INTRODUCTIONDiscovery of vitaminsThe discovery and isolation of many of the vitamins were originally achieved through work on rats given diets of purified proteins, fats, carbohydrates and inorganic salts. Using this technique, Hopkins in 1912 showed that a synthetic
diet of this type was inadequate for the normal growth of rats, but that when a small quantity of milk was added to the diet the animals developed normally. This proved that there was some essential factor, or factors, lacking in the pure diet.
About this time the term ‘vitamines’, derived from ‘vital amines’, was coined by Funk to describe these accessory food factors, which he thought contained amino-nitrogen. It is now known that only a few of these substances contain amino-nitrogen and the word has been shortened to vitamins, a term that has been generally accepted as a group name.
Although the discovery of the vitamins dates from the beginning of the twentieth century, the association of certain diseases with dietary deficiencies had been recognised much earlier. In 1753 Lind, a British naval physician, published a treatise on scurvy, proving that this disease could be prevented in human beings by including salads and summer fruits in their diet. The action of lemon juice in curing and preventing scurvy had been known, however, since the beginning of the seventeenth century. The use of cod-liver oil in preventing rickets has long been appreciated, and Eijkmann knew at the end of the nineteenth century that beri-beri, a disease common in the Far East, could be cured by giving the patients brown rice grain rather than polished rice.
Vitamins and biochemistryVitamins are usually defined as organic compounds that are required in small amounts for normal growth and maintenance of animal life. But this definition ignores the important part that these substances play in plants and their importance
generally in the metabolism of all living organisms. vitamins are not merely building blocks or energy-yielding compounds but are involved in, or are mediators of, the biochemical pathways.
For example, many of the B vitamins act as cofactors in enzyme systems but it is notalways clear how the symptoms of deficiency are related to the failure of the metabolic pathway.
In addition to avoiding explicit vitamin deficiency symptoms or a general depression in production due to a subclinical deficiency, some vitamins are added to the diet at higher levels in order to (1) enhance the quality of the animal
product, e.g. vitamin D for eggshell strength and vitamin E for prolonging the shelf
life of carcasses, or (2) improve health, e.g. vitamin A to improve the health status of the mammary gland in dairy cows.
Vitamins are required by animals in very small amounts compared with other nutrients; for example, the vitamin B1 (thiamin) requirement of a 50 kg pig is only about 3 mg/day. Nevertheless, a continuous deficiency in the diet results in dis-
ordered metabolism and eventually disease.
Some compounds function as vitamins only after undergoing a chemical change; such compounds, which include beta-carotene and certain sterols, are described as provitamins or vitamin precursors.
Many vitamins are destroyed by oxidation, a process speeded up by the action of heat, light and certain metals such as iron. This fact is important since the conditions under which a food is stored will affect the final vitamin potency. Some commercial vitamin preparations are dispersed in wax or gelatin, which act as a protective layer against oxidation.
The system of naming the vitamins by letters of the alphabet was most convenient and was generally accepted before the discovery of their chemical nature. Although this system of nomenclature is still widely used with some vitamins, the
modern tendency is to use the chemical name, particularly in describing members of the B complex.
At least 14 vitamins have been accepted as essential food factors, and a few others have been proposed. Only those that are of nutritional importance are dealt with in this chapter.
It is convenient to divide the vitamins into two main groups: fat-soluble and water-soluble. Table 5.1 lists the important members of these two groups.
Vitamins important in animal nutrition
FAT-SOLUBLE VITAMINSVitamin AChemical natureVitamin A (C20H29OH), known chemically as retinol, is an unsaturated monohydric alcohol with the following structural formula:
The vitamin is a pale yellow crystalline solid, insoluble in water but soluble in fat and various fat solvents. It is readily destroyed by oxidation on exposure to air and light. A related compound with the formula C20H27OH, originally found in fish, has been designated dehydroretinol or vitamin A2.
SourcesVitamin A accumulates in the liver and this organ is likely to be a good source; the amount present varies with species of animal and diet. Some typical liver reserves of vitamin A in different species, although these values vary widely within
each species.
