Biochemistry of vitamins for nurses

1. VITAMINS-
BIOCHEMISTRY
Mrs. Namita Batra Guin

2. DEFINITION
• They are organic constituents of the food. they
are called as protective accessory food factors.
• They are not generally synthesized by the body
and have to be supplied in the diet in very small
quantities.
• They are essential for life and well being.

3. TYPES
• Water soluble vitamins
• Fat soluble vitamins

4. WATER SOLUBLE
VITAMINS
• Dissolve in water
• Readily excreted by kidney
• Function as a coenzyme & in energy metabolism
• Vitamin C, thiamin and riboflavin are especially
susceptible to heat and alkalinity
• Hydrophilic compounds and water leach them from
vegetables
• Marginal deficiency more is common

5. FAT SOLUBLE
VITAMINS
• Adsorbed with dietary fat in micelles
• Excreted much more slowly
• Stored in adipose tissue & liver so pose a greater
risk of toxicity when consumed in excess
• Chylomicrons containing fat-soluble vitamins are
transported via the lymph to the bloodstream and
eventually to the liver.

6. CLASSIFICATION OF
WATER SOLUBLE
VITAMINS• Thiamine
• Pantothenic Acid
• Riboflavin
• Biotin
• Niacin
• Vitamin B-6
• Folate
• Vitamin B-12
• Vitamin C

7. VITAMIN B-Complex
• It includes a group of compounds most of which
are synthesized in the GI tract by microbial flora.
• Derivatives of these vitamins act as coenzymes.
• They are not stored in the body, thus their toxicity
is generally not observed.
• Most of these are heat stable except vitamin B1
(Thiamine)

8. THIAMIN
• Also called as Vitamin B1.
• Since Thiamin has important role in nervous
system, it is also called aneurine.
• Structurally it consists of pyrimidine ring which is
linked to thiazole ring.
• It occurs in nature as thiaminhydrochloride.

9. Structure of
Thiamin

10. Structure of
Thiamin

11. ABSORPTION OF
THIAMIN
• It is absorbed from proximal small intestine by active
transport and passive diffusion.
• 90% of the thiamin is carried in the form of TPP (Thiamin
pyrophosphate) by RBC’s
• Tissues retain thiamin as phosphate esters, which is
bound to proteins.
• TPP is catabolised into TMP.
• it is excreted in the urine along with other excretory
metabolites.

12. FUNCTIONS
• Synthesize and regulate neurotransmitters
• Functions in energy metabolism—vitamin portion
of TPP; plays role in decarboxylation and helps
form Acetyl Co A from pyruvate
• Acts as coenzyme with transketolase, an enzyme
of the HMP shunt.

13. Requirements And Sources
• 1.2-1.8mg/day
• Requirement is increased during fever and in hyperthyroidism,
alcoholics and pregnant women.
• Sources:
• White bread, cold cereal
• Enriched grains/ whole grains
• Thiaminase found in raw fish
• Yeast, liver, Kidney and Heart.

14. DEFICIENCY
• DRY BERIBERI
• Weakness, nerve degeneration, irritability, poor arm/leg coordination, loss
of nerve transmission, peripheral neuropathy, foot drop, wrist drop.
• WET BERIBERI
• Edema, enlarge heart, heart failure
• WERNICKE’S ENCEPHALOPATHY
• Generally observed in chronic alcoholics who may develop CNS
manifestations- ophthalmoplegia, cerebellar ataxia and mental
impairement.
• Deficiency is usually seen in the areas where people consume polished
rice or raw fish and are chronic alcoholics.

15. RIBOFLAVIN
• Also called as Vitamin B2 or lactoflavin- due to its
high content in milk.
• It is sensitive to light and UV rays.
• It is Heat stable in acidic as well as neutral
medium.
• It has a isoalloxazine ring which is attached to
ribitol side chain.

