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Water soluble vitamins

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Water soluble vitamins

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Water soluble vitamins

  1. 1. WATER SOLUBLE VITAMINS Presented By: Dr. Ifat Ara Begum Assistant Professor (Biochemistry) Dhaka Medical College, Dhaka
  2. 2. INTRODUCTION TO VITAMINS Organic nutrients required in small quantities for different biological functions & maintenance of normal metabolic integrity and which generally can not be synthesized in the body or can’t be synthesized enough to meet the body needs , so must be supplied in diet. Vitamin D, K, B12, Niacin (B3) & Biotin can be synthesized in body.
  3. 3. CONTD
  4. 4. CRITERIA OF WATER SOLUBLE VITAMINS Hydrophilic & soluble in aqueous media Retain shorter period of time in the body except vitamin B12 /folic acid which is stored in the liver No carrier protein (LP/specific protein) is needed for transport Are lost rapidly by urinary excretion Active absorption of vitamin B1/B2/ folic acid & vitamin C from intestinal tract. Rest are absorbed through intestinal mucosa by passive diffusion. Absorption is not dependent on fat absorption.
  5. 5. CONTD Precursors of coenzyme for enzymes of intermediary metabolism Susceptible to heat Toxicity: Rare Deficiency s/s occurs relatively quickly on an inadequate diet, correction/cure of s/s occurs rapidly as well on administration  Regular dietary supplementation is required
  6. 6. NAME OF WATER SOLUBLE VITAMINS 1. Vitamin B Complex: -Thiamin (B1) -Riboflavin (B2) -Niacin (B3) -Pantothenic acid (B5) -Pyridoxine (B6) -Biotin (B7) -Folic Acid (B9) -Cobalamin (B12) 2. Vitamin C (Ascorbic acid)/ Non-B complex
  7. 7. VITAMIN B ACTS AS CO-ENZYMES  Vit B as coenzymes:
  8. 8. VITAMIN B COMPLEX • These vitamins are chemically not related to one another. They are grouped together, because, all of them function in the cells as coenzymes.
  9. 9. CLASSIFICATION OF VITAMIN B COMPLEX Energy releasing vitamins: Vitamin B1, B2, B3, Biotin, Pantothenic acid (Vitamin B5) Hematopoietic vitamins: Folic acid, Vitamin B12 Others: Vitamin B6 (Pyridoxine)
  10. 10. VITAMIN B1 / THIAMINE Active form (Coenzyme form): Thiamine pyrophosphate (TPP) Dietary Source: Plant source ( Whole grain cereals, green leafy vegetables, legumes, peas, nuts, beans) & Animal source (Egg, meat, fish, liver, milk & milk products) RDA: 1.5-2 mg
  11. 11. CONTD
  12. 12. CONTD Function:  Serves as a coenzyme for PDH (that catalyzes breakdown of Pyruvate to Acetyl CoA & CO2) , α-KGDH (oxidative decarboxylation of α-KG to Succinyl CoA & CO2) and transketolase (in HMP shunt pathway of glucose)  Helps to maintain nerve conduction and functioning of nervous system.
  13. 13. CONTD Deficiency Symptoms :
  14. 14. CONTD  Beriberi: Early symptoms of beriberi are anorexia & weakness. It may be wet beriberi / dry beriberi / cerebral beriberi ( Wernicke- Korsakoff syndrome) Dry beriberi : CNS manifestations are major features. Peripheral neuritis with sensory disturbances leads to complete paralysis. Wet beriberi: Cardiovascular manifestations are prominent. Edema of leg, face & serous cavities are the main features. Death occurs due to heart failure.
  15. 15. CONTD Wernicke- Korsakoff syndrome /Cerebral beriberi: Clinical features are those of encephalopathy (occurring in acute thiamine deficiency & affects CNS) plus psychosis (occurring in chronic thiamine deficiency & affects CNS) . It is seen only when the nutrition is severely affected, either due to dietary insufficiency or due to impaired absorption of thiamine. Polyneuritis: Common in chronic alcoholics.
  16. 16. CONTD Things to remember: Oxidative decarboxylation of pyruvate and α- KG have key role in energy metabolism. In thiamine deficiency, ATP production is decreased with impaired cellular functions. Glucose is the only fuel for neurons & as optimum thiamine is specifically important for glucose oxidation, so deficiency of thiamine will affect the activity of nervous system.