The oils from livers of certain fish, especially cod and halibut, have long been used as an important dietary source of the vitamin. Egg yolk and milk fat also are usually rich sources, although the vitamin content of these depends, to a large ex-
tent, upon the diet of the animal from which it has been produced.
Vitamin A is manufactured synthetically and can be obtained in a pure form.
Some typical values for liver reserves of vitamin A in different species
ProvitaminsVitamin A does not exist as such in plants, but it is present as precursors or provitamins in the form of certain carotenoids, which can be converted into the vitamin. At least 600 naturally occurring carotenoids are known, but only a few of these are
precursors of the vitamin.
In plants, carotenoids have yellow, orange or red colours but their colours are frequently masked by the green colour of chlorophyll.When ingested, they are responsible for many of the varied and natural colours that occur in crustaceans, insects, birds and fish.They are also found in egg yolk, butterfat and the body fat of cattle and horses, but not in sheep or pigs. Carotenoids may be divided into two main categories: carotenes and xanthophylls. The latter include a wide range of compounds, for example lutein, cryptoxanthin and zeaxanthin, most of which cannot be converted into vitamin A. Of
the carotenes, beta-carotene is the most important member and this compound forms the main source of vitaminA in the diets of farm animals. Its structure is shown here:
The long unsaturated hydrocarbon chains in carotenes (and vitamin A) are easily oxidised to by-products that have no vitamin potency. Oxidation is increased by heat, light, moisture and the presence of heavy metals. Consequently, foods exposed to air and sunlight rapidly lose their vitamin A potency, so that large losses can occur during the sun-drying of crops. For example, lucerne hay has around 15 mg -carotene/kg, but artificially dried lucerne and grass meals have 95 mg/kg and 155 mg/kg, respectively. Fresh grass is an excellent source (250 mg/kg DM), but this is halved during ensilage.
Carotenoids and supplemental vitamin A are prone to destruction in the rumen, especially with high concentrate diets. Recent studies indicate that naturally occurring carotenoids in forages may not be degraded to the same extent as purified products used as supplements. The gelatin preparations of vitamin A, with stabilising agents, are intended to protect the vitamin from this destruction but still remain available to be absorbed from the duodenum. In monogastrics the availability varies between foods. In humans it has been found that oil solutions of carotenoids are more available than those naturally occurring in foods. This is reflected in the fact that the efficiency of absorption is largely dependent on the quality and quantity of fat in the diet. The measurement of availability of carotenoids in foods and factors that affect it are currently an active area of research in animals and humans.
Conversion of carotene into vitamin A can occur in the liver but usually takes place in the intestinal mucosa. Theoretically, hydrolysis of one molecule of the C40 compound beta-carotene should yield two molecules of the C20 compound retinol, but although central cleavage of this type is thought to occur, it is considered likely that the carotene is degraded from one end of the chain by step-wise oxidation until only one molecule of the C20 compound retinol remains. Although the maximum conversion measured in the rat is 2 mg beta-carotene into 1 mg retinol, authorities differ regarding the conversion efficiency in other animals with ranges from 3 : 1 to 12 : 1. Ruminants convert about 6 mg of beta-carotene into 1 mg of retinol.The corresponding conversion efficiency for pigs and poultry is usually taken as 11 : 1 and 3 : 1, respectively. Cats do not have the enzyme to convert carotene to vitamin A. Since their diet comprises meat, which usually contains sufficient vitamin A and low levels of carotenoids, the conversion pathway is redundant.The vitamin A values of foods are often stated in terms of international units (iu), one iu of vitamin A being defined as the activity of 0.3 µg of crystalline retinol.
MetabolismVitamin A appears to play two different roles in the body according to whether it is acting in the eye or in the general system.
In the retinal cells of the eye, vitamin A (all-trans-retinol) is converted into the 11-cis-isomer, which is then oxidised to 11-cis-retinaldehde. In the dark the latter then combines with the protein opsin to form rhodopsin (visual purple), which is the photoreceptor for vision at low light intensities. When light falls on the retina, the cis-retinaldehyde molecule is converted back into the all-trans form and is released from the opsin.This conversion results in the transmission of an impulse up the optic nerve. The all-trans-retinaldehyde is converted to all-trans-retinol, which re-enters the cycle, thus continually renewing the light sensitivity of the retina.
