VITAMIN A
A. History. It was first recognized as an essential nutritional factor by Elmer McCollum in 1915 and then isolated from fish-liver oil by Holmes in 1917. On account of its established role in the visual process, it is often called as antixerophthalmic factor or the “bright eyes” vitamin. It was first synthesized in 1946 by Milas.
B. Occurrence. Liver oils of various fishes are the richest natural sources of vitamin A. Shark and halibut contain maximum amount whereas the cod-liver has lowest amount. Depending upon the species of fish and the time of year of catch, the fish livers contain 2,000 to 100,000 I.U. per gram of vitamin A. The amount present in human liver is much less (500 to 1,000 I.U.per gram). However, polar bear liver is an extremely concentrated source of vitamin A. Other noteworthy sources are butter, milk and eggs and, to a lesser extent, kidney. In its provitamin form (i.e., as carotenes) it is supplied by all pigmented (particularly yellow) vegetables and fruits such as carrots, pumpkins, cantaloupes, turnips, peppers, peas, sweet potatoes, papayas, tomatoes, apricots, peaches, plums, cherries, mangoes etc. Yellow corn is the only cereal containing significant amounts of carotene. New-born infants have low quantities of vitamin A content that is rapidly augmented because colostrum and breast milk furnish large amounts of the vitamin. The milk of well-fed mothers, however, contains sufficient amounts of vitamin A (in ester form) for the infant's need. However, vitamin A is absent from vegetable fats and oils (olive oil, linseed oil, groundnut oil). It is added to margarine during its manufacture from these oils.
The β-carotene content of some items are presented in Table Vitamin A originates in marine algae, and then passes up the food chain to reach the large carnivorous animals. Toxic levels of vitamin A may accumulate in the livers of a wide range of creatures such as Polar bears, seals, porpoises, dolphins, sharks, whales, Arctic foxes and huskies. Even a small meal of southern Australian seal liver, say 80g, may produce illness in man. Most of the foods recommended as source of vitamin A contain well below the toxic levels of vitaminA, but one– Halibut liver oil– contains dangerously high amounts of vitamin A.
As regards the vitamin A contents of polar animals, one can see that, in reality, very little quantities of livers of these animals are required to kill a human being : 30–90 g of polar bear liver or halibut liver, 80–240 g of bearded seal liver and 100-300 g of Antarctic husky liver is enough to kill a human being.
C. Structure. Vitamin A is found in two forms A1 and A2. The carotenoids that give rise to vitamin A in animal body is named as provitamin A. These inculde α-, β- and γ-carotenes and cryptoxanthin. β-carotene is most potent of all these forms. A molecule of β-carotene is made of eight 5-carbon isoprenoid units, linked to form a long chain of 40 carbon atoms with an ionone ring at each end. It is an orange-red hydrocarbon and upon hydrolysis yields 2 moles of vitamin A1 . During hydrolysis, a cleavage occurs at the mid point of the carotene in the polyene chain connecting the 2 β-ionone rings. This conversion usually takes place in livers of fishes and mammals. Vitamin A1 is a complex primary alcohol called retinol, having the empirical formula, C20H29OH. The
terminalhydroxyl group is ordinarily esterified. It contains β-ionone ring. Another form of vitamin A, present in fresh-water fishes, is known as vitamin A2. It differs from vitamin A1, which is found in salt-water fishes, in possessing an additional conjugate double bond between carbon atoms 3 and 4 of the β-ionone ring. Its potency is 40% that of vitamin A1.
D. Properties. Ordinarily retinol is a viscid, colourless oil but by careful fractionation it has also been isolated as pale yellowish needles. It gives a characteristic absorption band in ultraviolet (UV) spectrum at 328 mμ. It is soluble in fat and fat solvents but insoluble in water. Loss of vitamin A in cooking, canning and freezing of foodstuffs is small; oxidizing agents, however, destroy it. It is destroyed on exposure to UV light. Vitamin A is relatively unstable in air unless protected by antioxidants including vitamin E.
E. Metabolism. In the tissues, the metabolic transformation of retinol is carried out by enzymes. The dietary β-carotene is split into retinal by an enzyme of the intestine. Retinal is then reduced by another enzyme to retinol which, in turn, is converted to retinyl ester by reacting with a fatty acid like palmitic. The retinyl ester, on the contrary, is enzymatically hydrolyzed t to produce retinol which is re-esterified with palmitic acid to produce retinyl ester. This is absorbed
through the lymphatic system and is stored in the liver.