  17. 17. CONTD Impaired oxidation of pyruvate to acetyl CoA forces the pyruvate to be converted to lactate. Lactate acts as vasodilator leading to increased venous return, high output heart failure and edema. Thiamine is useful in the treatment of beriberi, alcoholic polyneuritis, neuritis of pregnancy & neuritis of old age.
  18. 18. VITAMIN B2 / RIBOFLAVIN Active form (Coenzyme form): FMN (Flavin + Ribitol + Phosphate), FAD (FMN + AMP) RDA: 1.5- 2 mg Dietary Source: Same as thiamine.
  19. 19. CONTD Rich sources are liver, dried yeast, egg & whole milk. Good sources are fish, whole cereals, legumes & green leafy vegetables .
  20. 20. CONTD Function:  Coenzyme in 0xidation & reduction reaction (dehydrogenation process)  Concerned with energy metabolism as prosthetic group of flavoproteins: Enzymes containing riboflavin are called flavoproteins. The 2 coenzymes are FMN & FAD. The enzyme complex contains molybdenum and iron also. During oxidation, FAD accepts 2 hydrogen atoms from substrate. In turn, FAD is reduced to FADH2
  21. 21. CONTD FADH2 when oxidized in ETC, will generate ATP molecules. FAD dependent enzymes: Succinate DH, PDH, Xanthine oxidase, α-KGDH , Acyl CoA DH
  22. 22. CONTD Deficiency Symptoms:
  23. 23. CONTD Deficiency symptoms are confined to skin & mucous membrane: i. Glossitis (Tongue) ii. Magenta colored tongue iii. Cheilosis (Lip) iv. Angular stomatitis (Angle of mouth) v. Circumcorneal vascularization vi. Dermatitis
  24. 24. VITAMIN B3 / NIACIN / NICOTINIC ACID / NICOTINAMIDE Active form (Coenzyme form): NAD (Nicotinamide + ribose + phosphate + AMP) & NADP (NAD + phosphate)
  25. 25. CONTD
  26. 26. CONTD Dietary Sources:
  27. 27. CONTD Endogenous source: Produced from amino acid, tryptophan. 1 mg niacin (nicotinic acid) is produced from 60 mg tryptophan Exogenous source: plant & animal source like thiamine. RDA: 16-20 mg (Tryptophan provides only 10% of RDA)
  28. 28. CONTD Functions:  Coenzyme in 0xidation & reduction reactions  Functional part of NAD & NADP  Role in energy metabolism. NAD dependent enzymes: PDH, LDH
  29. 29. CONTD Therapeutic use: Reduction of plasma LDL-C and raises plasma HDL-C (treatment of type IIb hyperlipoproteinemia, which is featured by raised VLDL& LDL) At a dose of 1.5 gm/D, niacin inhibits lipolysis in adipose tissues & reduces plasma FFA. Decreased plasma FA concentration causes reduced FA influx into hepatocytes leading to decreased production of VLDL & LDL
  30. 30. CONTD Deficiency symptoms:
  31. 31. CONTD Pellagra: 3D Dermatitis: Bright red erythema esp. in feet, ankles & face. Increased pigmentation around the neck is know as Casal’s necklace. Diarrhoea: Mild to severe with blood & mucous. Nausea & vomiting may also present. Dementia: Seen frequently in chronic cases. Delirium is common in acute pellagra. Irritability, inability to concentrate & poor memory are more common in mild cases.
  32. 32. VITAMIN B5 / PANTOTHENIC ACID Active form (Coenzyme form): Coenzyme A (CoA-SH) & Acyl carrier protein (ACP) RDA: 5-10 mg
  33. 33. CONTD
  34. 34. CONTD Dietary Sources: Same as thiamine. Yeast, liver & eggs are good sources.
  35. 35. CONTD Functions: Formation of active acetate (acetyl CoA), which is used as raw material for synthesis of FA, cholesterol, ketone bodies, Ach etc & can be oxidized in TCA cycle as common end product of CHO, protein & fat catabolism. Formation of active succinate (succinyl CoA), which is used for synthesis of heme and ketolysis. CoA-SH helps in FA oxidation & ACP helps in FA synthesis.
  36. 36. CONTD Deficiency symptoms: Peripheral nerve damage, burning feet syndrome, staggering gait, mental symptoms.
  37. 37. VITAMIN B6 / PYRIDOXINE Chemistry: Family of 3 closely related pyridine derivatives: Pyridoxine (alcohol-plant source), Pyridoxal (aldehyde-animal sources) & Pyridoxamine (animal source).
  38. 38. CONTD
  39. 39. CONTD Active form (Coenzyme form): Pyridoxal phosphate (PLP) RDA: 1.5-2.0 mg
  40. 40. CONTD Dietary sources: Same as thiamine.
