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V ITAMINS

Vitamins are a group of organic substances essential in small quantities for normal metabolism.
They are found in minute amounts in natural foodstuffs & are sometimes produced synthetically.
They cannot be synthesized by the body. Must be obtained by outside sources like diet, rumen
bacteria & sun. Deficiencies of vitamins cause specific diseases & disorders.
A. Characteristics: Two characteristics mark a compound to be assigned as a vitamin:
1. It must be a vital organic dietary substance, which is neither a carbohydrate, fat, mineral nor protein,
but is necessary in very small quantities to the performance of particular metabolic functions or to the
prevention of an associated deficiency disease.
2. It cannot be manufactured by the body & therefore must be supplied in food.
B. Megavitamin Therapy: is the excessive intake of multivitamins to overcome a deficiency in
daily requirements. Vitamins in excess of body needs will be excreted.
C. Classification of Vitamins: Vitamins are usually grouped according to their solubility:
1. The fat-soluble group includes vitamins A, D, E & K.
2. The water-soluble group includes vitamin C & the B-Complex vitamins.
I. Fat Soluble Vitamins
Absorption of fat soluble vitamins depends upon:
o Presence of fats in the GIT.
o Hepatic function.
o Bile contents.
A. Vitamin A (Retinol): Vitamin A is an alcohol & because it has a specific function in the retina of
the eye, it has been given the name Retinol. However, it is still commonly referred to as vitamin A.
-carotene (pro-vitamin A) is the precursor of vitamin A.

1. Physiologic functions of vitamin A:
o Vision: Vitamin A is necessary for the proper functioning of some inner parts of the eye that are
concerned with night vision.
o Epithelial Tissue: Vitamin A has an important role in the formation & maintenance of healthy,
functioning epithelial tissue, the body's 1ry barrier to infections.
o Growth: It has been observed that vitamin A deficiency is associated with retarded growth
(mechanism unknown). Vitamin A is essential for the growth of skeletal, soft tissues, bones & teeth.
2. Hypovitaminosis “A”: A deficiency in vitamin A may occur for 3 basic reasons:
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o Inadequate dietary intake.
o Poor absorption.
o Inadequate conversion of carotene (liver or intestinal disease).
This deficiency can lead to:
o Night blindness: a condition known as nyctalopia.
o Xerophthalmia
o Keratinization of epithelial cells of the cornea of the eye.
o Keratinization of epithelial cells, these become dry, flat, & gradually harden to form scales that
will peel off; leading to infection.
o Loss of appetite and ruffled feathers
o Decrease in the egg production and hatchability.
4. Food sources of vitamin A:
o Animal sources: fish-liver oil, liver, kidney, milk, butter & egg yolk,
o Plant sources: are the yellow & green vegetables & fruit sources of carotene; e.g. carrots, sweet
potatoes, apricots, spinach & cabbage.
B. Vitamin D (Calciferol): Vitamin D is unique among the vitamins in two respects:
o It occurs naturally in only a few common foods (mainly fish oil & a little in egg & milk).
o It can be formed in the body by exposure of the skin to UV rays either from the sun or a lamp.
7-hydroxy ergosterol
Ergosterol
UV / activation in the liver
Cholicalciferol (vitamin D3) (natural)
UV
Calciferol (vitamin D2) (synthetic)
Cholicalciferol is 100 times as active as ergocalciferol.
1. Physiologic function of vitamin D: Vitamin D has hormone-like (para-hormone) functions closely
inter-balanced with the parathyroid hormone in calcium & phosphorus metabolism.
o Absorption of calcium & phosphorus from the small intestine.
o Calcification: Vitamin D works with calcium & phosphorus in the calcification aspect of bone
formation. It increases the mobilization of Ca++ from blood to bones.
2. Hypovitaminosis "'D": can happen due to inadequate exposure to sunlight (UV) &/or dietary deficiency.
This can lead to:
o Rickets (in young): a disease directly related to impaired metabolism of Ca & P, due to vitamin
D deficiency. Characteristic clinical manifestations of rickets result from failure of calcification
of growing bones. Several deformities of bones develop e.g. softening of cranial bones, bowed
thighs & knock-knees.
o Osteomalacia (soft bones): in adults.
o Hypo-parathyroidism: in adults.
o Increase the production of eggs with thin shell.
o And then decrease eggs production and hatchability.
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o Squatting in chicken.
3. Hypervitaminosis "'D": ingestion of excessive quantities of vitamin D can produce toxicity. Symptoms
of vitamin D toxicity are:
o Calcification of soft tissues such as lungs & kidney (kidney stones).
o Hyper-calcemia (increased Ca++ levels in blood).
o Bone fragility.
o Increased toxicity.
o Mental retardation.
4. Food sources of vitamin "D": The 2 basic food sources are yeast & fish liver oils. The main food
sources are those to which vitamin D has been added or produced by irradiation, especially milk.
Vitamin D is completely absorbed from the GIT. Absorption depends on hepatic & biliary functions.
Drugs that increase hepatic microsomal enzymes (anti-coagulants, barbiturates, rifampicin & antidepressants) lead to increased elimination of vitamin D and may cause its deficiency.
5. Uses of vitamin D:
o Anti-rickettic: in young (it promotes calcification of organic matrix of bone structure).
o Treatment of hypo-parathyrodism.
6. Daily requirements: 1000 IU / day.
One IU vitamin D = 0.025 g vitamin D2.