16. Structure of
Riboflavin

17. ABSORPTION OF
RIBOFLAVIN
• It is absorbed from proximal small intestine in the free form, by a
carrier mediated process that requires ATP.
• As most foods contain this vitamin in its coenzyme form-FMN and
FAD, absorption occurs only after the hydrolytic cleavage of free
riboflavin from its various flavoproteins complex by phosphatase.
• It is transported in plasma as free riboflavin and FMN, mainly
bound to albumin.
• It also functions in transplacental movement of vitamins.
• Riboflavin is converted to its coenzyme forms by flavokinase.
• Excess of riboflavin is excreted as such in the urine.

18. FUNCTIONS
• Accepts electrons in Electron Transport Chain
• Citric Acid Cycle
• Beta oxidation
• Electron transport chain
• Coenzymes:
• Flavin mononucleotide (FMN)
• Flavin adenine dinucleotide (FAD)
• Oxidation-reduction reactions
• Catabolism of fatty acids

19. Requirements And Sources
• 1-2mg/day
• Sources:
• Liver, kidney
• Most plant and animal foods
• Milk and milk drinks and yogurt supply.
• Fortified cereals, bread and bread products
contribute about 10%

20. DEFICIENCY
• Deficiencies are rare although some people may take in
marginal amounts
• Long term phenobarbital use, alcoholics, restricted caloric
intake
• Ariboflavinosis
• Glossitis, cheilosis, seborrheic dermatitis, stomatitis, eye
disorder, throat disorder, nervous system disorder
• Occurs within 2 months
• Usually in combination with other deficiencies

21. NIACIN
• Also known as pellagra preventive factor
because of its role in the prevention of pellagra.
• It includes two compounds which are derivatives
of pyridine ring. These are: nicotinic acid and
nicotinamide.
• It is present in tissues as nicotinamide.
• Vitamin B3 or Nicotinic acid

22. Structure of Niacin

23. ABSORPTION OF
NIACIN
• It is absorbed in duodenum and jejunum by the
process of diffusion.
• It can be biosynthesized in the body from
tryptophan. 60mg of tryptophan form 1mg of
Niacin.

24. FUNCTIONS
• NAD+ is used as coenzyme with several dehydrogenase
as such malate dehydrogenase, (converts malate to
oxaloacetate), lactate dehydrogenase( lactate to pyruvate)
• NADP+ is used as coenzyme with iso citrate
dehydrogenase, glucose-6-phosphate dehydrogenase.
• It is given in large doses to lower the cholesterol in
hyperlipoproteinemias. A reduction in glucose level is also
observed.

25. Requirements And Sources
• 10-20mg/day
• Sources:
• Rice-polish, Yeast, liver poultry and green
vegetables.
• Milk and milk products sources of high
tryptophan contents.

26. DEFICIENCY
• Pellagra occurs due to its deficiency
• Characterised by 3D’s- dermatitis, diarrhoea and dementia.
• Dermatitis: Results in pain in the parts which are exposed to the sun like:
face, neck, hands and feet. These parts become bronze, resembling sun
burn and later becoming thickened.
• Diarrhoea: Accompanied with anorexia, abdominal discomforts and
various other symptoms of the GI tract.
• Dementia: Due to impaired ability of the brain to utilise carbohydrates.
Symptoms like depression, confusion and psychosis are commonly
observed.
• Prolonged deficiency of Niacin can lead to death.
• Generally occurs in people whose staple food is maize and jowar.

27. PYRIDOXINE
• It occurs in nature in the form of pyridoxal
phosphate and pyridoxamine phosphate, which
acts as coenzyme for several enzymes.
• Pyridoxine, pyridoxal and pyridoxamine are
grouped under Vitamin B6.
• Also referred to as pyridoxal-5-phosphate (PLP)

28. Structure of
Pyridoxine

29. ABSORPTION OF
PYRIDOXINE
• Pyridoxine, PLP and pyridoxamine phosphate
are absorbed in duodenum and jejunum.
• The main urinary end product of Vitamin B6 is 4-
pyridoxic acid.