In its second role, in the regulation of cellular differentiation, vitamin A is involved in the formation and protection of epithelial tissues and mucous membranes. In this way it has particular importance in growth, reproduction and immune response. Vitamin A is important in the resistance to disease and promotion of healing through its effect on the immune system and epithelial integrity. In addition, it acts, along with vitamins E and C and -carotene, as a scavenger of free radicals .
The placental transfer of vitamin A to the foetus is limited and the neonate has low stores of the vitamin and relies on consumption of colostrum to establish adequate tissue stores.
The role of vitamin A (retinol) in the visual cycle.
Deficiency symptomsAbility to see in dim light depends upon the rate of resynthesis of rhodopsin; when vitamin A is deficient, rhodopsin formation is impaired. One of the earliest symptoms of a deficiency of vitamin A in all animals is a lessened ability to see in dim light, commonly known as ‘night blindness’. It has long been realised that vitamin A plays an important role in combating infection, and it has been termed the ‘anti-infective vitamin’. In several species, vitamin A deficiency has been shown to be accompanied by low levels of immunoglobulins, although the exact function of the vitamin in the formation of these important proteins is uncertain.
In adult cattle, a mild deficiency of vitamin A is associated with roughened hair and scaly skin. If it is prolonged the eyes are affected, leading to excessive watering, softening and cloudiness of the cornea and development of xerophthalmia, which is characterised by a drying of the conjunctiva. Constriction of the optic nerve canal may cause blindness in calves. In breeding animals a deficiency may lead to infertility, and in pregnant animals deficiency may lead to failure of embryo growth, disrupted organ development, abortion, short gestation, retained placenta or the production of dead, weak or blind calves. Less severe deficiencies may result in metritis and dermatitis and calves born with low reserves of the vitamin; it is then imperative that colostrum, rich in antibodies and vitamin A, should be given at birth, otherwise the susceptibility of such animals to infection leads to scours and, if the deficiency is not rectified, they frequently die of pneumonia. The National Research Council of the United States has increased the recommended allowance for dairy cows in order to
improve the health of the mammary gland and reduce mastitis.
In practice, severe deficiency symptoms are unlikely to occur in adult animals except after prolonged deprivation. Grazing animals generally obtain more than adequate amounts of provitamin from pasture grass and normally build up liver reserves. If cattle are fed on silage or well-preserved hay during the winter months, deficiencies are unlikely to occur. Cases of vitamin A deficiency have been reported among cattle fed indoors on high cereal rations, and under these conditions a high vitamin supplement is recommended.
In ewes, in addition to night blindness, severe cases of deficiency may result in lambs being born weak or dead. A deficiency is not common in sheep, however, because of adequate dietary intakes on pasture.
In pigs, eye disorders such as xerophthalmia and blindness may occur. A deficiency in pregnant animals may result in the production of weak, blind, dead or deformed litters. In view of the apparent importance of vitamin A in preventing
reproductive disorders in pigs, it has been suggested that the retinoids may have a role in embryo development (cell differentation, gene transcription). Alternatively, they may regulate ovarian steroid production and influence the establishment and maintenance of pregnancy. In less severe cases of deficiency, appetite is impaired and growth retarded. Where pigs are reared out of doors and have access to green food, deficiencies are unlikely to occur, except possibly during the winter. Pigs kept indoors on concentrates may not receive adequate amounts of vitamin A in the diet and supplements may be required.
In poultry consuming a diet deficient in vitamin A, the mortality rate is usually high. Early symptoms include retarded growth, weakness, ruffled plumage and a staggering gait. In mature birds, egg production and hatchability are reduced. Since most concentrated foods present in the diets of poultry are low or lacking in vitamin A or its precursors, vitamin A deficiency may be a problem unless precautions are taken. Yellow maize, dried grass or other green food, or alternatively cod- or other fish-liver oils or vitamin A concentrate, can be added to the diet.