C. Vitamin E (-Tocopherol): is known as the antisterility vitamin, but it has been
demonstrated to have this effect only in the rat & not in man.

Antioxidant.
•
Reduce the energy of the free radical
•
Stop the free radical from forming in the first place
•
Interrupt an oxidizing chain reaction to minimize the damage of free radicals
1. Physiologic function of vitamin E:

Because of its reducing properties, Vitamin E protects the body against peroxides that
can destroy capillary walls & RBCs.

Required for proper development and functioning of reproductive organs.
2. Hypovitaminosis “E”:
 anemia.
 Muscular dystrophy.
 Male sterility.
 Habitual abortions in females.
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 Encephalomalacia in chicken.
3. Hypervitaminosis “E”: Vitamin E is a safe drug that can be given in large doses.
4. Food sources of vitamin E: Richest sources are vegetables & seed oils. Others: milk, eggs, meat, fish.
5. Uses of vitamin E: Vitamin E is used to increases absorption of vitamin A. Additionally, because of
its reducing properties; it is used in commercial products (oily solutions) to prevent spoilage, & is added
to therapeutic forms of vitamin A to prevent oxidation.
6. Daily requirements:
5 – 15 IU
Vitamin E is carried in the plasma by -lipoproteins. It is incompatible with minerals e.g. Fe3+ & Ca2+
D. Vitamin K: is a group of fat-soluble vitamins that promote blood clotting. It is synthesized by the
normal intestinal bacteria so that an adequate supply is generally present.
It is a naphtoquinon derivative that exists in 3 forms:
o Vitamin K1 (phytoquinon):
of plant origin.
o Vitamin K2 (menaquinon):
of bacterial origin (in the GIT).
o Vitamin K3 (menadion):
Synthetic, wear soluble (inactive).
1. Physiologic functions of vitamin K: The major function of vitamin K is to increase the hepatic
synthesis of prothrombin. Prothrombin is an essential factor in blood coagulation.
2. Hypovitaminosis “K”:
The main symptom of vitamin K deficiency in the body is characterized by lack of clotting of blood after
haemorrhage.
4. Food sources of vitamin K: Green leafy vegetables (cabbage, spinach), cheese, egg yolk & liver.
5. Daily requirements: No requirement for vitamin K is stated since adequate amount is usually ensured
through intestinal bacteria & the body requires vitamin K in very small amounts.
1 – 2 uc
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II. Water Soluble Vitamins
A. Vitamin C (Ascorbic Acid):
Vitamin C or L-ascorbic acid, or simply ascorbate (the anion of ascorbic acid), is an essential
nutrient for humans and certain other animal species. Vitamin C refers to a number of vitamers that have
vitamin C activity in animals, including ascorbic acid and its salts, and some oxidized forms of the
molecule like dehydroascorbic acid.
1. Physiological functions of vitamin C:
o Required in various oxidation and reduction processes. Vitamin C helps in the absorption of iron
from the GIT.
o Building & maintaining collagen, cartilage, bone matrix & connective tissue.
3. Deficiency of vitamin C: Scurvy is the nutritional disease associated directly with vitamin C
deficiency. Tissue deterioration & changes of hemorrhagic origin take place. The skin becomes dry,
rough & has a brown color. Hemorrhages occur in the gums, muscle tissue & in the cavities of
joints, Lesions in teeth, bones & blood vessels.