30. FUNCTIONS
• It is used as coenzyme for glutamate pyruvate transaminase (GPT)
and glutamate oxaloacetate transaminase (GOT)
• PLP is involved in the synthesis of GABA and catecholamines.
• It helps in active transport of amino acids and certain metallic ions
across cell membrane.
• it is involved in the synthesis of heme.
• It is required as coenzyme in tryptophan metabolism.
• In B6 deficiency, Niacin synthesis from tryptophan does not take
place.
• It plays an important role in chain elongation of fatty acids.
• It is essential for glycogen metabolism in muscles and liver, as it is
used as coenzyme for phosphorylase.

31. Requirements And Sources
• 1-2mg/day. Requirement is very low, because
most of the requirement is met by the bacterial
synthesis in intestine.
• Sources:
• Yeast, wheat, maize, fish, liver, kidney
• Milk, fresh vegetables, eggs and meat.
• Banana, spinach , potato.

32. DEFICIENCY
• Mostly shown in patients with T.B. taking Anti-tubercular drug INH,
since the drug act as an antagonist to Vitamin B6.
• Deficiency symptoms include: cheilosis, glossitis and hypochromic
anaemia.
• In infants deficiency of Vitamin B6 affects CNS and results in
convulsions, demyelination of peripheral nerves and degeneration
of axons.
• It has been shown helpful in the treatment of nausea and vomiting
during pregnancy, radiation therapy and muscular dystrophy.

33. DEFICIENCY
• Many neurological conditions, treatment of
autism, down syndrome and seizures are treated
with pyridoxine.
• In deficiency of pyridoxine, peripheral neuropathy
results. So pyridoxine supplements are given.

34. PANTOTHENIC ACID
• It is a dipeptide and consists of a derivative of
butyric acid and beta-alanine.
• It is a part of coenzyme A and acyl carrier protein
(ACP) required for fatty acid synthesis.

35. Structure of
Pantothenic Acid

36. ABSORPTION OF
PANTOTHENIC ACID
Free pantothenic acid is absorbed into intestinal cells
via a saturable, sodium-dependent active transport
system.
At high levels of intake, when this mechanism is
saturated, some pantothenic acid may also be
absorbed via passive diffusion.

37. FUNCTIONS
• Forms prosthetic group of acyl carrier protein and participates
in fatty acid synthesis.
• CoA acts as a carrier for acetate i.e. acetyl CoA which is used
in the synthesis of acetylcholine and in cholesterol
biosynthesis.
• CoA is also used for oxidative decarboxylation of pyruvate to
acetyl CoA.
• CoA is essential in metabolism of branched chain amino acids
• CoA is also required for the activation of fatty acids and for
their subsequent oxidation.
• It is required for the activation of succinic acid and thus in
biosynthesis of heme.

38. Requirements And Sources
• 5-10mg/day. Requirement increases in acute
illness, burns and severe injuries.
• Sources:
• Yeast, liver, kidney, eggs, peas and
wheat.(rich)
• Milk, beef, pork, chicken, oats and sweet
potato. (moderate amount)

39. DEFICIENCY
• Deficiency affects both nervous system and
digestive system.
• Deficiency also results in adrenal insufficiency.
• Symptoms include: headache, fatigue, impaired
motor activity, muscle cramps and GI
disturbances.
• It is used in treatment of burning feet syndrome
and healing of ulcers and bed sores.

40. BIOTIN
• Also known as anti-egg white injury factor since it
protects animals against the toxicity of raw-egg
white.
• Structurally, biotin is a cyclic derivative of urea
which is fused to the thiophene ring.
• Occurs in both bound and free form.
• It is usually bound to the amino acid lysine forming
biocytin.

41. Structure of Biotin

42. ABSORPTION OF
BIOTIN
• Intestinal biotinidase releases free biotin from biocytin
and biotin peptide.
• Free biotin is absorbed in the proximal small intestine,
primarily by carrier- mediated diffusion.
• Biotin is transported in the plasma, primarily as free
biotin. It is taken into cells by a specific carrier
mediated process.
• Vitamin is rapidly excreted in the urine as free biotin as
well as its oxidised products, as biotin sulfoxides.