In horses, the signs of deficiency include the catalogue of symptoms seen in other farm animals: night blindness, keratinisation of the skin and cornea, susceptibility to infection and infertility.
Dogs and cats show similar symptoms. In addition dogs have ataxia and anorexia and cats have reproductive and developmental disorders.
It has been suggested that, in addition to vitamin A, some species may have a dietary requirement for -carotene per se. The ovaries of bovine species are known to contain high concentrations of -carotene during the luteal phase – indeed, it is an integral component of the mucosal membrane of luteal cells – and it has been postulated that certain fertility disorders in dairy cattle, such as retarded ovulation and early embryonic mortality, may be caused by a deficiency of the provitamin in the diet. In sows, injections of -carotene have reduced embryonic mortality and increased litter sizes. It is suggested that it influences steroidogenesis and, through its antioxidant properties, it may protect the highly active ovarian cells from damage by free radicals. Supplementation of the diet of dogs with -carotene resulted in increased plasma progesterone concentration.
Vitamin DChemical natureA number of forms of vitamin D are known,although not all of these are naturally occurring compounds.The two most important forms are ergocalciferol (D2) and cholecalciferol (D3).The term D1 was originally suggested by earlier workers for an activated sterol, which was found later to be impure and to consist mainly of ergocalciferol, which had already been designated D2.The result of this confusion is that in the group of D vitamins, the term vitamin D1 has been abolished.The structures of vitamins D2 and D3 are:
The D vitamins are insoluble in water but soluble in fats and fat solvents. The sulphate derivative of vitamin D present in milk is a water-soluble form of the vitamin. Both D2 and D3 are more resistant to oxidation than vitamin A, D3 being more
stable than D2.
SourcesThe D vitamins are limited in distribution. They rarely occur in plants except in sundried roughages and the dead leaves of growing plants. In the animal kingdom vitamin D3 occurs in small amounts in certain tissues and is abundant only in some
fishes. Halibut-liver and cod-liver oils are rich sources of vitamin D3. Egg yolk is also a good source, but cow’s milk is normally a poor source, although summer milk tends to be richer than winter milk. Colostrum usually contains six to ten times the amount present in ordinary milk.
Clinical manifestations of avitaminosis D, and other vitamin deficiencies, are frequently treated by injection of the vitamin into the animal.
ProvitaminsReference has been made (p. 49) to two sterols, ergosterol and 7-dehydrocholesterol, as being precursors of vitamins D2 and D3, respectively.The provitamins, as such, have no vitamin value and must be converted into calciferols before they are of any use to the animal. For this conversion it is necessary to impart a definite quantity of energy to the sterol molecule, and this can be brought about by the ultraviolet light present in sunlight, by artificially produced radiant energy or by certain kinds of physical treatment. Under natural conditions activation is brought about by irradiation from the sun. The activation occurs most efficiently with light of wavelength 290–315 nm, so that the range capable of vitamin formation is small. The amount of ultraviolet radiation that reaches the earth’s surface depends upon latitude and atmospheric conditions: the presence of clouds, smoke and dust reduces the radiation. Ultraviolet radiation is greater in the tropics than in the temperate regions, and the amount reaching the more northern areas in winter may be slight. Since ultraviolet light cannot pass through ordinary window glass, animals housed indoors receive little, if any, suitable radiation for the production of the vitamin. Irradiation is apparently more effective in animals with light-coloured skins. If irradiation is continued for a prolonged period, then the vitamin may be altered to compounds that can be toxic.
The chemical transformation occurs in the skin and also in the skin secretions, which are known to contain the precursor. Absorption of the vitamin can take place from the skin, since deficiency can be treated successfully by rubbing cod-liver oil into the skin.
Vitamin D requirements are often expressed in terms of international units (iu). One iu of vitamin D is defined as the vitamin D activity of 0.025 µg of crystalline vitamin D3.
