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Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
Vit dental tutorial
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Vit dental tutorial

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Biochemistry …

Biochemistry
Second Year

Published in: Health & Medicine
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  • 1. Vitamins. Dr. Arafat Ahmad Asst. Prof. Biochemistry College of medicine, UOD
  • 2. Definition & Classification. • Vitamins are organic compound required by the body in trace amounts to perform specific cellular functions. • Vitamins classified according to their solubility and there function in metabolism. • Vitamins cannot be synthesized by humans and therefore must be supplied by the diet.
  • 3. FAT SOLUBLE VITAMINS • GROUP CHARACTERISTICS • Vitamin A,D, E, K are 4 fat soluble vitamins. As a group have the following characteristics. • They are absorbed in the lymphatic system with fat. Fat soluble vitamin deficiency can occurs secondary to any condition that interfere with fat absorption such as mal nutrition, pancreatic and biliary disease.
  • 4. Deficiency and Toxicity • Must be attached to protein carriers in order to be transported through the blood in the liver and adipose tissue. • Fat soluble vitamin deficiency are slow to develop. • STORES : • Do not have to consume every day because they have body storage reserve. They can be toxic when consumed in large doses over a prolonged period of time, particularly Vit. A , and Vit D.
  • 5. RDA • RDA = RECOMMENDED DAILY ALLOWANCE • It is the amount needed / day to maintain optimal health and prevent chronic disease
  • 6. Vitamin A • Active forms : • Retinol. • Retinal. • Retinoic acid. • Beta carotene ( Plant ).
  • 7. Retinol • Retinol ( Vitamin A alcohol ) • It is primary alcohol containing beta ionone ring. • The side chain has two isoprenoid units,4 double bonds and one hydroxyl group. • Retinol is present in animal tissue as retinol esters with long chain fatty acids.
  • 8. Retinal and Retinoic acid • Retinal ( Vitamin A aldehyde) : This is an aldehyde form obtain by oxidation of retinol. • Retinol and Retinal are inter convertible. • Retinoic acid ( Vitamin A acid ).This is produced by oxidation of retinal. • Retinoic acid cannot form retinal or retinol.
  • 9. Beta carotene • Beta carotene ( pro-vitamin A ) This is found in plants. • It is cleaved in the intestine to produced 2 molecule of retinal. • In human this conversion is inefficient. • Beta carotene in human possesses only one sixth vitamin activity compared to retinal.
  • 10. RDA • Children = 400 – 600 mcg/day. • Men = 750 – 1000 mcg/day. • Women = 750 mcg / day. • Pregnancy = 1000 mcg / day.
  • 11. Absorption ,Transport and Mobilization • Dietary retinyl esters are hydrolyzed by pancreatic or intestinal brush border hydrolases in the intestine releasing retinol and free fatty acid. • Carotene are hydrolyzed by beta carotene 15 -15’-di oxygenase of intestinal cell producing two molecule of retinal which is reduced to retinol.
  • 12. In the intestinal mucosal cells • Retinol is re- esterified to long chain fatty acids, incorporated to chylomicrons and transferred to lymph. • The retinol esters are taken up by liver and stored. • Vitamin A is released from the liver as free retinol. • Zink plays and important role in retinol mobilization.
  • 13. • Retinol is transported in the circulation by the plasma retinol binding protein ( RBP). In association with pre albumin. • The Retinol –RBP complex bind to specific receptor on the cell membrane of peripheral tissue and inters the cells • Many cells of target tissue contain a cellular retinol binding protein that carries retinol to nucleus and bind to DNA like a steroid hormone.
  • 14. Wald’ visual cycle (George Wald- Nobel Prize -1968) • Rhodopsin is a conjugated protein in rods cells of retina. • It contains 11-cis retinal and the protein opsin. • The aldehyde of retinal is linked to epsilon amino group of lysine of opsin. • On exposure to light ----isomerization of 11-cis retinal to All trans retinal occurs. • This leads to a conformational changes in opsin
  • 15. Retinal epithelium • This conformational change in opsin is responsible to generation of nerve impulse. • The All trans –retinal is immediately isomerizes to 11-cis retinal by enzyme retinal isomerase. • This combine with opsin to regenerate Rhodopsin and complete the visual cycle.
  • 16. In liver • Conversion of all trans retinal to 11 cis retinal is incomplete in retinal epithelium. • Most of All trans retinal is transported to liver. • Converted to all trans retinol by enzyme alcohol dehydrogenase. • The All trans retinol is isomerizes to 11 -cis retinol which is again oxidized to 11 cis- retinal to participate in visual cycle.
  • 17. Colour Vision • Retinal –opsin complex---for colour vision • Porphyropsin----Red. • Idopsin-----------Green. • Cynopsin--------Blue. • These pigments are bleached on exposure to light, and nerve impulse is generated.
  • 18. Vitamin A-(Functions-cont.) • Growth • Reproduction ( Retinol and Retinal ) • Maintenance of epithelial cells • ( retinoic acid ) • SOURCES : Liver, kidney, cream, butter, cream, yellow of eggs, green vegetables, and fruits.
