nutrition

1. Fat soluble vitamins
• Fat soluble vitamins are required for normal color vision, blood
clotting, bone formation and maintenance of membrane structure.
• Vitamins A and D act as steroid hormones.
• Deficiency of fat soluble vitamins produce night blindness, skeletal
deformation, haemorrhages and hemolysis.
• However, excessive consumption of fat soluble vitamins leads to
toxicity.

2. VITAMIN A
• They are retinol (Vitamin A alcohol), retinal (Vitamin A aldehyde) and
retinoic acid (Vitamin A acid). These forms are sometimes referred to as
retinoids
• Vitamin A is a derivative of certain carotenoids which are hydrocarbon
pigments (yellow, red).
• These are widely distributed in the nature. These are called as
“Provitamins A” and are α, β and γ-carotenes.
• They are composed of β−ionine ring and side chain containing two
isoprene units with four conjugated double bonds.
• Due to the presence of double bonds in isoprenoid side chain vitamin A
exhibits cis-trans isomerism.
• cis indicates that the functional groups are on the same side of the carbon
chain while trans conveys that functional groups are on opposing sides of
the carbon chain

3. • Due to the presence of 4 double bonds vitamin A can be oxidized by
air or light slowly.

4. VITAMIN A In nature
Vitamin A occurs in two forms
• Retinolesters -In the foods of animal origin. Present in Liver oil, butter, milk,
cheese, egg yolk.
• in plant foods as provitamin carotenes, tomatoes, carrots, green-yellow
vegetables, spinach, and fruits such as mangoes, papayas, corn, sweet
potatoes
Absorption of Vitamin A
• In the intestine pancreatic esterase hydrolyzes retinolesters present in the
diet to retinol and free fatty acid in presence of bile salts. Retinol is absorbed
by mucosal cells.
• Dietary β-carotene is cleaved into two molecules of retinal by a dioxygenase
present in the intestinal mucosa. It is transported by lipoprotein.

5. Functions of vitamin A
The three major retinoids: retinal, retinol and retinoic acid have unique functions.
1. Retinal is required for normal and color vision.
2. Retinol is required for reproduction and growth.
3. Retinol is also required for differentiation and function as steroid hormone.
4. Retinoic acid is required for the synthesis of glycoproteins or mucopolysaccharides.
5. Retinoic acid also act as steroid hormone. It also promote growth and differentiation.
6. Retinol and retinoic acid are involved in regulation of gene expression.
Retinal and color vision
• Three light sensitive pigments present in cones are responsible for color vision. They
are porphyropsin, iodopsin and cyanopsin.
• All three pigments contain 11-cis retinal and are sensitive to red, green and blue colors
respectively.
• When the photon (light) strikes retina depending on the color of the light a particular
pigment is bleached. This leads to generation of nerve impulse and perception of color
by brain.
• Defective apoprotein production due to faulty genes leads to color blindness.

6. • Retina contains two types of photoreceptor cells:
• (i) Cones: Specialized for color and detail vision in bright light contains iodopsin.
• (ii) Rods: Specialized for visual activity in dim light (night vision), contains rhodopsin.
• When the light falls on rhodopsin it is split into opsin and all-trans-retinal in a series of
events. It first forms photorhodopsin, bathorhodopsin, then lumirhodopsin, then
metarhodopsin I, II and III. Finally metarhodopsin gets split into opsin and all-trans-
retinal.
• At this stage the eye becomes less sensitive to light. All-trans-retinal is inactive in
synthesis of rhodopsin, it has to be converted to 11-cis-retinal so that it can combine
opsin to form rhodopsin . It can take place in two main pathways:
• First of which is operated in the eye, the all-trans-retinal is converted to 11-cis-retinal by
the enzyme retinal isomerase and combine with opsin to reform rhodopsin
• Now the second pathway which is operated in the liver here the enzyme is the alcohol
dehydrogenase, first the all trans retinal is converted to all trans retinol and then by the
enzyme isomerase to 11-cis-retinol
• 11-cis-retinol acted upon by the enzyme retinene reductase to 11-cis-retinal
• Now 11-cis-retinene which is active, can combine with opsin to form back rhodopsin in
dark. Thus the visual process involves continual removal of the active cis-retinol from
blood into retina.

