Vitamins
i. The term vitamin is defined as an organic compound required in small amounts for the maintenance of normal
metabolic functions.
ii. A balanced diet should contain vitamins in addition to carbohydrates, proteins, fats, inorganic salts and water.
iii. Scurvy disease occurs due to the deficiency of vitamin C. This disease was common among the sailors who remained
on diets without fresh fruits or vegetables. British navy introduced the use of lime juice (contain vitamin C) by which
the scurvy disease reduced noticeably.
iv. Beriberi disease can be controlled by addition of rice husk to the diet. Later, substance present in rice husk which cured
beriberi was isolated that has nitrogen in it and thus it has been considered as an amine. The term vitamin was
abbreviated from “vital” and “amines”. Now days, the presence of amine group is not necessary for a substance to be
called a vitamin.
v. Some vitamins are synthesized by the body e.g. tryptophan can form nicotinic acid. Intestinal bacteria can synthesize
vitamin K and B12 etc. Vitamin D3 is synthesized in the skin when exposed to the sunlight.
The term vitamin is conditional both on the circumstances and the particular organism. A compound is called
a vitamin when it cannot be synthesized in sufficient quantities by an organism. Ascorbic acid is functions as
vitamin C for some organisms but not for others. Vitamins D and K are required in the human diet only in
certain circumstances. The term vitamin does not include other essential nutrients such as dietary minerals,
essential fatty acids, or essential amino acids and large number of other nutrients that promote health but
otherwise required in less amount.
B. Classification of vitamins
Vitamins are generally classified on the basis of their solubility in either fats or in water. According to their
solubility, vitamins are of two types:
1. Fat soluble vitamins that are A, D, E and K
2. Water soluble vitamins that are vitamin C (ascorbic acid), member of B complex including vitamin B1
(thiamine), vitamin B2 (riboflavin), B3 or nicotinic acid (niacin), vitamin B5 (pantothenic acid), vitamin B6
(pyridoxine), vitamin B7 (biotin), vitamin B9 (folic acid) and vitamin B12 (cyanocobalamin). Other substances
like choline, inositol, PABA, carnitine, lipoic acid, and bioflavonoids (vitamin P) are also considered vitamin
like substances. Several compounds other than a vitamin may possess the activity of a certain vitamin. Such
compounds are termed as vitamers.
https://www.ncbi.nlm.nih.gov/books/NBK22549/table/
Vitamin A
Chemistry
•Vitamin A is a complex alcohol called as retinol.
•Its aldehyde derivative is called as retinal (retinaldehyde).
•There are several isomers of vitamin A and the most important of these are the 13-cis retinol that is found in many
fishes and 11-cis retinol that occurs in retina.
•Vitamin A is quite stable but destroyed at high temperatures in the presence of oxygen.
•Now, it has been synthesized.
•Retinoids are a class of chemical compounds that are related chemically to vitamin A.
Occurrence
i. Vitamin A, present only in animals. Richest sources are the liver oil of certain fishes e.g. halibut, shark and
cod. It is also occur in livers of other animals, egg yolk, butter, cheese and milk.
ii. Colostrum is very rich in vitamin A. (Colostrum is a form of milk produced by the mammary glands of
mammals in late pregnancy). Most species produce colostrum within one day of giving birth.
iii. In plants, Vitamin A occurs as of its precursor or provitamin A i.e. carotenes which are yellow-red pigments
found in carrots, yellow corn, sweet potato, peaches and spinach.
iv. Carotenes do not have any vitamin A activity but are converted to vitamin A in liver.
Physiological role and deficiency effects
1. Role in Vision
This vitamin has best defined role in vision. The 11-cis retinaldehyde (vitamin A isomer) occurs only in
retina. It combines with a protein namely opsin to form a conjugated protein called rhodopsin. Rhodopsin is
responsible for vision in dim light. In the presence of light, rhodopsin hydrolyzes to opsin and All-trans
retinal (All-trans retinal is converted to retinoic acid in vivo by the action of retinal dehydrogenase. ... Retinal
isomers are also chromophores that bind to opsins, a family of G-protein-linked transmembrane proteins, to
form photosensitive receptors in visual and nonvisual systems. All-trans retinal is a potent photosensitizer). In
intense light, all the rhodopsin is hydrolyzed and the person becomes unable to see in the dark. In darkness,
the synthesis of rhodopsin restarts and after some time the person can see more clearly in dims light. If
vitamin A is not available in the body then synthesis of rhodopsin cannot take place and the person become
unable to see in the dim light (disease is called as night blindness). Night blindness is the earliest symptom of
vitamin A deficiency followed by degenerative changes in retina.