  41. 41. CONTD Functions: Coenzyme for transamination & deamination (during amino acid metabolism) & glycogen phosphorylase (during glycogenolysis) Helps in all decarboxylation reaction of AAs (like decarboxylation of histidine and glutamate to produce histamine & GABA respectively) Porphyrin & heme synthesis Synthesis of catecholamine & serotonin
  42. 42. CONTD Deficiency symptoms: Neurological: PLP dependent enzymes function poorly. So, serotonin, epinephrine, noradrenalin & GABA are not produced properly and therefore, neurological symptoms are quite common. In children: Convulsion due to decreased formation of GABA PLP is involved in synthesis of sphingolipids, so, B6 deficiency leads to demyelination of nerves & consequent peripheral neuritis.
  43. 43. CONTD Dermatological: Deficiency of vitamin B6 affects tryptophan metabolism. Since niacin is produced from tryptophan, there will be development of niacin deficiency (Pellagra) Hematological: Hypochromic microcytic anemia occurs due to inhibition of heme synthesis. Impaired antibody production is reported as well. Disorders of AA metabolism
  44. 44. CONTD Causes of B6 deficiency: i. Treatment of TB with INH (Common cause) ii. Rare causes: Newborn infant fed with infant formula, women taking OCP, Alcoholics. Link of INH with B6 deficiency: INH forms an inactive derivative with Pyridoxal phosphate. So it is recommended to prescribe B6 rich diet during treatment with INH
  45. 45. VITAMIN B7 / BIOTIN Biotin has one carboxyl group which links with a lysine residue in the apo-enzyme. It is also known as vitamin H or coenzyme R.
  46. 46. CONTD Active form (Coenzyme form): Covalently bound prosthetic group of carboxylase enzyme. It is active as biotin. RDA: 200 microgram
  47. 47. CONTD Dietary sources: Endogenous source: Produced by gut flora which is almost sufficient to meet the body need. Exogenous source: plant & animal source like thiamine.
  48. 48. CONTD Functions: Coenzyme for carboxylation reactions / cofactor responsible for CO2 transfer in several carboxylase enzymes, like Acetyl CoA carboxylase alpha, Acetyl-CoA carboxylase beta, Propionyl-CoA carboxylase, Pyruvate carboxylase, etc. Biotin is important in fatty acid synthesis, branched-chain amino acid catabolism, and gluconeogenesis.
  49. 49. CONTD Biotin antagonists: Avidin, a protein present in egg white, has great affinity to biotin. So, addition of raw egg white in diet may cause biotin deficiency. Avidin tightly binds with biotin hampering absorption of biotin. Deficiency symptoms: Impaired fat & carbohydrate metabolism Dermatitis
  50. 50. VITAMIN B9 / FOLIC ACID / FOLATE The terms “Folic acid” and “Folate” are often used interchangeably. Folic acid, the more stable form, occurs rarely in foods or the human body but is the form most often used in vitamin supplements and fortified foods. Naturally occurring folates exist in many chemical forms. Folates are found in foods as well as in metabolically active forms in the human body.
  51. 51. VITAMIN B9 / FOLIC ACID Chemistry: It is composed of 3 constituents. The pteridine group linked with PABA is called pteroic acid. It is then attached to glutamic acid to form pteroylglutamic acid or folic acid.
  52. 52. CONTD
  53. 53. CONTD Dietary sources: Same as thiamine. Rich sources are yeast, green leafy vegetables. Moderate sources are cereals, pulses, oil seeds & egg.
  54. 54. CONTD RDA: Infant: 50 microgram Children: 100-300 microgram Adult: 400 microgram Pregnancy: 800 microgram Lactation: 500 microgram
  55. 55. CONTD Metabolism of folic acid: Natural folic acid (usually in polyglutamate form) cleaves in intestinal lumen to monoglutamyl folate & absorbed. But dietary folic acid is absorbed as such followed by its deglutamination to monoglutamyl folate in intestinal cell, from which it goes to blood.
  56. 56. CONTD Absorbed folic acid is then activated to FH4 (tetrahydrofolate) via FH2 (dihydrofolate) through 2 steps reduction process in liver. Folic acid is stored in liver to some extent . Total body store is 12-15 mg, that can support body demand for 4-6 months after stoppage of folic acid intake.
