The below mentioned article provides a study note on Vitamin B:- 1. Introduction to Vitamin B 2. Chemistry of Vitamin B 3. Absorption 4. Transportation 5. Excretion 6. Sources 7. Functions 8. Deficiency Symptoms 9. Management 10. Maintenance Treatment 11. Toxic Effects.
Contents:
- Essay on the Introduction to Vitamin B
- Essay on the Chemistry of Vitamin B
- Essay on the Absorption of Vitamin B
- Essay on the Transportation of Vitamin B
- Essay on the Excretion of Vitamin B
- Essay on the Sources of Vitamin B
- Essay on the Functions of Vitamin B
- Essay on the Deficiency Symptoms of Vitamin B
- Essay on the Management of Vitamin B
- Essay on the Maintenance Treatment by Vitamin B
- Essay on the Toxic Effects of Vitamin B
Essay # 1. Introduction to Vitamin B:
a. In 1926, Minot and Murphy discovered that liver can cure pernicious anemia.
b. In 1948, Smith and Parker in Great Britain and Rickes et al in U.S.A. independently isolated Vitamin B12.
c. It is identical with extrinsic factor present in liver which cures pernicious anemia. It was found effective in curing pernicious anemia when administered intramuscularly in small quantities (5 to 10 µg.).
d. Although vitamin B12 is synthesized exclusively by microorganisms, for practical purposes it is found only in foods of animal origin but no plant sources of this vitamin. This indicates that the strict vegetarians are at risk of developing B12 deficiency.
The small amounts of the vitamin formed by bacteria on the surface of fruits may be adequate to meet requirements. The preparations of vitamin B12 made by bacterial fermentation are available.
Essay # 2. Chemistry of Vitamin B:
a. The structure of vitamin B12 is given below. The central portion of the molecule consists of 4 reduced and substituted pyrrole rings surrounding a single cobalt atom. The central structure is referred to as a “Corrin” ring system.
Two of the Pyrrole rings (rings A and D) are joined directly rather than through a single methylidyne carbon. Below the corrin ring system there is a 5, 6-dimethylbenzi-midazole riboside that is connected at one end to the central cobalt atom and at the other end from the ribose moiety through phosphate and amino-propanol to a side chain on ring D of the tetrapyrrole nucleus.
Addition of cyanide forms “Cymocobalamin” which is identical with the originally isolated vitamin B12 and the removal of cyanide group results in the formation of the compound “Cobalamin”. Cyanide group, if substituted by hydroxy group, forms “hydroxocobalamin”, by a nitro group forms “nitro-cobalamin ” by a methyl group forms “methylacobalamin”. It contains cobalt 4 to 5 per cent.
b. It has molecular weight of 1,355 and an empirical formula C63H88N14O14PCO.
c. Aqueous solution of vitamin B12, when exposured to sunlight, results in the destruction of the vitamin.
d. If ascorbic acid is added to a solution of vitamin B12, the B12 activity is slowly destroyed due to the reducing action of ascorbic acid on vitamin B12.
e. Crystalline vitamin B12 is stable to heating at 100°C for long periods and aqueous solutions at pH 4.0-7.0 can be autoclaved with very little loss. Destruction is rapid when the vitamin is heated at pH 9.0 or above.
Essay # 3. Absorption of Vitamin B:
a. Vitamin Bl2 is absorbed from the ileum. Its absorption depends on the presence of hydrochloric acid and a constituent of normal gastric juice called the Intrinsic factor (IF), a mucopolysaccharide, secreted by the parietal cells of the gastric mucosa.
b. Free vitamin B12 (cobalamin) is bound to intrinsic factor in the proportion of 2 mol of cobalamin to 1 mol of IF. Intrinsic factor is found in the cardia and fundus of the stomach. The combination of B12 with intrinsic factor results in the formation of a complex which is resistant to intestinal digestion. Vitamin B12 also binds to the proteins of gastric juice, bile and saliva.
c. It is currently believed that intrinsic factor possesses 2 receptor sites, one for B12 and the other for ideal intestinal microvilli. The former receptor site requires a neutral pH and the presence of calcium ions (Ca++). The latter receptor site is readily saturated which limits the absorption of Bl2 to 1.5 µg after a single dose.
The intrinsic factor is released within the intestine liberating B12 to pass into the intestinal mucosal cell. Intrinsic factor protects vitamin B12-peptide against bacterial attack, and in the peptide form the vitamin is absorbed.
d. About 1% of the large concentration of the vitamin is also absorbed by passive mechanism.