MetabolismDietary vitamins D2 and D3 are absorbed from the small intestine and are transported in the blood to the liver, where they are converted into 25-hydroxycholecalciferol. The latter is then transported to the kidney, where it is converted into
1,25-dihydroxycholecalciferol, the most biologically active form of the vitamin. This compound is then transported in the blood to the various target tissues, the intestine,
Metabolic pathway showing production of the hormonally active form of vitamin D
bones and the eggshell gland in birds. The compound 1,25-dihydroxycholecalciferol acts in a similar way to a steroid hormone, regulating DNA transcription in the intestinal microvilli, inducing the synthesis of specific messenger RNA
which is responsible for the production of calcium-binding protein. This protein is involved in the absorption of calcium from the intestinal lumen. The various pathways involved in these transformations are summarised in Fig. 5.3. Cats do not obtain vitamin D by exposure to sunlight.The natural diet of the cat contains adequate amounts of vitamin D to meet their requirements.Their metabolism has become adapted such that 7-dehydroxycholesterol is converted to cholesterol and is not available for vitamin D synthesis.
The amount of 1,25-dihydroxycholecalciferol produced by the kidney is controlled by parathyroid hormone. When the level of calcium in the blood is low (hypocalcaemia), the parathyroid gland is stimulated to secrete more parathyroid
hormone, which induces the kidney to produce more 1,25-dihydroxycholecalciferol, which in turn enhances the intestinal absorption of calcium.
In addition to increasing intestinal absorption of calcium, 1,25-dihydroxycholecalciferol increases the absorption of phosphorus from the intestine and also enhances calcium and phosphorus reabsorption from the kidney and bone.
Recently it has been discovered that 1,25-dihydroxycholecalciferol regulates the expression of genes and the activity of cells associated with the immune system.
Deficiency symptomsA deficiency of vitamin D in the young animal results in rickets, a disease of growing bone in which the deposition of calcium and phosphorus is disturbed; as a result the bones are weak and easily broken and the legs may be bowed. In young cattle the symptoms include swollen knees and hocks and arching of the back. In pigs the symptoms are usually enlarged joints, broken bones, stiffness of the joints and occasionally
paralysis.The growth rate is generally adversely affected.The term ‘rickets’ is confined to young growing animals; in older animals vitamin D deficiency causes osteomalacia, in which there is reabsorption of bone already laid down. Osteomalacia due to vitamin D deficiency is not common in farm animals, although a similar condition can occur in
pregnant and lactating animals, which require increased amounts of calcium and phosphorus. Rickets and osteomalacia are not specific diseases necessarily caused by vitamin D deficiency; they can also be caused by lack of calcium or phosphorus or an imbalance between these two elements.
In poultry, a deficiency of vitamin D causes the bones and beak to become soft and rubbery; growth is usually retarded and the legs become weak. Egg production is reduced and eggshell quality deteriorates. Most foods of pigs and poultry, with the possible exception of fishmeal, contain little or no vitamin D, and the vitamin is generally supplied to these animals, if reared indoors, in the form of fish-liver oils or synthetic preparations.
The need for supplementing the diets of cattle and sheep with vitamin D is generally not so great as that for pigs and poultry. Adult ruminants can receive adequate amounts of the vitamin from hay in the winter months, and from irradiation while grazing. However, since the vitamin D content of hays is extremely variable, it is possible that vitamin D supplementation may be desirable, especially with young growing animals or pregnant animals, on winter diets. There is a considerable lack of information about the vitamin D needs of farm animals under practical conditions. For cattle, sheep and pigs vitamins D2 and D3 have the same potency, but for poultry vitamin D2 has only about 10 per cent of the potency of D3.
Certain foods, such as fresh green cereals and yeast, have been shown to have rachitogenic (rickets-causing) properties for mammals, and raw liver and isolated soya bean protein have a similar effect on poultry. In one study it was shown that in order to overcome the rachitogenic activity of whole raw soya bean meal, a tenfold increase in vitamin D supplement was necessary. Heating destroys the rachitogenic activity.
Vitamin EChemical natureVitamin E is a group that includes a number of closely related active compounds. Eight naturally occurring forms of the vitamin are known, and these can be divided into two groups according to whether the side chain of the molecule, as shown
below, is saturated or unsaturated.