  • 19. Deficiency • Night blindness : difficult to see in dim light. • Xeropthalmia : The conjunctiva become dry, thick and wrinkled. The conjunctiva get keratinized. • Bitot’s spots : grayish-white triangular plaques firmly adherent to conjunctiva. • Keratomalacia : softening of cornea due to persistent xeropthalmia. • Blindness.
  • 20. Clinical use of Vitamin A • Acne and psoriasis : • Dermatological problem such as acne and psoriasis and skin aging are treated with retinoic acid. • Prevention of chronic disease : • Beta carotene decreased the incidence of heart disease and lung and skin cancer.( anti oxidant action ).
  • 21. Toxicity of Vitamin A • Excessive intake of vitamin A produces toxic syndrome called Hyper Vitaminosis A. • Dermatitis-(Dry-red pruritic skin), Hepatomegaly. Long bone tenderness( pain on touch) • Rise in intracranial pressure. • Congenital malformation of developing foetus.
  • 22. Vitamin D • Sources : Sun light, Fish liver oil, fish , egg yolk. • Requirement : 1. Children : 10 microgram ( 400 IU ) / Day. 2. Adults : 05 micro gram( 200 IU ) / Day. 3. pregnancy, Lactation : 10mcg (400)/ Day. 4. Above the age of 60 : 15mcg ( 600 ) / Day.
  • 23. Vitamin D • Pro vitamin : • 1. Ergosterol ( Plants ). • 2. 7-dehydrocholesterol( Animal ). • Endogenous Vitamin Precursor. • 7- dehydrocholesterol ( skin ). • Active form : Pro vitamin converted to cholecalciferol by ultraviolet light.( In skin ) • Vitamin is hydroxylated in liver to – • 25- hydroxy cholecalciferol. • Kidney forms-1,25 dihydrocholecalciferol ( Active)
  • 24. Functions • 1. Regulation of Ca and phosphates levels. • A) Increase uptake of calcium by the intestine. • (through synthesis of calcium binding protein) • B) decrease loss of calcium from kidney. • C) Increase bone resorption. • DEFICIENCY : Nutritional rickets ( children). • Osteomalacia : (adult) and renal rickets. • Most toxic of all vitamins.
  • 25. Body can make Vitamin D Sun Light-----→Skin ( 7- Dehydrocholesterol) ↓ In skin Cholecalciferol is formed ↓ In liver,25-hydroxycholecalciferol is formed ↓ In kidney,1,25-dihydrocholecalciferol is formed.
  • 26. Activation of VIT.D. • Vitamin D is a pro hormone. The cholecalciferol is first transported to liver, where hydroxylation at 25th position occurs to form 25- hydroxycholecalciferol( 25-HCC). • 25-HCC is major storage form. • In plasma, 25-HCC is bound to vitamin D binding protein. • In kidney- hydroxylation at position 1st occurs thus 1,25-dihydroxy cholecalciferol( Calcitriol) is generated----This is the active form of Vit. D.
  • 27. REGULATION OF CALCITRIOLE • The level of calcitriole is maintained by feed back control. • The rate of production is modulated by serum levels of------- • calcium,phosphorus,parathyroid hormone and calcitriole itself. • The major site of control is on the 1 alpha- hydroxylase is through PTH. • Hypercalcemia decreases calcitriole.
  • 28. • Low dietary calcium and hypocalcemia increases the rate of production of 1,25- DHCC. • The stimulatory effect of hypocalcemia on 1- alpha hydroxylase is through PTH. • The half life of calcitriole is 6-8 hrs and is mainly excreted through bile.
  • 29. Deficiency of Vitamin D • ADULTS-------- Osteomalacia • Children------- Rickets
  • 30. Causes of Vitamin D Deficiency • In people not exposed to sun light properly. • Nutritional deficiency of calcium and phosphate may produce similar clinical picture • Malabsorption of vitamin ( Obstructive jaundice and steatorrhea). • High phytate content in diet reduce the absorption of vitamin. • Abnormal Vit.D activation.
  • 31. Osteomalacia • Greek Words • Osteo = bone. • Malakia = soft. • Insufficient mineralization and increased osteoporosis, more prone to fractures. • Serum calcium and phosphate levels are low. • Serum alkaline phosphatase is markedly increase.
  • 32. Rickets • A deficiency of vitamin D or an inability to utilize vitamin D may lead to a condition called rickets. • In this condition there is weakening and softening of the bones due to extreme loss of calcium.
  • 33. Different types of rickets • 1. Classical Vitamin D rickets can be cured by giving vitamin D. • 2.The Hypophosphatemic rickets is due to defective resorption of phosphate from kidney • 3.Vitamin D and phosphate is used in treatment. • Vitamin D resistant rickets found with fanconi syndrome in which renal resorption of bicarbonate , phosphate , glucose , amino acids are deficient.
  • 34. Cont……. • Renal rickets : In kidney diseases even if vitamin D is present calcitriole is not formed. • This will respond to calcitriole administration. End organ refraction to vitamin D( Bone disease) Respond to mega dose of calcitriole.