Liver stores vitamin A in large quantities mainly in the form of retinyl ester. But the vitamin A that circulates in the blood is in the form of retinol and is bound to a specific carrier protein called retinol binding protein (RBP). The retinyl ester present in the liver, therefore, has to be converted to retinol before it mixes with the blood. Liver can also successively convert retinol to retinal and retinal to retinoic acid. Retinoic acid is quickly absorbed from the intestine through the portal system and is rapidly excreted back into the intestine through the bile. Vitamin A helps maintain the epithelial cells of the skin and the linings of the digestive, respiratory and genito-urinary systems. These linings play a protective role against cancer-causing agents (or carcinogens), viruses and bacteria and are rendered vulnerable by a deficiency of vitamin A. Vitamin A guards against cancer by protecting cell walls from undesirable oxidation, and scavenging the products of oxidation— free radicals, which are linked to the development of cancer.
F. Deficiency. Vitamin A is perhaps the most important as it affects the various metabolic processes in the body. It has profound effect on epithelial structures, in general. Vitamin A deficiency leads to the onset of many diseases like nyctalopia or night blindness (inability to see in night), xerophthalmia (scaly condition of the delicate membrane covering the eyes), keratomalacia (softening of the cornea), phrynoderma or “toad skin” (hard and horny skin) and stunted growth. Xerophthalmia or xerosis is a major cause of blindness in childhood and is still a major health problem in Far East such as Hong Kong, Jakarta, Manila and Dhaka. The disease affects large number of children but few adults. Xerophthalmia is characterized by drying of the eyes and hence so named (xerosG = dry ; ophthalmosG = eyes). The lacrymal glands become stratified and keratinized and cease to produce tears. This makes the external surface dry and dull. The ulcers develop. The bacteria are not washed away. The eyelids swell and become sticky. This results in frequent exudation of blood, causing severe infection to the eye. If left untreated, blindness results. Incredible, yet true, about 1400 cases of xerophthalmia were reported in 1904 among Japanese children. Besides, during World War I, many xerophthalmic cases were reported in Denmark because of the fact that butterfat was shipped out of that country in huge quantities and people had to live on substitutes with no retinol.
Keratomalacia (keratoG = hair ; malakiaG = softness) is a corneal disease, occurring maximally in pre-school children of 3–4 years. This usually happens suddenly in young children with kwashiorkor esp., after an episode of diarrhea or infection. At first the cornea loses its lustre, undergoes a necrosis and develops a few pin-point ulcers, which later coalesce to form a large, white ulcerative area. The perforation of the cornea may follow sometime, causing the release of aqueous humour and prolapse of the iris. Occasionally, instead of extensive ulceration and perforation of the cornea, the whole eyeball may shrink. Keratomalacia is unfortunately still prevalent on a wide scale in many parts of India (South and Eastern) and Indonesia and some other countries of Asia and Africa. Phrynoderma is a skin lesion and is characterized by follicular hyperkeratosis. In it, the skin esp., on the outer aspects of forearms in the regions of the elbows and of the thighs and buttocks becomes rough and spiky. In severe cases, the trunk is also affected. Also, the damaged epithelial structures in diverse organs such as the eyes, the kidneys or the respiratory tract often become infected. It is for this reason that vitamin A has been called an ‘anti-infection’ vitamin. The vaginal epithelium may become cornified, and epithelial metaplasia of the urinary tract may contribute to pyuria and hematuria. Increased intracranial pressure with wide separation of cranial bones at the sutures may occur.
In the alimentary tract, the deficiency of vitamin A causes damage to the intestinal mucosa, resulting in diarrhea. Vitamin A is an important factor in tooth formation. In its deficiency, there is a defective formation of enamel so that the dentin is exposed. Evidently, sound tooth formation does not occur. Vitamin A deficiency may result in retardation of mental and physical growth and in apathy. Anemia with or without hepatosplenomegally is usually present. Other deficiency diseases that have been attributed to vitamin A are atrophy of the testes and disturbances of the female genital organs.