Figure: Rhodopsin Cycle
2. Effect on Epithelium
i. Vitamin A is necessary for the maintenance of healthy epithelium of the body.
ii. Vitamin A is necessary in the formation of glycolipids and glycoproteins.
iii. When epithelium becomes stratified (separated into layers), dry, keratinized (tough), susceptible to irritation and
infection it results in following problems;
a. Eyes: Xerophthalmia (the condition in which eyes fails to produce tears due to dryness of the conjunctiva and
cornea) and keratomalacia (cornea become dry, dull and insensitive).
b. Respiratory Tract: The cilia are lost and respiratory infections take place.
c. Changes in genito-urinary tract.
d. Kidney stones,
e. Infertility.
3. Effect on Bones
Vitamin A in necessary for bone growth and development. The deformed skull bones may lead to nerve degeneration
and paralysis.
4. Effect of tooth
Vitamin A is necessary for normal bone growth.
5. Role in Metabolism
This vitamin is necessary for fetal and cell development throughout life. Its optimum concentration is required for
normal activity of mitochondria.
6. Role in Immune System
Enhances the activity of immune system and control infections and malignancies
7. Role in Gene Expression
Vitamin A binds to transcription regulatory protein and control the gene expression.
Hypervitaminosis A
• headache, nausea, vomiting, drowsiness, peeling of skin.
• Chronic hypervitaminosis A causes anorexia, dry itchy skin, alopecia, cracking of the lips, painful areas over
bones, hepatomegaly, splenomegaly, hypothyroidism, leukopenia, anemia, bleeding tendency, increased serum
alkaline phosphatase level. The symptoms disappear after excessive vitamin A intake is stopped.
Vitamin D
Chemistry
Many compounds have anti-rickets properties but only two of them are designated as vitamin D. Those are
called as vitamin D2 and vitamin D3. Vitamin D2 is also called as ergocalciferol that is produced by
ergosterol, isolated from ergot (vegetable origin). Vitamin D3 is also called as cholecalciferol and is of
animal origin. It is produced in the human epidermis by UV irradiation which convert provitamin D3 (7dehydrocholesterol) to cholecalciferol.
Figure: Synthesis of Vitamin D3 in skin
Vitamin D Deficiency
Vitamin D deficiency disease is known as rickets in children and osteomalacia in adults. In rickets bones of children
becomes undermineralized due to poor absorption of calcium. Osteomalacia in adults results from demineralization of
bone in women who have little exposure to sunlight, often after several pregnancies.
Hypervitaminosis D
i. Increased serum calcium level
ii. Nausea
iii. Anorexia
iv. Digestive disturbances
v. Formation of kidney stones
vi. Calcification of body tissues e.g. heart, stomach etc.
vii.Increased serum phosphorus level.
viii.Increased plasma cholesterol level
ix. Growth retardation in infants
Vitamin E
Chemistry
There are eight compounds with vitamin E activity. All are tocopherols and named as alpha, beta, gamma, delta, epsilon,
zeta, eta and theta tochopherols. All of these are derivatives of tocol. D-α-tocopherol is most active and abundantly found
vitamin E and is 5,7,8-trimethyltocol.
Figure: Structure of D-α-tocopherol.
Other tocopherols differ from each other in having different distribution of methyl groups. Vitamin E is a yellow oil,
stable to heat and acids. It is destroyed by commercial cooking and food processing including deep-freezing.
Occurrence
This vitamin occurs in animals and plants. Animal sources are meat, liver, eggs, fish, milk and butter. Plants sources are
wheat germ oil, and to lesser extent cottonseed oil, corn oil and peanut oil.
Physiological role
i. Vitamin E mainly functions as antioxidant.
ii. It is free radical trapping agent in the body.
iii. It is used in chain breaking reactions. In which, it reacts with the lipid peroxide radicals formed by peroxidation of
polyunsaturated fatty acids before they can establish a chain reaction (A chain reaction is a sequence of reactions
where a reactive product or by-product causes additional reactions to take place.
Vitamin E Deficiency
i.
Dietary vitamin E deficiency in humans is unknown.
ii. In experimental animals, vitamin E deficiency results in resorption of fetuses and testicular atrophy (Testicular atrophy is a medical
condition in which the male reproductive organs diminished in size and may be accompanied by loss of function).
iii. Deficiency of vitamin E leads to severe fat malabsorption, cystic fibrosis (conditions causes progressive disability and early death),
and some forms of chronic liver disease.
iv. Nerve and muscle damage occur.
v. Premature infants are born with inadequate reserves of the vitamin E and they suffer with hemolytic anemia.