  • 35. Hyper Vitaminosis D • Doses above 1500 IU/day for long period causes toxicity. • Symptoms are : weakness, polyurea, Intense thirst, difficulty in speaking, hypertension, weight loss. • Calcification of soft tissue called calcinosis especially in vascular and renal tissue. • Excessive sunlight does not causes Hyper Vitaminosis D.
  • 36. Vitamin K • RDA------70 mcg ( 50- 100 mcg ) • FAT Soluble • Sources : Cabbage, cauliflower, spinach, other green vegetables, and cereals. • Major role is in blood clotting.
  • 37. Vitamin K • ACTIVE FORM ----- : • PHYLLOQUINONE ( PLANTS )----K1 • MENAQUINONE ( ANIMALS )----K2 • MENADIONE ( SYNTHETIC FORM)---K3
  • 38. Absorption and storage • Absorption of vitamin K occurs in the intestinal mucosa along with chylomicrons. • Bile salts are required for the normal absorption. • Vitamin K may derived from diet or intestinal bacterial synthesis. • It is stored in the liver and transported in the plasma along with beta lipoprotein.
  • 39. FUNCTIONS • POST TRANSLATIONAL MODIFICATION OF VARIOUS BLOOD CLOTTING FACTORS LIKE , II,VII, IX, AND X. • THIS IS DONE BY CARBOXYLATION OF GLUTAMIC ACID RESIDUE WITH THE FORMATION OF GAMA-CARBOXYGLUTAMATE • CARBXYLATION OF BONE AND KIDNEY PROTEIN
  • 40. Biochemical role of Vitamin K • Vitamin K is necessary for the coagulation. • Factors dependent on Vitamin K are 1.Factor II ( prothrombin); • 2.Factor VII • 3.Factor IX ( Charismas factor). • 4. Factor X ( Stuart power factor ). • All these factors are synthesized in the liver as inactive zymogen.
  • 41. • Zymogens undergo post translational modification ( Gama carboxylation of Glutamic acid residues ). • Gama carboxy glutamic acid synthesis require vitamin K as co factor. • This is also needed for the functional activity of osteocalcin(osteoblasts of bone) as well as structural proteins of kidney, lung and spleen
  • 42. Vitamin K dependent Carboxylase • It is microsomal enzyme. • It requires reduced vitamin K , oxygen , NADPH and CO2 . In this process vitamin passes through a cycle. This process is inhibited by warferin and dicomurol.
  • 43. DIETARY DEGICIENCY • VITAMIN K –Deficiency is unusual unless the bacterial flora in gut decreased by antibiotics or other drugs or in new born babies. • TOXICITY : Vitamin K can produces hemolytic anemia due to toxic effects on the membrane of red cells.
  • 44. Clinical manifestations • 1. Hemorrhagic disease of new born is due to Vit. K deficiency. • Premature infants are having great chance to develop the deficiency state, this is due to lack of hepatic stores, limited oral intake, and absence of intestinal bacterial floora. • Prophylactic dose in new born is 1mg Menadione.
  • 45. Warferin and Dicomurol. • Competitively inhibit the gama carboxylation. • They are structurally similar to vitamin K. • They are widely used as anti coagulant drugs. • Treatment with warferin in pregnant women may lead to foetal bone abnormalities known as foetal warferin syndrome.
  • 46. Hyper Vitaminosis K • Hemolysis • Hyperbilirubinemia • Kernicterus • Brain damage. • Due to administration of large amount of vitamin K.
  • 47. VITAMIN E • RDA : 10 mg • Active form –alpha tocoferol. • Functions : Antioxidant in prevention of - non enzymatic oxidation of cell component by molecular oxygen and free radicals. Helps in RBC formation and the use of vitamin K, promotes functions of healthy circulatory system • Sources : Vegetable oil, liver, egg and wheat germ oils , nuts and green leafy vegetables.
  • 48. Deficiency • In premature infants • With defective lipid metabolism in adults. • Toxicity : • Very less toxic .
  • 49. Prevention of chronic disease • Vitamin C , vitamin E and beta carotene are known as antioxidant vitamins. • Supplementation of the diet with these vitamins, decrease the incidence of chronic diseases such as coronary heart disease and cancers. • The common chemical property though to be central to their ability to inactivate toxic oxygen free radicals
  • 50. Reactive oxygen radical arise from 1. By product of normal metabolism. 2.By exposure to sun light. 3.Ozone 4.Tobacco smoking. 5.Environmental pollution.
  • 51. Free radicals…….. • Free radicals are known to damage lipid membrane, protein and cellular DNA. • Free radicals are thought to play a role in the development of heart and lung disease, cancer and aging. • GliSODin activates the most powerful anti oxidant known , the body’s own internal defense system, including superoxide dismutase( SOD ), catalase and glutathione peroxidase(Gpx).
  • 52. Inter-relation of Vitamin E and Selenium • Selenium is present in glutathione peroxidase, an important enzyme that oxidizes and destroys the free radicals. • Selenium has found to decrease the requirement of Vitamin E and vice versa. • They act synergistically to minimize lipid peroxidation.

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