects. Folic acid supplementation before conception and during the first trimester has been shown to significantly reduce the defects. Therefore, all women of childbearing age are advised to consume 0.4 mg/day of folic acid to reduce this risk. 24  COBALAMIN (VITAMIN B12) 25 When the vitamin B12 is deficient, unusual fatty acids accumulate and become incorporated into cell membranes, including those of the nervous system causing neurological manifestation. In contrast to other water-soluble vitamins, significant amounts (4–5 mg) of vitamin B12 are stored in the body. 26 Pernicious anemia: Vitamin B12 deficiency is rarely a result of an absence of the vitamin in the diet. Malabsorption of cobalamin in the elderly is most often due to reduced secretion of gastric acid and less efficient absorption of vitamin B12 from foods. A severe malabsorption of vitamin B12 leads to pernicious anemia. 27 Reference Book: Champe, P. C., Harvey, R. A. and Ferrier, D. R., 2005. Biochemistry “Lippincott’s Illustrated Reviews”, 5th or 6th Edition 28