Vitamin K
Three compounds have the biologic activity of vitamin K. These compounds are;
a. Phylloquinone (Vitamin K1) – the normal dietary source, found in green vegetables.
b. Menaquinones (Vitamin K2) – synthesized by intestinal bacteria with varying side chain lengths.
c. Menadione, menadiol, and menadiol diacetate (Vitamin K3) – synthetic compounds that can be metabolized to
phylloquinone.
Occurrence of vitamin K
i. The best dietary sources of vitamin K are spinach, cabbage, cauliflower and other green vegetables.
ii. Other sources are tomatoes, egg yolk and liver.
iii. The normal bacterial flora especially gram positive bacteria of intestinal tract contribute significant amount of vitamin K2.
Functions
i. Required for synthesis of blood-clotting factors II (prothrombin), VII, IX and X by liver.
ii. It is also use as cofactor for the carboxylation of glutamate residues of proteins to form γ-carboxyglutamate, which chelates
the calcium ion.
iii. Vitamin K is also important in the synthesis of bone calcium-binding proteins.
Deficiency
i. Inhibition of γ-carboxylation of glutamate residues results in lack of physiological activity.
ii. Clotting time is prolonged.
iii. Tendency to bleed from minor wounds.
Vitamin C
Chemistry
i. Vitamin C is also called as Ascorbic acid. L-isomer of ascorbic acid is (L-ascorbic acid) is biologically active in
man while D-isomer (D-ascorbic acid) is biologically inactive.
ii.
It is odorless, white, crystalline substance with sour taste, destroyed by heat and exposure to air
and soluble in water.
iii.
It is a valuable vitamin for human beings but not for the majority of other animals because they
can synthesize it from glucose.
iv.
Human beings, guinea pig, bats, passerine birds (like sparrow), most fishes and invertebrates
can’t synthesize vitamin C due to the lack of enzyme L-gulonolactone oxidase.
Occurrence
1. Fresh fruit and vegetables are good source of vitamin C while animal tissues are not good source.
2. Guava, citrus fruits and tomatoes are the best sources and other sources are green pepper, onion, spinach,
cabbage, turnip, melons and potatoes.
Biochemical Role
1. Vitamin C is involved in oxidation reduction reactions of the body.
2. Vitamin C is involved in synthesis of the steroids hormones.
3. Vitamin C helps in reduction of Fe3+ (ferric) to Fe2+ (ferrous) which can only be absorbed from GIT for
utilization in the body.
4. Vitamin C is used in the treatment of met-hemoglobinemia (met-hemoglobinemia is a disorder
characterized by the presence of a higher than normal level of met-hemoglobin (metHb) in the blood. Methemoglobin is a form of hemoglobin that does not bind oxygen. When its concentration is elevated in red
blood cells, tissue hypoxia can occur).
5. Vitamin C has specific roles in the reactions of hydroxylases especially copper-containing and iron-containing
hydroxylases.
6. Vitamin C takes part in the reduction of folic acid to tetrahydrofolic acid. This reaction is necessary for utilization
of folic acid in the body. Deficiency of this vitamin in the infants results in the megaloblastic anemia (megaloblastic
anemia is inhibition of synthesis of red blood cell by DNA) due to non utilization of folic acid.
7. Vitamin C is involved in the conversion of proline to hydroxylproline present in collagen of normal tissue.
Collagen is main protein of the connective tissues.
8. Vitamin C is used as antioxidant.
9. Vitamin C has a vital role in hydroxylation of dopamine to noradrenaline, synthesis of carnitine, formation of bile
acids and microsomal drug metabolism.
Deficiency
Vitamin C deficiency causes Scurvy (signs of scurvy include changes in skin, fragility of blood capillaries, tooth loss
and bone fracture). Many of these deficiency symptoms can be attributed to deficient collagen synthesis.
Vitamins of B complex
The B vitamins are eight water-soluble vitamins, once they thought to be a single vitamin, called as
vitamin B. Later research showed that they are chemically distinct vitamins that often coexist in the same
foods. Supplements containing all eight vitamins are generally referred to as a vitamin B complex.
Individual B vitamin supplements are;
1.
Vitamin B1 (thiamine)
2.
Vitamin B2 (riboflavin)
3.
Vitamin B3 (niacin or niacinamide)
4.
Vitamin B5 (pantothenic acid)
5.
Vitamin B6 (pyridoxine, pyridoxal, or pyridoxamine, or pyridoxine hydrochloride)
6.