  57. 57. CONTD Functions: Carrier of 1-C units of different AAs to use them for synthesis of purines, pyrimidines, DNA, RNA, methionine, choline etc. [Common 1-C units are methyl (CH3) / methylene (CH2) / methenyl (CH) / formyl (CH=O) group] Helps in neural tube development in early fetal life.
  58. 58. CONTD Causes of folate deficiency: Increased demand but lack of intake / absorption as seen in dietary deficiency, pregnancy, drugs (like anticonvulsant drugs, etc), hemolytic anemia
  59. 59. CONTD Deficiency symptoms:  Megaloblastic anemia: Reduced DNA synthesis is the cause. In folic acid deficiency, thymidylate synthase enzyme is inhibited , so dTTP is not available for DNA synthesis. Very rapidly dividing cells in bone marrow & intestinal mucosa are therefore most seriously affected.
  60. 60. CONTD Due to failure of rapid DNA synthesis, large proerythroblasts can’t divide rapidly to make small sized mature RBC, rather premature relatively large blast cells appear in circulation leading to megaloblastic anemia  Growth failure GIT disturbances NTDs in fetus during pregnancy like spina bifida, anencephaly etc  Hyperhomocysteinemia
  61. 61. CONTD Folate Antagonists: Sulfonamides: They have structural similarity with PABA. Bacteria synthesizes folic acid from pteridine, PABA & glutamate. When sulfonamides are given , microorganisms can’t synthesize folic acid & hence their growth is inhibited. Thus sulfonamides are very good antibacterial agents, which do not affect the human cells.
  62. 62. CONTD Aminopterin & Amethopterin (methotrexate): These are powerful inhibitors of folate reductase & THFA generation. Thus these drugs decrease the DNA formation & cell division. They are widely used as anti-cancer drugs.
  63. 63. VITAMIN B12 / COBALAMIN /EXTRINSIC FACTOR OF CASTLE / ANTIPERNICIOUS ANEMIA FACTOR Chemistry: It contains one cobalt atom. Four pyrrole rings coordinated with a cobalt atom is called a Corrin ring. The 5th valency of the cobalt is linked to a benzimidazole ring. This is then called cobalamin. The 6th valency of cobalt is satisfied by any of the following groups: cyanide, hydroxyl, adenosyl or methyl.
  64. 64. CONTD Functional types:  Cyanocobalamin: Cobalamin + Cyanide. This is the commercial form. Methyl cobalamin: Cobalamin + Methyl group. It is the main circulating form.  5’-deoxy adenosyl cobalamin: Cobalamin + 5’- deoxyadenosine. It is the main storage form.  Hydroxy cobalamin: Cobalamin + Hydroxyl group. Injectable preparations are in this form.
  65. 65. CONTD Active form (coenzyme form):  Methyl cobalamin  5’-deoxy adenosyl cobalamin RDA: Infant & children: 1.0 – 1.5 microgram Adult: 3 microgram Pregnancy & lactation: 6 microgram
  66. 66. CONTD Dietary sources: Endogenous source: Produced by gut flora (negligible). Exogenous source: only animal source. Liver is the richest source.
  67. 67. CONTD Absorption of vitamin B12: Dietary vitamin B12 in intestine complexes with IF (a glycoprotein secreted by parietal cell of gastric mucosa , which is essential for absorption of vitamin B12) The complex travels through gut & eventually binds to its specific receptor in ileal mucosa Transport of bound cobalamin from ileum into the mucosal cells, where the complex is cleaved to yield free B12 that is subsequently absorbed into blood.
  68. 68. CONTD In blood B12 is transported with a protein called transcobalamin. Absorbed B12 is stored in liver , which is not depleted until 5-6 years after cessation of intake or absorption,
  69. 69. CONTD  Functions:  Interconversion of homocysteine & methionine to maintain methionine store & ensure availability of FH4 to participate in purine, pyrimidine & NA synthesis  Conversion of propionyl CoA to succinyl CoA (during metabolism of odd chain FA) and this succinyl CoA enters into TCA cycle later.  Maintains myelin sheath & epithelial cells  Helps in hemopoiesis by ensuring availability of FH4 (FH$ is needed for DNA synthesis & rapid DNA synthesis is necessary for hemopoiesis).
  70. 70. CONTD Deficiency disorders: Megaloblastic anemia: Happens due to 2ndary deficit of FH4 as a result of accumulation of folic acid as non-functional methyl-FH4 (folate trap). In FH4 deficiency, there is failure of rapid DNA synthesis, so proerythroblasts can’t divide rapidly to make small sized mature RBC and hence premature relatively large blast cells appear in circulation leading to megaloblastic anemia.