According to a report, presented at a meeting of the National Seminar on Corneal Disasters held in New Delhi (1981), India accounts for about one-third of the total blind population of the world, that is about 9 million blind people and that every year about 25,000 children go blind in India due to malnutrition. Researches conducted by the National Institute of Nutrition (NIN), Hyderabad (1978), show that about 30% of the blind in India lost their sight before they were 21. NIN studies have also revealed that about 10% of the school children belonging to the poorer socioeconomic groups show signs of vitamin A deficiency. It is however, worth-mentioning that the vitamin A deficiency is mainly a result of ignorance rather than the non-availability of food or of the resources to acquire the food as is the case with protein calorie malnutrition. According to NIN researches, if 40 g of green leafy vegetables are included in the existing diet without any other changes, the child will get the necessary vitamin A.
G. Hypervitaminosis A. Vitamin A is less toxic to man and other animals when it is taken in large doses over a long period of time. The children receiving overdosages of 500,000 units of
vitamin A per day exhibit tender swellings over the bones, limited motion and definite hyperosteoses. Human adults consuming 500,000 units or more show nosebleed, weakness, headache, anorexia and nausea. Continuous excessive intake of the vitamin is dangerous because it results in fragile bones and abnormal fetal development. In the case of plant carotenoids, a dietary oversupply (for example, eating too many carrots on a daily basis) results in carotenosis, a condition readily diagnosed by yellowing of the skin. These toxic effects develop presumably due to the fact that viatmin A, like vitamin D, is not readily excreted and consequently tissue levels may build up dangerous concentrations.
H. Human requirements. The recommended dietary allowance (RDA) of vitamin A is about 5,000 International Unit (I.U.). Growing children, adults and pregnant and lactating mothers require high doses of up to 8,000 I.U. It is also possible that some individuals require more than the minimal requirement due to either faulty absorption or some other reason. For vitamin A, the World Health Organization (WHO) has chosen as one International Unit the biologic activity of 0.000344 mg (0.344 μg) of synthetic vitamin A-acetate, which is equivalent to 0.30 μg of retinol.
In fact, one μg of β-carotene, the provitamin form, gets converted to about 0.167 μg of retinol, the true vitamin form. Another way of putting it is that the retinol equivalent of 1 μg of β-carotene is 0.167. A diet consisting of 1/2 pint of milk, 1 ounce of butter and an adequate amount of green vegetables or carrots daily is sufficient enough to meet minimal requirement. The optimal requirement of this vitamin is met with by taking 1 pint of milk and cod liver oil daily.
I. Treatment. For xerophthalmia, the treatment consists in giving 1,500 μg/kg/24 hr of vitamin A orally for 5 days and then continued with intramuscular injection of 7,500 μg of vitamin A in oil daily until recovery occurs.
J. Vitamin A and the vision. George Wald (Nobel Laureate, 1966) of Harvard University
has made major contributions to our understanding of the role of vitamin A in visual process. The retina of the human eye contains 2 types of receptor cells, rods and cones. Animals which have vision only in bright light (“day vision”) like pigeons have only cones while animals which can see in night or dim light (“night vision”) like owls have only rods. Thus, the rods are concerned with seeing at low illumination and the cones are responsible for colour vision.
I. Rod vision. The rods contain a photosensitive visual pigment known as rhodopsin. It is conjugated protein and upon illumination splits into a protein called opsin and a carotenoid called retinene1 . It is actually this reaction which may initiate an enzymic reaction responible for visual mechanism. The retinene1, released by bleaching of rhodopsin, is reduced to vitamin A1 by NADH in the presence of retinene1 reductase, an enzyme present in the retina. Vitamin A1 of mammals is in all-trans form like the retinene liberated by bleaching rhodopsin. The isomerization of all-trans retinene1 and vitamin A1 to Δ”-cis forms is catalyzed by the enzyme
retinene isomerase. The major site of this reaction is the liver. Opsin in dark reacts with Δ”-cis retinene1 to regenerate rhodopsin. The series of reactions leading from vitamin A1 to rhodopsin constitutes the major events in ‘dark adaptation’. And the reactions leading to bleaching of rhodopsin constitute what is known as ‘light adaptation’. Whereas the retina of mammals, birds, frogs and marine fishes contain rhodopsin, all freshwater fishes have another visual pigment porphyropsin in their retina. Wald has shown that porphyropsin undergoes the same cyclic changes on bleaching and regeneration as in the case of rhodopsin except that here retinene A2 and vitamin A2 come in picture.
II. Cone vision. According to Young-Helmholtz trichromatic theory, there are present at least 3 closely related pigments in cones. These are iodopsin, chlorolabe and erythrolabe. The last two pigments absorb actively in the green and the red portions of the spectrum respectively. When light strikes the retina, it bleaches one or more of these pigments based upon the quality of light. The pigments are converted to all-trans retinene and the protein, opsin. This reaction produces the nerve impulse which is read as blue, green or red based on the pigment affected.