43. FUNCTIONS
• Carboxylation of acetyl-CoA to form malonyl-
CoA for the elongation of a fatty acid chain
• Addition of CO2 to pyruvate to yield
oxaloacetate
• Breaks down leucine
• Allows 3 essential amino acids metabolism

44. Requirements And Sources
• 15-30mg/day.
• Sources:
• Rice-polish, whole cereals, milk, yeast and
organ meat such as liver and kidney.
• Also found in fruits and vegetables.

45. DEFICIENCY
• Deficiency is generally not seen as it is synthesized by
intestinal flora.
• Deficiency of Biotin may cause mild dermatitis, nausea
and loss of appetite, muscular pain and anaemia.
• Deficiency is induced by the ingestion of large amount
of raw-egg white, as it contains heat labile biotin
binding protein called avidin.
• Heating egg white prevents this effect since heating
denatures avidin.

46. FOLIC ACID
• Folic acid and related compounds are referred to
as folacin since it is derived from the word folium.
• It has pteridine nucleus as molecule of p-
aminobenzoic acid and glutamate in its structure.
• Number of glutamate molecules may vary from 1-
7.
• Major active form of folic acid is 5,6,7,8-
tetrahedron derivative of folic acid.

47. Structure of Folic
Acid

48. ABSORPTION OF FOLIC
ACID
• Monoglutamate forms of folic acid are absorbed by active
transport, mainly in the jejunum.
• When ingested in large amounts, folate can also be
absorbed by passive diffusion.
• Folate taken up by the intestinal mucosal cell is reduced to
tetrahydrofolate which is either transferred to the portal
circulation or converted to 5-methyl FH4 before entering
the circulation.
• Monoglutamate derivatives are taken up by the cells using
an energy dependent process.

49. ABSORPTION OF FOLIC
ACID
• Liver is the most important depot for folate, containing
about half of the total body’s store.
• Folates are metabolised in 3 ways:
• Reduction to derivatives with single carbon units
• Tissue floats turnover by cleavage of their pteridine
and paraminobenzoyl polyglutamate moieties.
• Degraded to a variety of water soluble side chain
metabolites that are excreted in the urine and bile.

50. FUNCTIONS
• Used as coenzyme (tetrahydrofolate, FH4) in
several reactions in metabolism of amino acids
and nucleotides.
• It is essential for the synthesis of purines and
thymine.
• It is also involved in the catabolism of histidine

51. Requirements And Sources
• 400-500 𝝁g. Demand increases during pregnancy
and lactation. It increases dramatically as blood
volume and number of cells increase. By the third
trimester, folic acid requirements double.
• Sources:
• Green leafy vegetables such as cabbage and
spinach
• Yeast, liver, kidney, beef and wheat.

52. DEFICIENCY
• Deficiency may arise due to the destruction of
intestinal bacteria, or may be due to certain
inhibitors of folic acid.
• Macrocytic or megaloblastic anemia, retardation
of growth, weakness, infertility and inadequate
lactation in females.
• Neural tube defects in the foetus is caused by
folic acid deficiency.

53. CYANOCOBALAMIN
• Also called as Vitamin B12, Extrinsic factor of Castle,
due to presence of cyan group and cobalt atom.
• It is a deep crystalline compound soluble in water.
• It is stable to heat in neutral solution but destroyed in
acidic or alkaline solution.
• Central ring structure has a corrin nucleus.

55. ABSORPTION OF VITAMIN
B12
• It is bound to protein and is released from it by pepsin
digestion in the stomach.
• It then combines with R proteins in the stomach and
moves to SI.
• R proteins are hydrolysed and intrinsic factor binds the
cobalamin.
• From IF-Vitamin B12, vitamin is taken into the
erythrocytes by a process involving binding to a specific
membrane receptor on the ideal brush border.

56. ABSORPTION OF VITAMIN
B12
• After absorption, cobalamin binds to the plasma R
proteins- trans cobalamin.
• Cellular uptake of the vitamin is mediated by a
specific TC receptor.
• In adequately nourished individual, vitamin B12 is
stored in liver in form of adenosylcobalamin.
• Free cobalamin is excreted intact by renal and
biliary routes.