  71. 71. CONTD Neurological disorders: Due to progressive demyelination. e.g. Sub acute combined degeneration of spinal cord, peripheral neuropathy, dementia, optic atrophy Hyperhomocysteinemia & atherosclerosis: Homocysteine level in blood is related with MI.
  72. 72. CONTD Folate trap: Both B12 & folic acid participate in purine, pyrimidine & NA synthesis. Folic acid in its active form, FH4 participates directly as a carrier of 1-C unit from AAs, whereas, B12 in its active form (methyl cobalamin) acts indirectly by ensuring the conversion of methyl FH4 back to FH4, so that FH4 can again carry 1-C units to participate again in the synthesis of purine, pyrimidine & NA.
  73. 73. CONTD In B12 deficiency, methyl FH4 can’t be converted back to FH4. So, available folate is trapped in the form of non-functional methyl-FH4. This is called folate trap. It leads to impairment of the synthesis of purine, pyrimidine & NA with consequent megaloblastic anemia.
  74. 74. PERNICIOUS ANEMIA A form of megaloblastic anemia that occurs in vitamin B12 deficiency following failure of gastric parietal cells to secret IF, which is necessary for vitamin B12 absorption. Lack of IF for absorption of vitamin B12 is more common than dietary deficiency.  IF deficiency is usually caused by autoimmune disease of gastric parietal cells or by generation of anti-IF antibodies. It may be due to total / partial gastrectomy even.
  75. 75. CONTD Vitamin B12 deficiency blocks the metabolism of folic acid via folate trap metabolism, leading to functional / secondary folic acid deficiency. As FH4 is needed for DNA synthesis, there occurs impaired erythropoiesis & large proerythroblasts fails to divide rapidly to make mature RBC and blast cells appear in blood. Severe vitamin B12 deficiency following IF deficiency cause severe form of megaloblastic anemia, hence the name is pernicious anemia.
  76. 76. CONTD Megaloblastic anemia vs Pernicious anemia: Megaloblastic anemia refers to any condition which causes large red blood cells (folate deficiency, Vitamin B12 deficiency, etc.) Pernicious anemia can be thought of as a *type* of megaloblastic anemia which is caused by Vitamin B12 deficiency secondary to malabsorption of vitamin B12 due to deficiency of IF.
  77. 77. VITAMIN C / L-ASCORBIC ACID / ASCORBATE Chemistry: Water soluble and easily destroyed by heat, alkali & storage. In process of cooking, 70% of vitamin C is lost. Structural formula closely resembles that of carbohydrate (hexose) A reducing agent & the strong reducing property depends on the double bonded carbons Readily oxidized by oxygen.
  78. 78. CONTD Ascorbate means anion form of ascorbic acid. Readily excreted in urine. Since vitamin C is a strong reducing agent, the Benedict’s test will be positive in the urine sample after the vitamin administration. Active form: Ascorbic acid / Ascorbate RDA: 60-80 mg
  79. 79. CONTD Dietary sources: Citrus fruits (lemon, orange, amoloki, guava, tomato, etc) , green chili & green leafy vegetables.
  80. 80. CONTD Functions: Post-translational maturation of collagen: Done by vitamin C dependent hydroxylation of proline & lysine residues of collagen following their synthesis. Hydroxyproline & hydroxylysine are essential for the formation of cross-linking in collagen, which gives the tensile strength of the fibers.
  81. 81. CONTD Enhances absorption of iron: By reducing dietary iron (which is mostly in ferric form and cant be absorbed in such) in to readily absorbable ferrous form. Reduces serum cholesterol concentration : By synthesis of bile acids and bile salts from cholesterol in liver and thus facilitating cholesterol excretion in the form of bile salts through fecal routes.
  82. 82. CONTD Acts as anti-oxidant: Therefore, diet rich in vitamin C may reduce risk of coronary heart disease & certain cancers but clinical trials about these claims are not yet very much convincing. Helps in catecholamine synthesis Participates in steroid hormone synthesis Therapeutic use of vitamin C: Recommended for treatment of ulcer, trauma & burns.
  83. 83. CONTD Deficiency symptoms: “Scurvy” which is characterized by swollen, spongy and bleeding gums with loosened teeth, fragile blood vessels, bleeding under the skin and in deep tissues (cutaneous bleeding leading to woody leg due to capillary hemorrhage, spontaneous bruising, joint hemorrhage, epistaxis, hemorrhage in GIT, etc) , soreness and stiffness of the joints and lower extremities, swollen joints, slow wound healing, and anemia (iron deficiency anemia).

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