loosening or loss of teeth

swelling of joints

rarefaction of bones and dentine

Anemia
3. Food sources of vitamin C: Citrus fruits & tomatoes are well known sources of vitamin C. Other
sources include cabbage, potatoes as well as green & yellow vegetables.
4. Uses of vitamin C
o Wound healing: The important role of vitamin C in cementing supportive tissue makes it an
important agent in wound healing. This has evident importance for vitamin C therapy in surgery
or burns especially where extensive tissue regeneration is involved.
o Fevers & infections: infections, especially bacterial infections, decrease tissue stores of vitamin
C, & additional intake is required to help maintain resistance to infection.
o Reaction to Stress: Any body stress such as fracture, general illness & shock requires vitamin C.
o Treatment of mega-hemoglobinemia: because of its reducing properties.
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5. Daily requirements:
 In young animal:
 Adults:
> 20 mg / day
> 150 mg / day
B. Vitamin B1 (Thiamine): is the anti-beriberi factor & is an essential co-enzyme in carbohydrate
metabolism . If Thiamine is not present in sufficient amounts, clinical effects will be reflected in the GI,
CV, & nervous system.
1. Deficiency of vitamin B1: causes beriberi. The disease results from the consumption of white wheat,
polished rice & alcoholics. The 2 general types of beriberi are infantile & adult. It is characterized by
convulsive disorders, respiratory difficulties & GI problems (constipation & vomiting). Symptoms include:
o Peripheral neuritis.
o Tachycardia.
o Cardiac hypertrophy.
o Cardiac hypertrophy.
o Weakness of the legs and walking unstable.
o The lack of progress shows virtual paralysis of the muscles, especially extensor muscles of the legs, wings
2. Toxicity of vitamin B1: because vitamin B1 is very safe, toxicity is not marked.
3. Food sources of thiamine:

Milk and dairy by-products.
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Yeast.
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green forages
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Whole grains.
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Wheat bran and synthetic riboflavin rumen synthesis.
4. Uses of vitamin B1: Vitamin B1 is useful in the treatment of
o Beriberi.
o Neuralgia (nerve inflammation).
o Peripheral neuritis in diabetic patients.
o Mental disorders.
Vitamin B1 may be administered orally, or by subcutaneous or IM injection.
5. Daily requirements:
o Adults:
> 0.6 mg (4.5 mg)
o Children:
> 0.4 mg
o 10 mg for calves and cows.
o 1.5 – 2.5 mg for chicken
C. Vitamin B2 (Riboflavin): is a yellow-green fluorescent pigment that is found in milk. It is an
important factor in protein metabolism .
1. Vitamin B2 deficiency:
o Riboflavin deficiency chiefly causes tissue inflammation & breakdown.
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o Wounds become easily aggravated.
o Lips & nose crack easily (cheilosis – cracks in the corner of the mouth)
o Glossitis (inflammation of the tongue)
o Seborrheic dermatitis (scaly, greasy eruption of the skin), Keratitis
o Photophobia due to corneal vascularization.
o Toxicity of the embryo in pregnants.
o Riboflavin deficiencies seldom occur alone, they are especially likely to occur in conjunction
with deficiencies of other B vitamins & protein.
o Curled toe paralysis in chicken.
o Reduced eggs production and hachability.
2. Food sources of riboflavin: Most important food sources are milk. Other good sources are liver,
kidney , some vegetables and green forage . It is absorbed from the upper GIT.
3. Daily requirements:
o 6 – 8 mg for chicken.
o 20 mg for cattle.
Vitamin B1 may be administered orally, or by subcutaneous or IM injection. It is never given alone
but rather in combination with other B vitamins.
D. Vitamin B3 (Niacin, Nicotinic Acid)
o Vitamin B3 occurs either as Nicotinic acid or Nicotinamide.
CONH2
COOH
N
Nicotinic acid
N
Nicotinamide
1. Physiological functions of vitamin B3:
o Niacin is an important factor in the metabolism of proteins, fats & glucose.
o energy production
o maintenance of skin and tongue
o improves circulation
o maintenance of nervous system
o health of the digestive track
2. Vitamin B3 deficiency:
o The disease associated with niacin deficiency is “pellagra” which is characterized by a typical
dermatitis & often has fatal effects on the nervous system.
o The deficiency is manifested as:

Weakness, lassitude,
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
GIT effects including anorexia & indigestion.