B. Occurrence. Liver oils of various fishes are the richest natural sources of vitamin A. Shark and halibut contain maximum amount whereas the cod-liver has lowest amount. Depending upon the species of fish and the time of year of catch, the fish livers contain 2,000 to 100,000 I.U. per gram of vitamin A. The amount present in human liver is much less (500 to 1,000 I.U.per gram). However, polar bear liver is an extremely concentrated source of vitamin A. Other noteworthy sources are butter, milk and eggs and, to a lesser extent, kidney. In its provitamin form (i.e., as carotenes) it is supplied by all pigmented (particularly yellow) vegetables and fruits such as carrots, pumpkins, cantaloupes, turnips, peppers, peas, sweet potatoes, papayas, tomatoes, apricots, peaches, plums, cherries, mangoes etc. Yellow corn is the only cereal containing significant amounts of carotene. New-born infants have low quantities of vitamin A content that is rapidly augmented because colostrum and breast milk furnish large amounts of the vitamin. The milk of well-fed mothers, however, contains sufficient amounts of vitamin A (in ester form) for the infant's need. However, vitamin A is absent from vegetable fats and oils (olive oil, linseed oil, groundnut oil). It is added to margarine during its manufacture from these oils.
The β-carotene content of some items are presented in Table Vitamin A originates in marine algae, and then passes up the food chain to reach the large carnivorous animals. Toxic levels of vitamin A may accumulate in the livers of a wide range of creatures such as Polar bears, seals, porpoises, dolphins, sharks, whales, Arctic foxes and huskies. Even a small meal of southern Australian seal liver, say 80g, may produce illness in man. Most of the foods recommended as source of vitamin A contain well below the toxic levels of vitaminA, but one– Halibut liver oil– contains dangerously high amounts of vitamin A.As regards the vitamin A contents of polar animals, one can see that, in reality, very little quantities of livers of these animals are required to kill a human being : 30–90 g of polar bear liver or halibut liver, 80–240 g of bearded seal liver and 100-300 g of Antarctic husky liver is enough to kill a human being.
C. Structure. Vitamin A is found in two forms A1 and A2. The carotenoids that give rise to vitamin A in animal body is named as provitamin A. These inculde α-, β- and γ-carotenes and cryptoxanthin. β-carotene is most potent of all these forms. A molecule of β-carotene is made of eight 5-carbon isoprenoid units, linked to form a long chain of 40 carbon atoms with an ionone ring at each end. It is an orange-red hydrocarbon and upon hydrolysis yields 2 moles of vitamin A1 . During hydrolysis, a cleavage occurs at the mid point of the carotene in the polyene chain connecting the 2 β-ionone rings. This conversion usually takes place in livers of fishes and mammals. Vitamin A1 is a complex primary alcohol called retinol, having the empirical formula, C20H29OH. The
terminalhydroxyl group is ordinarily esterified. It contains β-ionone ring. Another form of vitamin A, present in fresh-water fishes, is known as vitamin A2. It differs from vitamin A1, which is found in salt-water fishes, in possessing an additional conjugate double bond between carbon atoms 3 and 4 of the β-ionone ring. Its potency is 40% that of vitamin A1.D. Properties. Ordinarily retinol is a viscid, colourless oil but by careful fractionation it has also been isolated as pale yellowish needles. It gives a characteristic absorption band in ultraviolet (UV) spectrum at 328 mμ. It is soluble in fat and fat solvents but insoluble in water. Loss of vitamin A in cooking, canning and freezing of foodstuffs is small; oxidizing agents, however, destroy it. It is destroyed on exposure to UV light. Vitamin A is relatively unstable in air unless protected by antioxidants including vitamin E.
E. Metabolism. In the tissues, the metabolic transformation of retinol is carried out by enzymes. The dietary β-carotene is split into retinal by an enzyme of the intestine. Retinal is then reduced by another enzyme to retinol which, in turn, is converted to retinyl ester by reacting with a fatty acid like palmitic. The retinyl ester, on the contrary, is enzymatically hydrolyzed t to produce retinol which is re-esterified with palmitic acid to produce retinyl ester. This is absorbed
through the lymphatic system and is stored in the liver.