8. Mechanism of Action of Transducin
• Photoactivated rhodopsin is converted metarhodopsin II
• Metarhodopsin II cause the activation of regulatory protein called
Transducin
• The activated transducin now activate phosphodiesterase (PDE)
• The activated PDE then catalyses the hydrolysis of second messenger
c-GMP to 5’-AMP, lowering the c-GMP level to the plasma membrane
of the outer segment, causing the Na+ channels to close.
• The c-GMP is the second messenger that regulates the opening and
closing of Na+ channels.

9. Conclusion
• In the dark, there are high level of c-GMP,
which binds to the Na+ channels, causing them
to open.
• In the light, photoactivated rhodopsin, through
transducin and phosphodiesterase, lowers the
levels of c-GMP, thus closing the most of Na+
channels
Night blindness (nyctalopia):
This is one of the earliest signals of vitamin A
deficiency which is impairment of dark
adaptation. Therefore continual supply of retinol
is essential for normal visual function. Vit A
deficiency depresses the resynthesis of
rhodopsin and interferes with the function of
rods resulting in night blindness.

10. Deficiency of Vitamin A
• 1. Night blindness • In early stages, the affected individual is not able to see clearly
in dim light or night due to block in the resynthesis of rhodopsin. • In the later
stage of deficiency the affected individual cannot see or read in dim light. • Thus
loss of night vision (night blindness) is the major initial symptom of Vitamin A
deficiency. • Night blindness in adults or in preschool children is common in
countries where intake of vitamin A is low.
• 2. Growth of bone and formation of tooth are defective. Thick and long bones are
formed.
• 3. Nerve growth also affected. Degeneration of myelin sheath occurs.
• 4. Keratinisation of mucous secreting epithelial cells (hyperkeratosis) lining
respiratory tract and reproductive tract occurs. Mucous secretion by salivary and
lacrymal glands is also affected.
• 5. Deposition of keratin in skin (xeroderma) gives rise to characteristic toad skin
appearance.
• 6. Reproductive disorders like testicular degeneration, resorption of foetus or foetal
malformation are observed.
• 7. Degenerative changes in kidneys.

11. • Sources (a) Animal sources.
• Marine fish oils like halibut liver oil, cod liver oil and shark liver oils are
excellent sources. Liver of sheep or goat is also excellent source.
• Butter, egg, and milk are good sources.
• Freshwater fish contain Vitamin A2 (dehydroretinol) which is only 40%
active.
• (b) Plant sources. In plant foods vitamin A is present as carotenes. Plant oil
like red palm oil is excellent source.
• Leafy vegetables. coriander leaves, curry leaves, spinach and cabbage are
good sources.
• Yellow vegetables like carrot, pumpkin and sweet potato and ripe
tomatoes also contain appreciable amounts of vitamin A.
• Fruits. Yellow pigmented fruits papaya, mango, jackfruit, banana and
oranges also contain vitamin A in good amounts.

12. VITAMIN D
Chemistry
• It is also called sunshine vitamins.
• Its active forms are vitamin D2 (ergo calciferol) and vitamin D3
(cholecalciferol).
• Calcitriol is the most active form of vitamin D that acts as steroid
hormone.
• They are formed from provitamins which are sterols.
• Absorption, transport and storage • Dietary vitamin D2 and vitamin D3
are absorbed in the small intestine in presence of bile salts.
• Absorbed Vit D is incorporated into chylomicrons and enters circulation
via lymph.
• Vitamin D is stored in liver and adipose tissue.

13. Biologically Active Form of Vitamin D (Calcitriol)
Formation of Calcitriol
• The biologically active form of vitamin D is called calcitriol, which is synthesised in liver and kidneys.
(a) Synthesis of 25-OH-D3 in Liver (Calcidiol)
• Vitamin D2 and/or D3 binds to specific D binding protein and is transported to liver.
• It undergoes hydroxylation at 25 position, by the enzyme 25-hydroxylase, in the endoplasmic
reticulum of the mitochondria of liver cells.
• Coenzyme/cofactors required are:
• Mg ++
• NADPH
• Molecular O2
• A cytoplasmic factor is also required, the exact nature not known. Two enzymes, an NADPH-
dependant cytochrome P450 reductase and a cytochrome P450 are involved also.
• 25-OH-D3 (calcidiol) is the major storage form of vitamin D in liver and found in appreciable amount
in circulation. The blood level of 25-OH-D3 exerts feedback inhibition on the enzyme 25-
hydroxylase.