The four saturated vitamins are designated ␣-, -, ␥- and ␦-tocopherol. Of these the ␣-form is the most biologically active and most widely distributed.
The -, ␥- and ␦-forms have only about 45, 13 and 0.4 per cent of the activity of the ␣-form, respectively. The unsaturated forms of the vitamin have been designated ␣-, -, ␥- and ␦-tocotrienols. Of these only the ␣-form appears to have any
significant vitamin E activity, and then only about 13 per cent of its saturated counterpart.
The ␣-tocopherol molecule has three centres where stereoisomers can occur. The naturally occurring molecule is the D-␣-tocopherol (or RRR-␣-tocopherol) configuration and has the highest vitamin activity. Synthetic DL-␣-tocopherol acetate (also called all racemic ␣-tocopherol acetate) is used as a vitamin E supplement and comprises all eight possible stereoisomers; only one molecule in eight is in the RRR form. The vitamin activity of the four stereoisomers in the L forms is considerably lower than the four that make up the D forms; in the latter the RRR form is the most
active.
SourcesVitamin E, unlike vitamin A, is not stored in the animal body in large amounts for any length of time and consequently a regular dietary source is important. Fortunately, the vitamin is widely distributed in foods. Green fodders are good sources
of ␣-tocopherol, young grass being a better source than mature herbage. The leaves contain 20–30 times as much vitamin E as the stems. Losses during haymaking can be as high as 90 per cent, but losses during ensilage or artificial drying are low.
Cereal grains are also good sources of the vitamin, but the tocopherol composition varies with species.Wheat and barley grain resemble grass in containing mainly ␣-tocopherol, but maize contains, in addition to ␣-tocopherol, appreciable quantities of ␥-tocopherol. During the storage of moist grain in silos, the vitamin E activity can decline markedly. Reduction in the concentration of the vitamin from 9 to 1 mg/kg DM has been reported in moist barley stored for 12 weeks.
Animal products are relatively poor sources of the vitamin, although the amount present is related to the level of vitamin E in the diet.
The vitamin E values of foods are often stated in terms of international units, one iu of vitamin E being defined as the specific activity of 1 mg of synthetic all-racemic ␣-tocopherol acetate. It is generally accepted that 1 mg of RRR-␣-tocopherol is equivalent to 1.49 iu vitamin E and 1 mg RRR-␣-tocopherol acetate is equivalent to 1.36 iu vitamin E. However, recent evidence suggests that the equivalence of allracemic to RRR forms is related to species, age and the criteria used to assess them and that it may be as high as 2 : 1.
MetabolismVitamin E functions in the animal mainly as a biological antioxidant; in association with the selenium-containing enzyme glutathione peroxidase and other vitamins and trace-element-containing enzymes, it protects cells against oxidative
damage caused by free radicals. Free radicals are formed during cellular metabolism and, as they are capable of damaging cell membranes, enzymes and cell nuclear material, they must be converted into less reactive substances if the animal is to survive. This protection is particularly important in preventing oxidation of polyunsaturated fatty acids, which function as primary constituents of subcellular membranes and precursors of prostaglandins. Oxidation of unsaturated fattyacids produces hydroperoxides, which also damage cell tissues, and more lipid free radicals, so that prevention of such oxidation is of vital importance in maintaining the health of the living animal. The animal has complementary methods of protecting itself against oxidative damage: scavenging of radicals by vitamin E and destruction of any peroxides formed by glutathione peroxidase
The regeneration of vitamin E
Vitamin E also plays an important role in the development and function of the immune system. In recognition of this the National Research Council requirements for dairy cows have been increased to reduce the incidence of mastitis. In studies
with several species, supplementation of diets with the vitamin provided some protection against infection with pathogenic organisms.
Recent research has indicated that vitamin E is also involved in the regulation of cell signalling and gene expression.
Like vitamin A, it was thought that the transfer of vitamin E across the placenta was limited, with the neonate relying on colostrum to meet its requirements. More recent evidence in sheep indicates that placental transfer does occur, with increased muscle and brain concentrations in lambs born from ewes fed higher levels. Nonetheless, colostrum is a very important source of vitamin E for the new born.