Liver stores vitamin A in large quantities mainly in the form of retinyl ester. But the vitamin A that circulates in the blood is in the form of retinol and is bound to a specific carrier protein called retinol binding protein (RBP). The retinyl ester present in the liver, therefore, has to be converted to retinol before it mixes with the blood. Liver can also successively convert retinol to retinal and retinal to retinoic acid. Retinoic acid is quickly absorbed from the intestine through the portal system and is rapidly excreted back into the intestine through the bile. Vitamin A helps maintain the epithelial cells of the skin and the linings of the digestive, respiratory and genito-urinary systems. These linings play a protective role against cancer-causing agents (or carcinogens), viruses and bacteria and are rendered vulnerable by a deficiency of vitamin A. Vitamin A guards against cancer by protecting cell walls from undesirable oxidation, and scavenging the products of oxidation— free radicals, which are linked to the development of cancer.F. Deficiency. Vitamin A is perhaps the most important as it affects the various metabolic processes in the body. It has profound effect on epithelial structures, in general. Vitamin A deficiency leads to the onset of many diseases like nyctalopia or night blindness (inability to see in night), xerophthalmia (scaly condition of the delicate membrane covering the eyes), keratomalacia (softening of the cornea), phrynoderma or “toad skin” (hard and horny skin) and stunted growth. Xerophthalmia or xerosis is a major cause of blindness in childhood and is still a major health problem in Far East such as Hong Kong, Jakarta, Manila and Dhaka. The disease affects large number of children but few adults. Xerophthalmia is characterized by drying of the eyes and hence so named (xerosG = dry ; ophthalmosG = eyes). The lacrymal glands become stratified and keratinized and cease to produce tears. This makes the external surface dry and dull. The ulcers develop. The bacteria are not washed away. The eyelids swell and become sticky. This results in frequent exudation of blood, causing severe infection to the eye. If left untreated, blindness results. Incredible, yet true, about 1400 cases of xerophthalmia were reported in 1904 among Japanese children. Besides, during World War I, many xerophthalmic cases were reported in Denmark because of the fact that butterfat was shipped out of that country in huge quantities and people had to live on substitutes with no retinol.
Keratomalacia (keratoG = hair ; malakiaG = softness) is a corneal disease, occurring maximally in pre-school children of 3–4 years. This usually happens suddenly in young children with kwashiorkor esp., after an episode of diarrhea or infection. At first the cornea loses its lustre, undergoes a necrosis and develops a few pin-point ulcers, which later coalesce to form a large, white ulcerative area. The perforation of the cornea may follow sometime, causing the release of aqueous humour and prolapse of the iris. Occasionally, instead of extensive ulceration and perforation of the cornea, the whole eyeball may shrink. Keratomalacia is unfortunately still prevalent on a wide scale in many parts of India (South and Eastern) and Indonesia and some other countries of Asia and Africa. Phrynoderma is a skin lesion and is characterized by follicular hyperkeratosis. In it, the skin esp., on the outer aspects of forearms in the regions of the elbows and of the thighs and buttocks becomes rough and spiky. In severe cases, the trunk is also affected. Also, the damaged epithelial structures in diverse organs such as the eyes, the kidneys or the respiratory tract often become infected. It is for this reason that vitamin A has been called an ‘anti-infection’ vitamin. The vaginal epithelium may become cornified, and epithelial metaplasia of the urinary tract may contribute to pyuria and hematuria. Increased intracranial pressure with wide separation of cranial bones at the sutures may occur.
In the alimentary tract, the deficiency of vitamin A causes damage to the intestinal mucosa, resulting in diarrhea. Vitamin A is an important factor in tooth formation. In its deficiency, there is a defective formation of enamel so that the dentin is exposed. Evidently, sound tooth formation does not occur. Vitamin A deficiency may result in retardation of mental and physical growth and in apathy. Anemia with or without hepatosplenomegally is usually present. Other deficiency diseases that have been attributed to vitamin A are atrophy of the testes and disturbances of the female genital organs.
According to a report, presented at a meeting of the National Seminar on Corneal Disasters held in New Delhi (1981), India accounts for about one-third of the total blind population of the world, that is about 9 million blind people and that every year about 25,000 children go blind in India due to malnutrition. Researches conducted by the National Institute of Nutrition (NIN), Hyderabad (1978), show that about 30% of the blind in India lost their sight before they were 21. NIN studies have also revealed that about 10% of the school children belonging to the poorer socioeconomic groups show signs of vitamin A deficiency. It is however, worth-mentioning that the vitamin A deficiency is mainly a result of ignorance rather than the non-availability of food or of the resources to acquire the food as is the case with protein calorie malnutrition. According to NIN researches, if 40 g of green leafy vegetables are included in the existing diet without any other changes, the child will get the necessary vitamin A.