14. (b) Synthesis of 1, 25-di –OH-D3 (Calcitriol) in Kidneys
• 25-OH-D3 is bound to a specific vitamin D binding protein and is carried to
kidneys.
• It undergoes hydroxylation at 1-position, by the enzyme 1 α -hydroxylase, in
the endoplasmic reticulum of mitochondria of proximal convoluted tubules
of kidney.
• The reaction is a complex three component monooxygenase reaction
requiring Mg++, NADPH and molecular O2 as coenzymes/cofactors.
• In addition, at least three more enzymes are required.
• Ferrodoxin reductase
• Ferrodoxin, and
• Cytochrome P450
• This system produces 1,25-di-OH-D3 (calcitriol) which is the most potent
metabolite of vitamin D

15. Mode of action of calcitriol:
Calcitriol acts in a similar way as the steroid hormone receptors. This binding is specific
and reversible. The receptor has a specific binding site on DNA that appears to contain
Zinc-finger motif characteristic of other steroid receptors.
Vitamin D as prohormone:
Since calcitriol is synthesised in the body and acts like steroid hormone and has a basic
sterol nucleus in its structure, it is now regarded as a hormone and vitamin D as a
prohormone.

16. Functions of calcitriol
• 1. Major action of calcitriol is to increase absorption of calcium and
phosphate in the intestine particularly in duodenum and jejunum.
• 2. Calcitriol is required for bone formation and mineralisation of bone. It
increases synthesis of osteocalcin a calcium binding protein of bone.
Osteocalcin is involved in deposition of calcium salts in bone.
• 3. Calcitriol affects calcium and phosphorus excretion by kidney. It reduces
the excretion of calcium and phosphorus.
• 4. Vitamin D is involved in maintenance of normal muscle tone.
• muscle tone prepares you for action, maintains your balance and posture,
generates heat that keeps your muscles healthy, and allows for a quick,
unconscious reaction to any sudden internal/ external stimuli.
• 5. Calcitriol is an immuno regulatory hormone. It stimulates cell mediated
immunity. It plays a vital role in monocyte/macrophage activation.

17. Vit D deficiency symptoms
• 1. Rickets • In children vitamin D deficiency causes rickets, results in soft bones. This
leads to deformities in skull, chest, spine, legs and pelvis.
• 2. Osteomalacia • Vitamin D deficiency causes osteomalacia in adults. It is seen in
pregnant women and women with inappropriate diet. Skeletal pain is early sign.
Deformities of ribs, spine, pelvis and legs are seen.
• 3. Osteoporosis • Vitamin D deficiency causes osteoporosis in old people. Photolysis of
provitamins dcreases with age. This and together with decreased sex hormone
production may lead to deficiency. Symptoms are bone pain and porous bones. Bone
fractures are common.
Sources
• Vitamin D is mostly present in foods of animal origin.
• Marine fish liver oils like halibut liver oil, cod liver oil and shark liver oil are good sources.
• Sardines, egg yolk and butter contains small amounts. However, milk is a poor source of
vitamin D, Mushrooms contain small amounts of vitamin D.
• Toxicity (Hyper vitaminosis) • Ingestion of mega doses of vitamin D results in toxicity of
Vit D.
• Signs and symptoms of vitamin D toxicity are loss of appetite, nausae, thirst, vomiting,
polyuria and calcification of lungs, renal tubules and arteries. Muscle wasting also occurs.
Demineralisation of bone similar to vitamin D deficiency is seen.

18. VITAMIN E
Chemistry:
• Chemically they are tocopherol
• They are derivatives of tocol or 6-hydroxy chromane ring with phytyl side chain.
• The tocopherols differ from each other in the number or position of methyl groups.
• • α-tocopherol: 5, 7, 8 trimethyl tocol
• • β-tocopherol: 5, 8 dimethyl tocol
• • γ-tocopherol: 7, 8 dimethyl tocol
• • δ-tocopherol: 8 methyl tocol
• The α-tocopherol is the most active in vitamin E activity.
• Tocopherols are alkaline sensitive and their vitamin activity is destroyed by oxidation.
• Among all tocopherols α-tocopherol is most potent and widely distributed in nature.
• Cooking and food processing may destroy vitamin E to some extent.