Vitamin B7 (biotin)
7.
Vitamin B9 (folic acid)
8.
Vitamin B12 (various cobalamins; commonly cyanocobalamin in vitamin supplements)
1: Thiamine or Thiamin (Vitamin B1)
Chemistry
1. Thiamine is white crystalline compound, soluble in water, slowly destroyed by moist heat, yeast like odor.
2. Thiamine has pyrimidine and thiazole part in its molecule linked by a methylene bridge.
Occurrence
1. Thiamine is present in outer layer of grains (outer layer of grain called bran) and rice polishing.
2. Best dietary sources of this vitamin include whole grains, legumes, beef, liver, nuts and yeast.
3. It is found in lesser amount in milk, eggs, fish and vegetables.
Biochemical Role
1. Thiamin has a key role in energy-yielding metabolism, especially in carbohydrate metabolism.
2. Thiamin diphosphate is the coenzyme for three multi-enzyme complexes that catalyze oxidative decarboxylation reactions.
3. It is also the coenzyme in the pentose phosphate pathway (This pathway is an alternative to glycolysis. While it does
involve oxidation of glucose, its primary role is anabolic rather than catabolic).
Deficiency
Vitamin B1 deficiency leads to beriberi that includes neurological disturbances, cardiac insufficiency and muscular
atrophy (symptoms of beriberi include weight loss, emotional disturbances, weakness, pain in the limbs and periods of
irregular heart rate. Edema is common. It may increase the amount of lactic acid and pyruvic acid within the blood. In
advanced cases, the disease may cause heart failure and death).
2: Riboflavin (Vitamin B2)
Chemistry
1. It is an orange yellow crystalline compound, soluble in water, stable by heat but sensitive to light.
2. Riboflavin consists of a heterocyclic dimethyl-isoalloxazine ring attached to a sugar alcohol called D-ribitol.
Occurrence
1. Riboflavin is widely distributed in nature and present in plant and animals.
2. Rich sources of riboflavin are liver, wheat germs, yeast, milk, meats, fish and eggs.
3. Poor sources of vitamin are leafy vegetables, fruits and root vegetables.
Biochemical Role
1. Riboflavin helps the different redox coenzymes like flavin mononucleotide (FMN) and flavin adenine dinucleotide
(FAD). FMN and FAD are cofactors for various oxidoreductases.
Deficiency
Riboflavin deficiency is widespread but not fatal. The deficiency is characterized by cheilosis (it is an inflammatory lesion
at corner of the mouth), lingual desquamation (it is the shedding of the outer layers of the skin) and seborrheic dermatitis
(it is a skin disorder causing scaly, flaky, itchy and red skin).
Niacin or Nicotinic acid or Vitamin B3
Chemistry
1. Niacin is a colorless, water soluble and heat stable solid. It is derivative of pyridine with a carboxyl group (COOH)
at its 3-position. Niacin is also called Nicotinic acid (pyridine 3-carboxylic acid). Amide derivative of niacin
(nicotinamide) also possess activity of niacin.
Occurrence
1. Richest source of vitamin B3 is liver and kidney. Good sources of vitamin B3 are meat, fish, eggs, milk, whole
wheat, dried legumes, unpolished rice, peanuts, tomatoes, tea, coffee and leafy vegetables.
2. In body it can be derived from tryptophan thus it is not considered a vitamin.
3. This vitamin is also synthesized by intestinal bacteria.
Biochemical Role
1. Niacin is vasodilator.
2. Niacin is part of structure of NAD+ and NADP+. These coenzymes have well defined role in biological
oxidation.
Deficiency
Deficiency of Niacin causes Pellagra which means rough skin. Pellagra is indicated by four Ds, dermatitis, diarrhea,
dementia, and if untreated then death.
4: Pantothenic Acid or Vitamin B5
Chemistry
1. Viscous yellow oil, stable to moist heat but destroyed by dry heat. Only dextrorotatory isomer possesses
biological activity.
Pantothenic acid
Occurrence
1. It is very widespread vitamin. It occurs in liver, kidney, eggs, milk, cauliflower, cabbage, peas, potatoes and tomatoes.
2. Intestinal E. coli can also synthesize this vitamin.
Biochemical Role
1. Pantothenic acid acts as a part of coenzyme A or acyl carrier protein. CoA takes part in reactions of the citric acid
cycle, fatty acid synthesis and oxidation, acetylations and cholesterol synthesis. Acyl carrier protein participates in
fatty acid synthesis.