G. Hypervitaminosis A. Vitamin A is less toxic to man and other animals when it is taken in large doses over a long period of time. The children receiving overdosages of 500,000 units of
vitamin A per day exhibit tender swellings over the bones, limited motion and definite hyperosteoses. Human adults consuming 500,000 units or more show nosebleed, weakness, headache, anorexia and nausea. Continuous excessive intake of the vitamin is dangerous because it results in fragile bones and abnormal fetal development. In the case of plant carotenoids, a dietary oversupply (for example, eating too many carrots on a daily basis) results in carotenosis, a condition readily diagnosed by yellowing of the skin. These toxic effects develop presumably due to the fact that viatmin A, like vitamin D, is not readily excreted and consequently tissue levels may build up dangerous concentrations.
H. Human requirements. The recommended dietary allowance (RDA) of vitamin A is about 5,000 International Unit (I.U.). Growing children, adults and pregnant and lactating mothers require high doses of up to 8,000 I.U. It is also possible that some individuals require more than the minimal requirement due to either faulty absorption or some other reason. For vitamin A, the World Health Organization (WHO) has chosen as one International Unit the biologic activity of 0.000344 mg (0.344 μg) of synthetic vitamin A-acetate, which is equivalent to 0.30 μg of retinol.
In fact, one μg of β-carotene, the provitamin form, gets converted to about 0.167 μg of retinol, the true vitamin form. Another way of putting it is that the retinol equivalent of 1 μg of β-carotene is 0.167. A diet consisting of 1/2 pint of milk, 1 ounce of butter and an adequate amount of green vegetables or carrots daily is sufficient enough to meet minimal requirement. The optimal requirement of this vitamin is met with by taking 1 pint of milk and cod liver oil daily.
I. Treatment. For xerophthalmia, the treatment consists in giving 1,500 μg/kg/24 hr of vitamin A orally for 5 days and then continued with intramuscular injection of 7,500 μg of vitamin A in oil daily until recovery occurs.J. Vitamin A and the vision. George Wald (Nobel Laureate, 1966) of Harvard University
has made major contributions to our understanding of the role of vitamin A in visual process. The retina of the human eye contains 2 types of receptor cells, rods and cones. Animals which have vision only in bright light (“day vision”) like pigeons have only cones while animals which can see in night or dim light (“night vision”) like owls have only rods. Thus, the rods are concerned with seeing at low illumination and the cones are responsible for colour vision.
I. Rod vision. The rods contain a photosensitive visual pigment known as rhodopsin. It is conjugated protein and upon illumination splits into a protein called opsin and a carotenoid called retinene1 . It is actually this reaction which may initiate an enzymic reaction responible for visual mechanism. The retinene1, released by bleaching of rhodopsin, is reduced to vitamin A1 by NADH in the presence of retinene1 reductase, an enzyme present in the retina. Vitamin A1 of mammals is in all-trans form like the retinene liberated by bleaching rhodopsin. The isomerization of all-trans retinene1 and vitamin A1 to Δ”-cis forms is catalyzed by the enzyme
retinene isomerase. The major site of this reaction is the liver. Opsin in dark reacts with Δ”-cis retinene1 to regenerate rhodopsin. The series of reactions leading from vitamin A1 to rhodopsin constitutes the major events in ‘dark adaptation’. And the reactions leading to bleaching of rhodopsin constitute what is known as ‘light adaptation’. Whereas the retina of mammals, birds, frogs and marine fishes contain rhodopsin, all freshwater fishes have another visual pigment porphyropsin in their retina. Wald has shown that porphyropsin undergoes the same cyclic changes on bleaching and regeneration as in the case of rhodopsin except that here retinene A2 and vitamin A2 come in picture.II. Cone vision. According to Young-Helmholtz trichromatic theory, there are present at least 3 closely related pigments in cones. These are iodopsin, chlorolabe and erythrolabe. The last two pigments absorb actively in the green and the red portions of the spectrum respectively. When light strikes the retina, it bleaches one or more of these pigments based upon the quality of light. The pigments are converted to all-trans retinene and the protein, opsin. This reaction produces the nerve impulse which is read as blue, green or red based on the pigment affected.
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