57. FUNCTIONS
• Used as coenzyme in conversion of
methylmalonyl CoA to succinylcholine CoA.
• It is also involved in the conversion of glutamate
to beta-methylaspartate and diols.
• It is required for protein synthesis.
• Methylcobalamin is used as coenzyme in the
formation of methionine from homocysteine.

58. Requirements And Sources
• 1-3 𝝁g.
• Sources:
• Liver, kidney, egg, fish and milk.

59. DEFICIENCY
• Can result in megaloblastic anaemia.
• Since significant amount of vitamin is stored in the body.
Therefore, clinical symptoms of the deficiency may
develop after a long time.
• In pernicious anaemia, lack of intrinsic factor prevents the
absorption of this vitamin.
• Deficiency also results in methylmalonic aciduria.
• Deficiency generally occurs in geriatric people, who are
strict vegetarian.

60. VITAMIN C
• Also called as ascorbic acid, anti-scurvy factor.
• It is a derivative of carbohydrates.
• It is a good reducing agent.
• Both oxidised and reduced forms are biologically
active.
• It can be destroyed by heat.

61. Structure of Vitamin C

62. ABSORPTION OF VITAMIN
C
• It is absorbed by active transport and passive diffusion.
• It is transported in the plasma in the reduced form (L-ascorbic
acid) in free solution.
• It is taken up by the cells though glucose transporter and
specific active transport system.
• Dehydroascorbic acid is readily reduced to ascorbate in the
cells.
• This system is stimulated by insulin and inhibited by glucose.
• The vitamin is concentrated primarily in many vital organs like:
adrenals, eye and brain.

63. FUNCTIONS• It is required for the hydroxylation of amino acids, particularly the
aromatic amino acids.
• Hydroxylation of proline and lysine.
• Essential for the absorption of iron from GI tract as well as its
release from ferritin.
• It has stimulating effect on phagocytic activity of leucocytes.
Thus, it provides resistance to the body.
• Ascorbic acid is also required for the synthesis of the steroid
hormones in the adrenal cortex. Thus, it helps in lowering blood
cholesterol level.
• Antioxidant.
• Synthesis of epinephrine and norepinephrine from tyrosine.

64. Requirements And Sources
• 40-60 mg.
• Sources:
• Amla is the richest source of Vitamin C.
• Citrus fruits, green vegetables, guava, berries
green chillies and tomato etc.

65. DEFICIENCY
• Causes Scurvy.
• Characterised by multiple haemorrhages.
• Early symptoms include: swollen, spongy and bleeding
gums; loosening of teeth; pain in joints.
• In severe cases, bleeding from nose, GI tract and
genitourinary tract.
• Increased susceptibility to infection, delayed wound healing.
• Anaemia, fatigue and lethargy.

66. APPLICATION and
TOXICITY
• Mega doses help in curing cancer.
• Used in treatment of copper sulphate poisoning
and acidification of urine.
• Excessive amount can cause diarrhoea.
• Oxalate stones can get deposited in the kidneys.

67. FAT SOLUBLE
VITAMINS
• It includes: Vitamin A, D, E and K.
• They are absorbed in the lumen, in the presence of
fat and are emulsified with bile.
• Their precursors are called provitamins, which
mostly occur in plants.
• They are stored in liver and several other tissues.
• Large doses of these vitamins may result in
hypervitaminosis leading to various toxic symptoms.

68. VITAMIN A
• Also called as anti-night blindness factor, retinoids.
• It refers to the collection of three forms: retinol, retinal and
retinoids acid.
• Retinol is a primary alcohol with unsaturated side chain. It
is transported in chylomicrons. Also secreted by liver.
• Retinal is aldehyde from, easily interconvertible to retinol.
• Retinoic acid is formed when retinal gets oxidized.
• It exists as provitamin, beta-carotene in plants.

69. Structure of Vitamin A

70. ABSORPTION OF VITAMIN
A
• Vitamin A and its provitamins are absorbed in small intestine.
• Approximately 95% of vitamin A is in the form of esters, which
are stored in the liver, largely as retinol palmitate.
• Small amounts of vitamin A are also present in other tissues
such as lactating breast, adrenals, lungs and intestines.
• In blood, vitamin esters, mainly palmitate, are attached to beta-
lipoproteins and are taken up by the liver.
• The liver contains almost all the body stores of vitamin.
• Being fat soluble, vitamin is then released and is carried by
RBP (retinol-binding protein) for the use in other tissues.