If deficiency continues, the skin & nervous system will be affected. The skin areas exposed to
sunlight develop a dark, scaly dermatitis (photosensitivity). Neuritis, confusion, apathy,
schizophrenia & disorientation also develop.
3. Uses of vitamin B3:
o Treatment of pellagra.
o Nicotinic acid (but not nicotinamide) in doses of > 3 gm / day, is hypocholesterolemic.
4. Food sources of niacin: Meat is the major source of niacin. Peanuts, beans & peas are good
sources. Corn, grain and wheat
5. Daily requirements:
o Adults:
> 6 mg – 45 mg
o Children:
> 4 mg
o 12 mg / kg for chicken.
o 12 – 25 mg/ kg for cattle.
60 mg of tryptophan = 1 mg of nicotinic acid (niacine).
N.B: When vasodilatation is contraindicated we can use nicotinamide instead of nicotinic acid.
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E. Vitamin B6 (Pyridoxine):
1. Physiological functions of vitamin B6:
o Vitamin B6 acts as a coenzyme in protein (amino acid) metabolism (in decarboxylation &
transamination).
o It is essential for the production of GABA (gamma-amino-butyric-acid) in the brain which is the
main neurotransmitter inhibitor to prevent convulsions.
Serotonin (5HT) decarboxy.
Tryptophan Pyridoxal 6 phosphate coenzyme
Nicotenic acid
2. Pyridoxine deficiency: Since pyridoxine plays an important role in several metabolic activities, it's
deficiency may cause the following problems:
o Anemia: Hypochromic, microcytic anemia has been observed in several patients even in the
presence of high serum iron levels.
o Central Nervous System Disturbances: epileptic convulsions & peripheral neuritis.
3. Food sources of pyridoxine: Yeast, wheat, corn, liver & kidney are good sources of vitamin B6.
There is evidence that intestinal bacteria produce this vitamin, but the full extent of this source & the
degree to which it is utilized by the body are not yet determined.
4- Daily requirements:

1 – 7 mg/kg for chicken.