Essay # 4. Transportation of Vitamin B:
a. Vitamin B12 is present in plasma as methylcobalamin, 5′-deoxyadenosylcobalamin or hydroxycobalamin bound to proteins, transcorrin I and transcorrin 11. Transcorrin I is a strong binder of cobalamin and transcorrin II is a weaker binder of cobalamin. 1-10% of B12 carried on transcorrin II is attached immediately after absorption and is readily released to be excreted in the urine.
b. Cobalamin bound to plasma protein fraction is carried to the tissues where it is bound to a variety of protein receptors. Any excess is stored in the liver as 5′-deoxyadenosylcobalamin. The total amount of cobalamin in the bodies of adults is 2.5 mg of which about 1.5 mg is in the liver.
Essay # 5. Excretion of Vitamin B:
a. B12 is excreted mainly by the way of the bile and by this pathway about 40 µg. pass into the jejunum daily. By an interohepatic circulation, most of this is reabsorbed in the ileum using the intrinsic factor mechanism.
b. Small amounts of the vitamin also enter the intestine from the gastric, pancreatic and intestinal secretions.
c. The unabsorbed vitamin leaves the body in the feces. This amount—together with that produced in the colon by bacterial synthesis—is about 3-6 µg daily.
d. Cobalamin unbound to protein is excreted in the urine. This amounts to 0.25 µg/day.
Normal Concentration of Vitamin B in Serum:
200 to 850 µg/dL.
Essay # 6. Sources of Vitamin B:
Essay # 7. Functions of Vitamin B:
a. Vitamin B12 along with folic acid is required for the development of red blood cells beyond megaloblast stage.
b. It stimulates the appetite and general health of the subject.
c. It cures the neurological symptoms of pernicious anemia.
d. Coenzyme activities:
(i) Vitamin B12, as the coenzyme, is involved with tetrahydrofolate in the synthesis of labile methyl groups which can be transferred to homocysteine to form methionine. This is not sufficient to supply the body with its total methionine requirement and the amino acid is, therefore, a member of the essential amino acid group.
(ii) The vitamin is also a coenzyme for the mutase which converts methyl- malonyl-CoA into succinyl-CoA, Hence, methylmalonate accumulates in the urine in deficiency states.
(iii) The vitamin is also involved in the maintenance of sulfhydryl groups in the reduced state. The deficiency of the vitamin produces the reduction of glutathione in the blood.
(iv) Vitamin B12 is also involved in the conversion of ribonucleotides to deoxyribonucleotide.
(v) It is also required in the dehydrase reactions in the conversion of ethylene glycol to acetaldehyde and glycerol to β-hydroxypropionaldehyde.
(vi) As coenzyme, it is required for the isomerisation of glutamic acid to threo-β-methyl aspartate.
(vii) It is involved in the biosynthesis of proteins.
Essay # 8. Deficiency Symptoms of Vitamin B:
In man, deficiency of vitamin B12 may result from poor dietary intake which occurs in the tropics, in strict vegetarians (vegans) and occasionally in the elderly.
It may result from a deficiency of intrinsic factor or from interference with the function of intrinsic factor and from intestinal malabsorption and also from the prolonged use of anticonvulsant drugs and of paraminosalicylic acid which is used in the treatment of tuberculosis.
In deficiency states, the symptoms are:
a. Megaloblastic macrocytic anemia (Pernicious anemia).
b. Mucosal atrophy and inflammation of tongue (glossitis) and mouth.
c. Severe disease of the nervous system both central and peripheral.
d. Psychiatric symptoms are not uncommon.
e. There may also be amblyopia.
f. A severe form of acidosis in children due to the excessive production of methyl-malonate due to congenital defect in the biosynthesis of 5′-de-oxy-adenosyl cobalamin.
Essay # 9. Management of Vitamin B:
(a) In the deficiency of vitamin B12, hydroxocobalamin is given parenterally in a dosage of 1,000 µg twice during the first week, then 100 µg weekly for a further 6 doses. Within 48 hours of the first injection the bone marrow shows a striking change from a megaloblastic to a normoblastic state.
(b) In some patients the rapid regeneration of the blood depletes the iron reserves of the body and recovery is stopped. To prevent this, ferrous sulphate 200 mg daily should be given soon after the commencement of the treatment. A combined deficiency of vitamin B12 and iron is found by the presence of macrocytosis and hypochromia.
Essay # 10. Maintenance Treatment by Vitamin B:
The patient must have regular parenteral doses of hydroxocobalamin indefinitely (1,000 µg i.m. every 3 months) for life. Blood counts should be performed annually.
Essay # 11. Toxic Effects of Vitamin B:
No ill-effects on excessive ingestion of the vitamin.