71. FUNCTIONS
• Role in Visual process.
• Helps in the synthesis of steroid hormones, particularly, synthesis of
cortisterone and cortisol.
• Vitamin A also plays an important role in cholesterol biosynthesis.
• It affects cell growth and differentiation.
• It helps in the synthesis of membrane glycoproteins.
• It is also required in the maintenance of integrity of the tissues lining
eyes, GI tract and respiratory system.
• It also ensures optimal functioning of the immune system.
• It also acts as anti-oxidants
• Used in the treatment of acne.

72. VISUAL CYCLE
• It is also known as rhodopsin cycle or Wald’s visual cycle.
• The processing of visual information begins with the detection of light on the
photoreceptors.
• To detect light, both rods and cones exploit the unique properties of 11-cis retinal, a
photosensitive derivative of vitamin A.
• Retina contains two types of receptors: CONES (specialized for colour and bright
light); and RODS (specialised for visual activity in dim light). Rods cells have a
photosensitive pigment called rhodopsin for visual activity. It contains opsin (an
apoprotein) and retinol as its prosthetic group.
• When light falls on rhodopsin, it splits up into opsin and all-trans retinal in a series
of events.
• It forms bathorhodopsin first, followed by lumirhodopsin, then metarhodopsin I and
II.
• Finally metarhodopsin gets split into opsin and all-trans retinal. At this stage eye
becomes sensitive to light.

73. VISUAL CYCLE
• All-trans retinal is inactive and has to be converted to 11-cis retinal.
• This reaction is catalysed in retina itself in dark by retinal isomerase. 11-cis retinal
combines with opsin to regenerate rhodopsin
• In Liver
• All-trans retinal is transported to liver and reduced to all-trans retinol by retinol
dehydrogenase.
• All-trans retinol is esterified to all-trans retinal ester and stored in liver.
• When retinol is required, hydrolysis of esters occurs.
• All-trans retinol is carried in blood via RBP(retinol binding protein).
• All-trans retinol is isomerised to 11-cis retinol.
• Regeneration of 11-cis retinal occurs by the action of retinol dehygenase to 11-cis
retinol. It is important because its deficiency leads to increase in dark adaptation
time and night blindness.

74. VISUAL CYCLE
• In cones: It has three pigments sensitive to three
primary colours i.e. porphyropsin (red), iodopsin
(green), cyanopsin (blue).
• Prosthetic group in these three pigment is same i.e.
11-cis-retinal.

75. VISUAL CYCLE

76. Requirements And Sources
• 4000-6000 IU (2000mg).
• Sources:
• Liver oil, fish-liver oil, egg, milk.
• Yellow fruits and vegetables like: papaya, carrot
.
• Sweet potato, green-leafy vegetables are good
sources of beta-carotenes.

77. DEFICIENCY
• Night Blindness (Nyctalopia): Vitamin A deficiency interferes with the
production of rhodopsin. Thus impairing rod functions and results in
night blindness. It responds to Vitamin A therapy rapidly.
• Dry eye (Xerophthalmia): thickening and loss of transparency and
loss of transparency of the conjunctiva with yellowish pigmentation
occurs. Major cause of blindness in childhood.
• Keratomalacia: resulting in softening of cornea and defective vision
due to keratinization of epithelium of cornea.
• Defective Teeth formation.
• Skin becomes dry, scaly and rough.
• Bitot’s spot is seen. These are greyish, glistening white plaques
formed of desquamated thickened conjunctival epithelium adhering
to the conjunctiva.

78. DEFICIENCY
• Corneal scar: Keratomalacia can lead to
perforation of the cornea. It remain forever.

79. BITOT SPOT

80. KERATOMALACIA

81. XEROPHTHALMIA

82. HYPERVITAMINOSIS
• Toxicity symptoms include skin abnormalities
such as dry and rough skin.
• scaly dermatitis, headache, nausea, vomiting
and loss of appetite.
• hepatomegaly, painful joints and several bone
abnormalities.

