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Essay on Vitamin A
- Essay on the Historical Review of Vitamin A
- Essay on the Chemical Structure of Vitamin A
- Essay on the Absorption of Vitamin A
- Essay on the Synthesis of Vitamin A
- Essay on the Properties of Vitamin A
- Essay on the Distribution of Vitamin A
- Essay on the Deficiency of Vitamin A
Essay # 1. Historical Review of Vitamin A:
In 1912 Hopkins reported normal and continued growth when whole milk was added to purified rations in young rats, and this study ultimately led up to the discovery of this vitamin by McCollum. In 1915 McCollum and Davis established the essential factors in eggs, butter and milk, i.e., ‘fat-soluble A’ in eggs and butter, and ‘water-soluble B’ in milk. ‘Fat-soluble A’ cured Xerophthalmia.
Includes A1 and A2. A2 is functionally almost similar to A1. Chemical structure is slightly different. Vitamin A2 has one more double-bond. It is a dehydrovitamin A1 and also known as 3-dehydroretinal. Its potency is 40% that of vitamin A1. Vitamin A1 may be derived from β-carotene by cleavage at the midpoint of the carotene molecule.
Essay # 2. Chemical Structure of Vitamin A:
Unsaturated primary alcohol (-ioninol). Empirical formula of vitamin A1 (retinol1) is C20H29OH and of vitamin A2 (retinol2) is C20H27OH. Structure closely similar to plant pigments carotenes, the pro-vitamin A.
Since β-ionone ring is essential part of vitamin A molecule and as β-carotene contains two β-ionone rings and α- and γ-carotenes contain β-ionone ring, so α- and γ-carotenes give one molecule of vitamin A but β-carotene gives two.
The chemical structure of β-carotene, vitamins A1 and A2 are shown below:
Vitamin A exists naturally in several isomeric forms. This is a cistrans isomerism which arises from configurational differences about the double bonds in the side chain. The most naturally occurring form of vitamin A is the all-trans isomer.
Retinene (Retinal) is the aldehyde form of vitamin A.
Essay # 3. Absorption of Vitamin A:
In the small intestine, the vitamin A esters of food are hydrolysed to fatty acids and free vitamin. Vitamin A1 and carotene are absorbed through the lymphatics and appear in the blood plasma as the ester, indicating re-esterification in the intestinal wall. Presence of fats and bile salts helps the process. Vitamin A1 is more quickly and completely absorbed than carotene and the latter which is not converted to vitamin A here is carried to the blood. The simultaneous presence of tocopherols and other antioxidants protects them against destruction in the intestinal lumen.
Chiefly in the liver (95%) as esters. Slightly in the lungs, lactating breasts, kidney, skin, etc. In liver vitamin A seems to be associated with lipoprotein.
The values for vitamin A and carotenes in the blood of normal subjects vary widely. Approximate concentrations are—vitamin A, 18 to 60 µ gm (60 to 200 i.u.) per 100 ml serum; carotenoids, 100 to 300 µ gm per 100 ml serum, carried mainly in the β-lipoprotein fraction.
Essay # 4. Synthesis of Vitamin A:
In the body from carotene. One molecule of β-carotene gives two molecules of vitamin A. Hence, carotene is called pro-vitamin A.
Conversion takes place in the intestinal mucosa by the enzyme carotinase in rats, pigs, goats, sheep, etc., although the liver may also participate. In man the liver is believed to be the only organ which performs this conversion. It has also been artificially synthesised.
Essay # 5. Properties of Vitamin A:
Soluble in fat-solvents, insoluble in water. Ordinarily it is a viscid colourless oil but by careful fractionation it has also been isolated as pale yellowish needles.
Heat-stable, provided contact with air is prevented. Easily destroyed on exposure to air or ultra-violet rays. It gives a characteristic absorption band in the ultra-violet spectrum at 328 mµ.
Essay # 6. Distribution of Vitamin A:
Vitamin A is present only in lipids of animal sources and carotenoid, in vegetable ones.
i. Animal Sources:
Cod-liver oil (400-4,000 i.u. per gm); halibut-liver oil (20,000 i.u. per gm); milk (2,000 i.u. per 600 ml); butter (20-50 i.u. per gm); one egg (200 i.u.). Fishes are also rich sources.
ii. Vegetable Sources:
Vegetable oils contain very little. Substances which are rich sources of carotene, e.g., carrots (20 i.u. per gm); spinach (100 i.u. per gm). Green leaves, yellow fruits such as mangoes, tomatoes, etc., are also good sources.
i. Essential for growth.