19. Absorption, transport and storage : Dietary tocopherols are absorbed in small
intestine in the presence of bile salts.
• Absorbed tocopherols are incorporated into chylomicrons in mucosal cells of
intestine and enters circulation via lymph.
• In plasma tocopherols are released from chylomicrons by lipoprotein lipase.
• Liver takes up half of tocopherol and it is stored.
• Skeletal muscle and adipose tissue also stores vitamin E.
• From the liver tocopherols are transported to other tissues in β-lipoprotein.

20. Functions of Vitamin E
• Antioxidant Property is this is the most important functional aspect of vitamin E.
• • Removal of free radicals: Vitamin E is involved in removal of free radicals and prevents
their peroxidative effects on unsaturated lipids of membranes and thus helps maintain
the integrity of cell membrane.
• Vitamin E prevents peroxidation. Vit E (α-tocopherol) reacts with the lipid peroxide
radicals formed by peroxidation of polyunsaturated fatty acids before they can establish
a chain reaction, acting as free radical trapping antioxidant.
• 1. α-tocopherol in cell membrane and cytosol function as antioxidant. It is present in
high concentration in tissues which are exposed to high O2 pressure like erythrocytes,
lungs, retina etc. It acts as chain breaking antioxidant.
• 2. Vitamin E is involved in maintenance of muscle tone
• 3. Vitamin E increases synthesis of hemeproteins
• 4. Vitamin E prevents dietary vitamin A and carotenes from oxidative damage.
Sources • Cereal germ oils like wheat germ oil, corn germ oil and vegetable oils like
coconut oil, sun flower oil, peanut oil, ricebran oil, palm oil, mustard oil, cotton seed oil
and soyabean oil are rich sources of vitamin E. • Vegetables, fruits and meat are relatively
poor sources of vitamin E.

21. • Role in Reproduction in Rats
• Vitamin E helps in maintaining seminiferous
epithelium intact. However, its deficiency
leads to irreversible degenerative changes
leading to permanent sterility. Motility of
sperms is lost and spermatogenesis is
impaired.
• In female rats the ovary is unaffected by
vitamin E deficiency, but the fetus does not
develop normally, dying in utero
undergoing resorption.
• Other Functions
• Tocopherol derivative tocopheranolactone
may be involved in synthesis of coenzyme Q
or ubiquinone.
• Vitamin E may have some role in nucleic
acid synthesis.

22. VITAMIN K
• Chemistry
• • Chemically they are quinones
• • Vitamin K1 also called as phylloquinone, is the major form of vitamin found in plants
particularly in green leafy vegetables.
• • Vitamin K2 also known as menaquinone is the vitamin K present in animals and
synthesized by intestinal flora.
• • They are derivatives of naphthoquinone and differ in side chain.
• • Phylloquinone contain phytylside chain where as
• • menaquinone contains polyisoprenoid side chain made up of 7 isoprene units.
Absorption and Transport
• Vitamin K of dietary origin is absorbed in small intestine in presence of bile salts. • In
mucosal cells of intestine absorbed vitamin K is incorporated into chylomicrons. • It
reaches liver after entering circulation through the lymph. • Liver distributes vitamin K
to other tissues. • It rarely accumulates in liver and peripheral tissues.

23. Functions of Vitamin K
• Vitamin K is required for the synthesis of blood clotting factors like prothrombin
(factor II), cothromboplastin (factor VII), (factor IX) and (factor X).
• It is required for the carboxylation of the γ-carbon atom of glutamic residues of
these factors. The γ-carboxylation generates calcium binding sites which is
essential for blood clotting process.
Deficiency Symptoms of vitamin K
• 1. Haemorrhage in the new born is most common vitamin K deficiency symptom.
uncontrolled bleeding through nose (epitaxis) and gastrointestinal tract is likely to
occur. However it can be treated successfully with intra muscular injections of
vitamin K.
• 2. In adults vitamin K deficiency rarely occurs. However prolonged use of
antibiotics may cause vitamin K deficiency due to elimination of intestinal flora.
• Sources
• Plant Sources • Cauliflower, Cabbage, spinach, turnip greens, peas and soybean
are rich sources. Animal sources • Dairy products like cheese, butter and farm
products like eggs and liver are good sources.