83. VITAMIN D
• It is also called as Calciferol or anti-rachitic factor. It is also
considered as pro hormone and synthesized in the body
• Vitamin D is a steroid. It is represented by a group of steroids
that occurs not only in animals but also in plants and yeast.
• Most important forms of Vitamin D are Vitamin D2 (in plants),
and Vitamin D3 (in animal tissues).
• D2 and D3 are not biologically active. They are converted into
active form in the body.
• Physiologically active form of Vitamin d is 1,25-
dihydroxycholecalciferol (1,25-DHCC). It functions as hormone.

84. Structure of Vitamin D

85. ABSORPTION OF VITAMIN
D• Dietary vitamin D is incorporated with other lipids into micelles
and absorbed with lipids into the small intestine by passive
diffusion.
• Inside the cells, vitamin is incorporated into chylomicrons, enters
the lymphatic system and enters plasma.
• It is then delivered to liver.
• Vitamin D synthesized in skin from cholesterol enters capillary
system and is transported to the peripheral tissues.
• Small amount of Vitamin D is stored in liver.
• Small amount of vitamin D is even excreted in bile and most of it is
reabsorbed in the intestine.
• It is not eliminated in the urine.

86. PROVITAMIN D
• A derivative of the cholesterol, called 7-
dehydrocholesterol, is a precursor of vitamin D3
in animals.
• It is also called provitamin D.
• It is synthesised in human being and is converted
to vitamin D3 by UV light in the skin.
• This process is referred to as photo biogenesis.

87. FUNCTIONS
• Acts on organs such as bone, kidneys, intestinal
mucosa for regulation of calcium and
phosphorous metabolism.
• It promotes intestinal absorption of calcium and
phosphorous. It also promotes bone resorption
and calcium mobilisation.
• Increases the citrate level of blood, bone,
kidneys and heart tissues.

88. • Calcium metabolism:
• Vitamin D3 induces synthesis of calcium binding protein, Ca2+
dependent ATPase and alkaline phosphatase, which are
essential for the regulation of serum calcium and phosphorous.
• In intestine, due to stimulation of synthesis of calcium binding
protein, 1,25-DHCC increases intestinal absorption of calcium
as well as phosphorus.
• In bone, calcitriol stimulates synthesis of osteocalcin, which in
turn mobilises calcium from bone. i.e. it causes
demineralization.
• In kidney, active vitamin D increases tubular reabsorption of
calcium and excretion of phosphorus.
• Overall effect of all three, increases the serum calcium level
towards normal.

89. Requirements And Sources
• 200 IU (5-10mg).
• Sources:
• Sunshine. It is synthesized in body by the
action of UV light on skin.
• Milk, butter.
• Liver oil, fish oil, egg yolk.

90. DEFICIENCY
• Leads to Rickets and Osteomalacia.
• Rickets
• Occurs during infancy and childhood. It is a nutritional disorder.
• Symptoms: enlarged wrists, ankles and poor structural
development affecting long bones, bowed legs and knock-
knees.
• Deformities of bone of skull, chest and spine. Late eruption of
teeth.
• Exposure to sunlight and vitamin D supplements has preventive
and curative effects.

91. DEFICIENCY
• Osteomalacia.
• Occur in adults. Also called as adult rickets.
• Commonly observed in females during
pregnancy and lactation or in those who are not
exposed to sunlight.
• Bone particularly of pelvic region show
characteristic deformities, which in turn may
complicate parturition.

92. DEFICIENCY
• Vitamin D resistant rickets.
• Also known as renal rickets. Low levels of
calcium are seen.
• it is inherited disease. Patients shoe
hypophosphataemia and severe rickets.
• Vitamin D does not reverse the disease.

93. HYPERVITAMINOSIS
• Extremely large doses may lead to
hypercalcemia, hyperphosphatemia, anorexia,
nausea, vomiting and diarrhoea.
• Bone pain and metastatic calcification of soft
tissues including kidneys, myocardium, pancreas
and uterus.