ii. It is a component of rhodopsin, hence essential for night vision (vide ‘Rhodopsin’).
iii. Maintains the integrity and activity of epithelial tissues and glands.
iv. Prevents infection (secondary to normal epithelial tissues).
v. It plays some part in protein synthesis.
vi. Controls the action of the bone cells, so that normal growth and shape of bone are maintained.
vii. Vitamin A is directly concerned both in the formation of mucopolysaccharides and also in the sulphation of it.
viii. Helps in keeping normal fertility.
ix. Vitamin A participates in reactions which affect the stability of cell membranes, and membranes of subcellular particles.
x. It also plays a stabilising role on the normal permeability of lysozymes and mitochondria.
xi. It is probable, that vitamin A has some specific functions on carbohydrate metabolism.
xii. Prevents the condition known as urolithiasis where urinary calculi in the form of calcium phosphate is present.
The protein carrier of vitamin A is similar to that of copper-carrying protein, ceruloplasmin, and both are stored predominantly in the liver. It has been observed that there may be inverse relationship between the vitamin and the metal. This indicates that there may be some reciprocating interplay between vitamin A and copper in their metabolism and mode of action.
Essay # 7. Deficiency of Vitamin A:
i. General Growth:
Failure of growth.
a. Night-Blindness (Nyctalopia):
The rhodopsin or visual purple is chromoprotein containing the carotenoid pigment retinene which is same as vitamin A aldehyde or retinal as a prosthetic group and a protein opsin. It is present in the outer limbs of the rods only. When exposed to light rhodopsin is split up into the yellow compound retinene and colourless protein opsin.
The retinene is actually retinene1 (vitamin A1 aldehyde). Under the influence of light, rhodopsin is converted to orange-red compound lumirhodopsin which becomes changed to metarhodopsin, ultimately forming a yellow mixture of trans-retinene and opsin.
In vitro, transretinene is converted to cis-retinene on exposure to blue light. But in the eye, transretinene is rapidly converted to trans-vitamin A by retinene reductase and NADH. In dim light during the process of resynthesis of rhodopsin active cis-vitamin A enters the retina from blood and is oxidized to cis-retinene by retinene reductase and NAD.
b. Degeneration of lachrymal glands.
c. Redness, abnormally dry and lusterless condition of the eye-ball (Xerophthalmia) (Fig. 11.2) with consequent keratinization and degeneration of cornea (Keratomalacia).
iii. Epithelial Tissues:
Thickening and keratinisation, follicular and popular eruptions (Phrynoderma or Toad skin), sebaceous and sweat glands degenerate.
b. Alimentary Tract:
The glands present in the alimentary tract and the epithelial linings degenerate.
c. Kidney and Urinary Tract:
Epithelium degenerates and becomes cornified, hence favours formation of renal stone.
d. Respiratory Passages:
The Epithelium becomes stratified and degenerates.
These degenerative changes of the epithelial tissues decrease the resistance of the local cells, hence infection in these regions easily takes place. For this reason vitamin A is called anti-infective vitamin.
iv. Nervous System:
Degeneration of the nervous system specially affecting the afferent tracts (resembles subacute combined degeneration). Retina also shows degenerative changes.
Abnormal bone growth in certain parts of vertebral column and skull. It is believed that effects on nervous system are partly due to the abnormal type of growth giving pressure effect on nerves.
In rats reproduction becomes defective. Interferes with the normal process of ovulation although it is not proved in man.
Equivalent to the activity of 0.6 micro-gram of carotene (same as 0.344 micro-gram of pure preparation of vitamin A1 acetate).
5,000 i.u. for adults. For growing children and during puberty, lactation and pregnancy—6,000-8,000 i.u.
In growing rats large doses (4,000 units per day) cause:
i. Loss of weight.
ii. Atrophy of skin.
iii. Loss of hair.
iv. Ulcerations in the eyes.
vi. Decalcification of bones with spontaneous fracture.
vii. Lowering of plasma prothrombin.
viii. Reduction of ascorbic acid content of the tissues.
Administration of vitamins K and C prevents these changes of hypervitaminosis A. Effects in man include drowsiness, sluggishness, severe headache, vomiting and peeling of skin of mouth and elsewhere.
The haemorrhagic manifestations associated with hypervitaminosis may be prevented by simultaneous administration of vitamin K. The effect may be due to interference with bacterial synthesis of vitamin K in the intestine. The antioxidant action of tocopherols is probably responsible for its sparing action on vitamin A and carotene. This protective effect of vitamin E is enhanced by other antioxidants, e.g., ascorbic acid, etc.