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Vitamins

Vitamins. Vitamin A: vision, epithelial tissue, growth in children Vitamin D: bone mineralization, blood Ca 2+ regulation Vitamin E: antioxidant Vitamin K: clotting factor. Fat-soluble. Vitamins. Water-soluble. Energy metabolism. Amino acid metabolism.

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Vitamins

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  1. Vitamins

  2. Vitamin A: vision, epithelial tissue, growth in children • Vitamin D: bone mineralization, blood Ca2+ regulation • Vitamin E: antioxidant • Vitamin K: clotting factor Fat-soluble Vitamins Water-soluble Energy metabolism Amino acid metabolism RBC/Neural development Collagen synthesis • Thiamine (B1) • Riboflavin (B2) • Niacin (B3) • Biotin • Pantothenic acid (B5) • Pyridoxine • pyridoxal, • pyridoxamine (B6) • Folic acid • Cobalamin (B12) • Ascorbic acid • (Vitamin C)

  3. Water-soluble Vitamins • B-Complex • Thiamine (B1) • Sources: whole-grain cereals, meats, legumes, nuts • Active form is thiamine pyrophosphate (TPP) • Functions : • Oxidative decarboxylation of pyruvicacids,conversion of pyruvic acid to acetyl coA. • In transketolationreaction,transfer of ketol group. • TPP is also essential for the process of nerve conduction and structure of nerve membrane. • Deficiency: most common in alcoholics and malnourished individuals • Decreased ATP production

  4. Manifestations • Wet beri-beri:Affects cardiovascular system • 1. Extensive edema. • 2. Congestive heart failure. • Dry beri-beri: Affects nervous system. • 1. Polyneuritis. • 2. Hyperesthesia • Muscle wasting and loss of weight. • Wernicke’s disease • 1. Occular distrubance • 2.Ataxia

  5. Cont. • Korsakoff’s syndrome • Defective memory. • Impaired learning ability. • Recommended dietary allowance:RDA • 1-1.5mg/day.

  6. 2. Riboflavin (B2)(UV sensitive) • Sources: milk, eggs, meat, poultry, fish, green leafy vegetables • Active forms are FMN and FAD • FAD: cofactor in succinate dehydrogenase reaction (TCA) • FMN: component of ETC – accepts 2 electrons from NADH in NADH dehydrogenase reaction • Deficiency: not associated with major human disease but commonly seen in conjunction with other vitamin deficiencies • Deficiency symptoms include: dermatitis • cheilosis • glossitis

  7. Cont. • Occular disturbance. • 1. photophobia • 2. vascularization of cornea. • Angular stomatitis: inflammation of angles of mouth. • 3. Seborrheic dermatitis:inflammtion of sebaceous glands of skin. • Requirements: 1.3 -1.7 mg/day.

  8. 3. Niacin (nicotinic acid) (B3) • Sources: meat, whole-grain cereals, synthesis from tryptophan-containing foods (milk, eggs) • Active forms are NAD+ and NADP+ • Excess tryptophan is metabolized to niacin and supplies approx. 10% of RDA • Clinical correlations: • deficiency causes pellagra(4D) • RDA effective in treatment of type IIbhyperlipoproteinemia ( reduces lipolysis of fatty acids, activates lipoprotein lipase , less VLDL and LDL)

  9. Requirements • Niacin 13-19mg/day depending upon the age and sex • Tryptophan 13 x 60 mg/day to 19 x 60 mg/day. • Hypervitaminonsis • 1. Skin flushing. • 2. Gastrointestinal disturbance. • 3. Pruritis

  10. 4. Pantothenic acid (B5) • present in a wide variety of foods esp. eggs, liver, yeast • Active form is Cofactor A (i.e. succinyl CoA, acetyl CoA, fatty acyl CoA) • part of fatty acid synthase complex • Clinical correlations: • deficiency is uncommon • no RDA established

  11. 5. Pyridoxine, pyridoxal, pyridoxamine (B6 derivatives) • Sources: whole-grain cereals, eggs, meat, fish, soybeans, nuts • Active form is pyridoxal phosphate • Important function in transamination, deamination, decarboxylation, and condensation reactions

  12. 5. Pyridoxine, pyridoxal, pyridoxamine (B6 derivatives) • Clinical correlations: • Isoniazid (isonicotinic acid hydrazide) used to treat TB may induce B6 deficiency -> need B6 supplement while taking isoniazid • Deficiencies seen in alcoholics, infants given deficient formula, and women on oral contraceptives • Toxicity: neurological symptoms if >2g/day

  13. 6. Cobalamin (B12) contains Co, corrin ring system • Sources: meats, shellfish, poultry, eggs, dairy products (not present in plants) • Active forms are 5’-deoxyadenosylcobalamin (fatty acid oxidation) and methyl cobalamin (met synthesis) • Needed for synthesis of methionine from homocysteine, forming tetrahydrofolate • isomerization of methyl malonyl CoA to succinyl CoA. • Vit B12 hepls in the formation of myelin sheath through the metabolism of odd numbers fatty acids.