Deficiency
1. Widely distributed in all foodstuffs and deficiency has not been clearly reported in humans.
2. In deficiency; neuromuscular degeneration and deficient functioning of adrenal cortex occur.
5: Pyridoxine or Vitamin B6
Chemistry
1. Pyridoxine is soluble in water, colorless crystals, sensitive to light, UV and alkalies.
2. Convertible to aldehyde form i.e. pyridoxal and amino form i.e. pyridoxamine
Occurrence
1. Pyridoxine is present in egg yolk, meat, fish and milk of the animal kingdom.
2. It is also present in yeast, whole grains, cabbage and legumes of the plants kingdom.
Biochemical Role
1. Pyridoxal phosphate is a coenzyme for many enzymes involved in amino acid metabolism, especially in
transamination and decarboxylation.
2. Cofactor of glycogen phosphorylase
Deficiency
Vitamin B6 deficiency is rare, it occurs in children and pregnant women, its deficiencies result in the abnormalities of
tryptophan and methionine metabolism.
6: Biotin or Vitamin B7 or Vitamin H
Chemistry
1. Biotin is colorless, needle-like crystals, slightly soluble in water, heat stable.
2. It is monocarboxylic acid.
Occurrence
1. It is widely distributed in nature. It is found especially in liver, kidney, milk, tomatoes, yeast and molasses.
2. It is occur in large amount in royal jelly produced by bees (Royal jelly is a honey bee secretion that is used in the
nutrition of larvae, as well as adult queens).
3. It is also synthesized by intestinal flora. It is an important source of biotin.
Biological role
Biotin is a coenzyme of carboxylases class of enzymes.
Deficiency
1. Deficiency is unknown except in people kept for many months on parenteral nutrition.
2. Deficiency of biotin can occur in very small number of people who eat abnormally large amounts of uncooked egg white,
which contains avidin, a protein that binds biotin and make it unavailable for absorption.
7: Folic Acid or Folacin or Vitamin B9
Chemistry
1. It is yellow, crystalline substance, slightly soluble in water, heat stable in neutral or alkaline medium but not in
acidic medium.
2. Its structure consists of three components;
a. A derivative of pteridine
b. Para-aminobenzoic acid (PABA)
c. Glutamic acid
Occurrence
1. Widely distributed in nature. Its name folic acid is because of its presence in foliage of plants.
2. It is found in liver, kidney, beef, cauliflower and wheat.
3. It is synthesized by intestinal bacteria.
Biochemical Role
Folic acid is not active as such. For activation, it is reduced to tetrahydrofolic acid. Folic acids are involved in the metabolisms
of nucleic acids, amino acids and phospholipids.
Deficiency
1. Folate deficiency causes megaloblastic anemia.
2. Deficiency of folic acid affects the cells that are dividing rapidly.
3. Its deficiency affects the bone marrow functions.
8: Cyanocobalamin or Cobalamin or Vitamin B12
Chemistry
1.
Also called anti-pernicious anemia vitamin (Pernicious anemia is a form of megaloblastic anemia,
due to vitamin B12 deficiency, caused by impaired absorption of vitamin B12 due to the immune destruction
of intrinsic factor, more specifically of loss of gastric parietal cells).
2.
This is only and naturally occurring organic compound that possess cobalt in their structure.
3.
It is deep red, tasteless crystalline compound, soluble in water, heat stable in neutral pH but not at
alkaline pH.
4.
Structure of vitamin B12 has four parts;
a.
Corrin ring
b.
A single cobalt atom with positive charge present in the center of corrin ring
c.
Dimethylbenzimidazole part
d.
Ribose phosphate part
Figure: Vitamin B12. X=CH3 in methylcobalamin; X=CN in
cyanocobalamin (commercial form).
Occurrence
1. This vitamin is not present in plants.
2. This vitamin is only found in bacteria and in animal tissues.
3. Best sources of vitamin B12 are liver and kidney.
4. It also occurs in milk, eggs and fish.
5. It is also synthesized by intestinal flora.
Biochemical Role
Vitamin B12 is involved in two reactions in the body:
a. The transfer of a methyl group to homocysteine to form methionine.
b. Rearrangement of the methyl group of L-methylmalonyl CoA to form succinyl CoA
Deficiency
Vitamin B12 deficiency causes pernicious anemia. Pernicious anemia arises when vitamin B12 deficiency
blocks the metabolism of folic acid. This impairs erythropoiesis, causing immature precursors of erythrocytes
to be released into the circulation (megaloblastic anemia). The commonest cause of pernicious anemia is
failure of the absorption of vitamin B12 rather than dietary deficiency.