4 mg/kg for cattle.
F. Pantothenic Acid (Panthenol):
o Pantothenic acid is available in all forms of living things & throughout body tissues.
o Intestinal bacteria synthesize considerable amounts of pantothenic acid. This, together with its
widespread natural occurrence, makes deficiency unlikely.
o Pantothenic acid plays a vital coenzyme role in overall body metabolism. It is converted to coenzyme A which is essential for the synthesis of acetylcholine & in fatty acid metabolism.
1. Food sources of pantothenic acid: Yeast, liver & kidney are rich sources, followed by egg, especially
the yolk, leafy vegetables & skimmed milk.
2. Uses of pantothenic acid:
o It is used locally to aid wound healing.
o It can be given IM to aid motility of the intestine after surgical operations.
G. Vitamin B12 (Cyanocobolamin): In 1948 vitamin B12 was discovered & was shown to have
control over the blood-forming defects & neurologic problems involved in pernicious anemia.
1. Physiologic function of vitamin B12:
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o Haematopoiesis: A well-established role of vitamin B12 is it participation in the formation of
RBCs, & therefore, in the control of pernicious anemia.
o Maintenance of the myelin sheath of the nervous tissue: its deficiency leads to neurologic signs.
o Production & normal growth of epithelial cells: in the GIT mucosa, cervix, vagina & tongue.
2. Deficiency of vitamin B12: Leads to pernicious anemia (macrocytic &/or megaloplastic anemia),
which affects all highly proliferating cells & is characterized by:
o RBCs large sized
o WBCs with polysegmented nucleus
o Platelets are giant
o Bone marrow with large cells
3. Uses of vitamin B12:
o Treatment of pernicious anemia (Addison’s pernicious anemia) which is a disease resulting
from the vitamin B12 deficiency. This deficiency can be either due to low vitamin B12 levels, or
defective vitamin B12 absorption due to deficiency of the GIT intrinsic factor.* Symptoms include
peripheral neuritis, gastric mucosal atrophy, glottitis, achlorohydria (lack of HCl secretions), &
megaloplastic anemia.
o The drug of choice for the treatment of pernicious anemia is vitamin B12 given by IM or
subcutaneous injection (oral B12 is of no value as it will not be absorbed due to lack of intrinsic
factor).
4. Food sources of vitamin B12: Vitamin B12 is supplied almost entirely by animal foods where it is
stored in organ meat. The richest sources are liver, kidney, meat, milk, eggs & cheese. 1ml of liver
extract = 10 mg of vitamin B12.
It is the only nutrient that needs a gastric secretion (intrinsic factor) to be absorbed from the GIT. The
intrinsic factor is glycoprotein in nature & is secreted by the parital cells of the stomach (that secrete HCl).
This glycoprotein forms a complex with vitamin B12. The ilial cells take up the formed complex
transporting it to the blood where plasma -globine transfer it to cobolamine II.
Intestinal bacteria also synthesizes some vitamin B12 although the amount supplied is not known.
H. Folic Acid (B9): belongs to group B-vitamins that have an important role in cell growth & bloodforming factors.
1. Physiologic function of folic acid:
o Folic acid is essential for the synthesis of purine & pyrimidine nucleotides.
Folic acid folate reductase enzyme tetra-hydro folinic acid synthesis reaction purine + pyrimidine
(puroyl glutamic acid).
o It's essential for the formation of RBCs.
2. Deficiency of folic acid:
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o Anemia: Simple folic acid deficiency can cause nutritional megaloblastic haematopiosis, a
condition that differs from megaloplastic anemia caused by vitamin B12 deficiency in lacking the
neurologic symptoms, i.e. no myelin damage. (Folic acid is not fully effective as a specific agent in
the control of pernicious anemia).*
o Sprue: Folic acid is effective in treating sprue, a GI disease characterized by severe diarrhea.
o In chicks cause in addition to anemia, slipped tendon, beak deformities,embryonic mortality and
the curve of the leg bone.
3. Toxicity of folic acid: Folic acid is not toxic by the oral route.
4. Food sources of folic acid: Liver, kidney & fresh green leafy vegetables are rich sources.
5. Uses of folic acid:
o Folic acid is used to treat nutritional megaloblastic haematopiosis
o It is also used, in comination with vitamin B12 to treat megaloplastic anemia.
o A metabolite of folic acid, is used to treat cancer, psoriasis and rheumatoid arthritis.
4. Daily requirements:
1.5 – 2 mg / kg for chicken.
0.5 mg / kg for cattle.
* Folic acid can mask the signs of perinaceous anemia but will not prevent the progression nor the
neurologic symptoms.
I. BIOTIN: is a member of the B-Complex group of vitamins. It has been called a
“micronutrient” because such minute traces of it perform its metabolic task.
It is composed of a ureido (tetrahydroimidizalone) ring fused with a tetrahydrothiophene ring.
A valeric acid substituent is attached to one of the carbon atoms of the tetrahydrothiophene
ring. Biotin is a coenzyme for carboxylase enzymes, involved in the synthesis of fatty
acids, isoleucine, and valine, and in gluconeogenesis
o It is synthesized by the intestinal flora or taken with ingested food.
o It has a high potency & a natural deficiency is unknown.
o Biotin is a coenzyme in carbon dioxide reactions in energy metabolism. It is involved in fatty acid
synthesis & in many carboxylation reactions.
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1. Food sources of biotin: excellent food sources include egg yolk, liver, kidney, tomatoes & yeast.
Large amounts of egg white causes its deficiency.
J- Choline:
o It is synthesized in the body from the amino acid methionine.
o It is essential for the synthesis of phosphatidyl-choline which is involved in lipid transport &
acetylcholine synthesis
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