  14. Vitamin B12 Metabolism • The absorption of vitamin B12 ,it combines with a glycoprotein secreted by the gastric parietal cells called intrinsic factors • This IF-B12 complex binds with specific ileal receptors. • A pH above 6 and Ca ions required to promote vitamin absorption. • Vitamin B12 passes via portal circulation to the liver to the general circulation. • Vitamin B12 is carried in the plasma by number of carrier globulins ,namely transcobalmin II ,transcobalmin I and R proteins.They transport B12 to the tissue .It bind to specific cell receptor cell surface to enter the cell.

  15. Clinical correlations: • Deficiency causes accumulation of abnormal fatty acids -> neurological effects • Pernicious anemia– not usually a vitamin deficiency but inability to absorb B12 (no intrinsic factor) because of autoimmune destruction of parietal cells • Treatment: Lifetime intramuscular injections of cyanocobalamin • Anemia reversible, but not CNS effects

  16. Clinical correlations: • deficiency in either vitamin B12 or folic acid causes increase in plasma homocysteine levels, which damages blood vessels and poses a risk for thrombosis • megaloblastic anemiamust be treated with both folate and vitamin B12 • other causes of B12 deficiency: • pure vegan diet • terminal ileal disease (i.e. Chron’s disease)

  17. 6. Biotin • Sources: bacterial synthesis in intestine,eggyolk,yeast, animal tissues and tomatoes. • Important function as cofactor in carboxylation reactions (I.e. pyruvatecarboxylase, acetyl CoAcarboxylase) • Clinical correlations: • Deficiency (uncommon) caused by: • 1. eating raw egg whites (contain avidin) • 2. broad-spectrum antibiotics (kill intestinal bacteria)

  18. 7. Folic acid • Sources: green leafy vegetables, liver, lima beans, whole-grain cereals • Active forms are tetrahydrofolate derivatives • Important in 1-C transfer reactions especially in DNA synthesis • Metabolism: • Folic acid ingested as polyglutamates -> converted to monoglutamates in jejunum by intestinal conjugase enzyme • Monoglutamate is reabsorned in jejunum. • Folic acid circulated and is measured in blood as methyltetrahydrofolate. • Only a 3-4 month supply is stored in the liver.

  19. Clinical correlations: • Folic acid deficiency is most common vitamin deficiency in U.S., most common in pregnant women and alcoholics • Folic acid before pregnancy reduces risk of neural tube defects.

  20. Deficiency caused by: 1. Diet lacking in fruit and vegetable 2. Drugs: methotrexate, trimethoprim (chemotherapeutic drugs which inhibit dihydrofolate reductase thus preventing purine and pyrimidine biosynthesis -> kills blast cells and causes macrocytic anemia) 4. Oral contraceptives (block reabsorption of monoglutamate in jejunum) 5. Alcohol (block reabsorption of monoglutamate in jejunum) 6. Rapidly-growing cancers (malignant cells use folic acid) 7. Small bowel malabsorption (I.e. celiac disease) 8. Sulfa drugs (sulfanilamide) inhibits folic acid synthesis

  21. B. Non-B-Complex • Ascorbic acid • Source: citrus fruits, potatoes, tomatoes, green vegetables • Action – coenzyme in hydroxylation reactions esp. proline and lysine in collagen synthesis • antioxidant activity – helps prevent formation of free radicals • Clinical correlations: • deficiency and cigarette smoking causes scurvy • megadoses claimed to be effective against common cold (very controversial) • no toxic effects but oxidized form (dehydroascorbic acid) is toxic • Excess intake may cause renal calculi (kidney stones)

  22. Classification and Functions of Vitamins • Vitamin A: vision, epithelial tissue, growth in children • Vitamin D: bone mineralization, blood Ca2+ regulation • Vitamin E: antioxidant • Vitamin K: clotting factor Fat-soluble Vitamins Water-soluble Energy metabolism Amino acid metabolism RBC/Neural development Collagen synthesis • Thiamine (B1) • Riboflavin (B2) • Niacin (B3) • Biotin • Pantothenic acid (B5) • Pyridoxine • pyridoxal, • pyridoxamine (B6) • Folic acid • Cobalamin (B12) • Ascorbic acid • (Vitamin C)