94. VITAMIN E
• Also called as tocopherol.
• It is an alcohol with a phytol and
trimethylhydroquinone.
• Natural Vitamin E is d-tocopheroland is a single
stereoisomer.
• Synthetic vitamin E - dl-tocopherol is produced
commercially.

95. Structure of Vitamin E

96. ABSORPTION OF VITAMIN
E
• Free tocopherols and their esters are readily
absorbed by the small intestine with the help of
bile acids.
• It is absorbed by micelle-dependent diffusion.
• It is incorporated into chylomicrons and is
transported via lymph into general circulation.
• It is delivered to liver. Cellular uptake occurs
either as receptor-mediated process or as
process mediated by lipoprotein lipase.

97. FUNCTIONS
• Functions as antioxidant
• Prevents oxidation of Vitamin A and carotenes
and reduces their wastage.
• Its derivatives are involved in the synthesis of
coenzyme Q.
• Protects cell membrane.
• Protects LDL from oxidation.

98. Requirements And Sources
• 10-30mg/day
• Sources:
• Green leafy vegetables- spinach, lettuce.
• Milk and milk products and egg yolk.
• Oils such as corn oil, cottonseed oil and
sunflower oil are rich in sources of vitamin E.

99. DEFICIENCY
• Results in range of degenerative diseases.
• Fat malabsorption, where it results in progressive
neuropathy and retinopathy.
• Hepatic necrosis, muscular dystrophy, defects in vascular
system and certain reproductive defects can occur.
• In infants, it s associated with increased erythrocyte
fragility. leading to haemolytic anaemia.
• Clinical Vitamin E deficiency occurs in patients with
obstructive jaundice, pancreatitis and steatorrhoea, where
fats and fat soluble vitamins fail to be absorbed.

100. HYPERVITAMINOSIS
• Causes haemorrhage.
• It is the least toxic fat soluble vitamin.

101. VITAMIN K
• Two naturally occurring forms of Vitamin K are
K1 and K2.
• K1- phylloquinone, found naturally in plant
sources.
• K2- menaquinone/ farnequinone, synthesized by
intestinal bacteria.
• A synthetic Vitamin K also known as K3 is
commercially available for therapeutic use.

102. Structure of Vitamin K

103. ABSORPTION OF VITAMIN
K
• It is absorbed by an energy dependent process
in small intestine.
• K2 and K3 are absorbed by passive diffusion in
SI and colon.
• It is incorporated into chylomicrons in the
lymph and taken to the liver where they are
incorporated into VLDL and subsequently
delivered to the peripheral tissues by LDL’s.
• It is excreted primarily in urine as phosphate,
sulphate or glucuronide derivative.

104. FUNCTIONS
• Maintenance for the normal levels of various blood-clotting
factors such as: prothrombin, factor VII, factor IX and
factor X.
• These proteins are synthesized in the liver in their inactive
form and get converted to active form with the help of
Vitamin K.
• Necessary for Oxidative phosphorylation process.
• Conversion of prothrombin to thrombin
• Formation of fibrinogen to fibrin.
• Stimulates bone formation and decreases bone resorption.

105. Requirements And Sources
• 70-140 𝝁g/day
• Sources:
• Green leafy vegetables- spinach, cabbage and
cauliflower.
• Milk and milk products.
• Soybean, wheatgerm, carrot, potato and fish.

106. DEFICIENCY
• Deficiency is rare as it is synthesized by the intestinal
bacteria.
• However, antibiotic treatment destroys the bacterial pool and
deficiency occurs.
• Bleeding tendencies occurs because of
hypoprothrombinemia.
• Symptoms of deficiency are observed in obstructive jaundice.
• Deficiency results in intestinal malabsorption in sprue,
obstructive jaundice and coeliac disease.
• Cutaeneous and intramuscular haemorrhage with bluish-red
coloration in different parts of the body.

107. HYPERVITAMINOSIS
• Leads to toxicity.
• Haemolysis, hyperbilirubinemia, kernicterus and
brain damage can occur. (In infants).
• Warfarin and dicoumarol acts as its antagonist.
They act as competitive inhibitors for the
enzymes.