  23. Vitamin A • Vitamin A consists of three biologically active molecules, retinol, retinal (retinaldehyde) and retinoic acid • Essential for vision, reproduction, growth and maintenance of epithelial tissues • Associated with reduced heart disease, lung cancer, skin cancer, lower cataract risk • Sources: liver, kidney, cream, butter, egg yolk • RDA: 1000 retinol equivalents (RE) for males • 800 retinol equivalents (RE) for females • 1 RE = 1 mg retinol, 6 mg b-carotene, or 12 mg of other carotenoids

  24. Each of these compounds are derived from the plant precursor molecule,b-carotene(a member of a family of molecules known ascarotenoids). • Beta-carotene, which consists of two molecules of retinal linked at their aldehyde ends, is also referred to as the provitamin form of vitamin A. • Retinol -> dietary supplements • Retinoic acid -> dermatological applications

  25. Metabolism of Vitamin A • Ingested b-carotene is cleaved in the lumen of the intestine by b-carotene dioxygenase to yield retinal. • Retinal is reduced to retinol by retinaldehyde reductase, an NADPH requiring enzyme within the intestines.

  26. Vision and the Role of Vitamin A • vision is the function of 11-cis retinal coupled to opsin to form • rhodopsin • Rhodopsin is coupled to a G-protein called transducin. When • exposed to light 11-cis is converted to all-trans-retinal. This • conformational change activates transducin. Increased GTP binding. • cGMP maintains Na+ channels in open state • activation of cGMP phosphodiesterase • drop in cGMP closes channels and leads to hyperpolarization of the • rod cell

  27. Additional Roles of Retinol • Growth – retinoic acid required for appetite, bone growth • Spermatogenesis (males) and prevention of fetal resorption (females) – requires retinal or retinol (retinoic acid doesn’t work!) • Maintenance of epithelial cells + mucus secretion

  28. Vitamin A - Clinical Correlations • 2. Acne, psoriasis • Retinoic acid used to treat mild acne (Darier’s disease) • Tretinoin (all-trans retinoic acid) used to treat skin aging (topical) • Isotretinoin (13-cis retinoic acid) used to treat severe acne (oral admin) • ** teratogenic • contraindicated for women with childbearing potential • prolonged treatment with isotretinoin causes hyperlipidemia and increased LDL/HDL ratio

  29. Vitamin A - Clinical Correlations • Dietary Deficiency • treated with retinol or retinyl esters • night blindness early sign of Vitamin A deficiency • increased susceptibility to infection and cancer • severe deficiency leads to progressive keratinization of the cornea • (xerophthalmia)

  30. Vitamin A - Clinical Correlations • 3. Toxicity • Hypervitaminosis A = > 7.5 mg per day • Early signs of Hypervitaminosis A : dry, pruritic skin, hepatomegaly, rise in intracranial pressure (can mimic brain tumor) • teratogenic

  31. Vitamin D(calciferol) • Sources : generated from the provitamin ergosterol(in plants)and 7-dehydrocholesterol(in human and animals) by ultra violet irradiation of sun. • Liver ,egg and yeast are rich diet • Fish liver oils.cod liver oil,shark liver oil.

  32. Metabolism of Vitamin D • D2 and D3 are activated in vivo by 2 sequential hydroxylation reactions • 1. 25-hydroxylase in liver • 25-cholecalciferol-1-hydroxylase in kidney • product is 1,25-dihydroxycholecalciferol (1,25-diOH D3)

  33. Function of Vitamin D – to increase plasma Ca2+ • stimulates calcium (and phosphate) uptake • by intestine by inducing synthesis of a • calcium-binding protein • increases calcium reabsorption by the • kidney • mobilizes bone calcium by resorption

  34. Vitamin D - Clinical Correlations • Deficiency of vitamin D • Rickets – in children • collagen matrix formed but mineralization is incomplete • soft pliable bones – “bow-legged” • mutation in vitamin D receptor can cause vitamin D-independent rickets • 2. Osteomalacia – in adults • demineralization of bones = fractures • (less sunlight) problem more severe • 3. Renal rickets(renal osteodystrophy) = chronic renal failure • results in low synthesis of 1,25 vitamin D3 (calcitrol) • calcitrol supplementation is effective treatment

  35. Vitamin D - Clinical Correlations • Toxicity • Very toxic • vitamin D can be stored -> accumulates in liver and fat • high doses = loss of appetite, nausea, thirst, hypercalcemia (leads to calcium deposits in arteries and kidneys

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