Deficiency symptomsThe most frequent and, from a diagnostic point of view, the most important manifestation of vitamin E deficiency in farm animals is muscle degeneration (myopathy). Nutritional myopathy, also known as muscular dystrophy, frequently occurs in cattle, particularly calves, when they are turned out on to spring pasture. It is associated with low vitamin E and selenium intakes during the in-wintering period and possibly the relatively high concentration of polyunsaturated fatty acids in the young grass lipids. The requirement for the vitamin increases with increasing concentrations of polyunsaturated fatty acids in the diet. The myopathy primarily affects the skeletal muscles and the affected animals have weak leg muscles, a condition manifested by difficulty in standing and, after standing, a trembling and staggering gait. Eventually, the animals are unable to rise, and weakness of the neck muscles prevents them from raising the head. A popular descriptive name for this condition is ‘white muscle disease’, owing to the presence of pale patches or white streaks in the muscles.The heart muscle may also be affected and death may result. Serum creatine phosphokinase and glutamic oxaloacetic transaminase levels are elevated in animals deficient in vitamin E.
Nutritional myopathy also occurs in lambs, with similar symptoms to those of calves. The condition is frequently referred to as ‘stiff lamb disease’. Dietary supplements of vitamin E given to pregnant ewes have resulted in increased birth weight and improved vigour and viability of neonatal lambs through quicker times to stand and suck. The National Research Council has recently increased the dietary recommendation for vitamin E several fold owing to its beneficial effects on prolonging the shelf life of lamb at retail.
In pigs, the two main diseases associated with vitamin E and selenium deficiency are myopathy and cardiac disease. Nutritional myopathy affects in particular young fast-growing pigs, but it may occur at any age.The pigs demonstrate an uncoordinated staggering gait or are unable to rise. In contrast to other animals, it is the pig’s heart
muscle that is more often affected. Sudden cardiac failure occurs; on post-mortem examination, large amounts of fluid are found around the heart and lungs and the lesions of the cardiac muscles are seen as haemorrhagic and pale areas.This condition is commonly known as ‘mulberry heart disease’. Sometimes the liver is also affected and it becomes enlarged and mottled. Supplemental vitamin E has improved litter size in pigs, probably through its antioxidant properties protecting arachidonic acid and maintaining the functional integrity of the reproductive organs.
Vitamin E deficiency in chicks may lead to a number of distinct diseases: myopathy, encephalomalacia and exudative diathesis. In nutritional myopathy the main muscles affected are the pectorals, although the leg muscles also may be involved. Nutritional encephalomalacia, or ‘crazy chick disease’, is a condition in which the chick is unable to walk or stand and is accompanied by haemorrhages and necrosis of brain cells. Exudative diathesis is a vascular disease of chicks characterised by a generalised oedema of the subcutaneous fatty tissues, associated with an abnormal permeability of the capillary walls. Both selenium and vitamin E appear to be involved in nutritional myopathy and in exudative diathesis, but the element does not seem to be important in nutritional encephalomacia. It should be stressed that selenium itself is a very toxic element and care is required in its use as a dietary additive. The toxic nature of selenium is discussed in Chapter 7 In horses, vitamin E deficiency results in the previously mentioned problems, i.e. lameness and muscle rigidity (‘tying up’) associated with skeletal and heart muscles.
The red blood cells become fragile and the release of myoglobin from damaged muscle cells gives rise to coffee-coloured urine.
Vitamin KVitamin K was discovered in 1935 to be an essential factor in the prevention of haemorrhagic symptoms in chicks.The discovery was made by a group of Danish scientists, who gave the name ‘koagulation factor’ to the vitamin, which became shortened to the K factor and eventually to vitamin K.
Chemical natureA number of forms of vitamin K are known to exist. All compounds exhibiting vitamin K activity possess a 2-methyl-1,4-naphthoquinone ring (menadione), which animals are unable to synthesise but plants and bacteria can.
The form of the vitamin present in plants is 2-methyl-3-phytyl-1,4-naphthoquinone, generally referred to as phylloquinone or vitamin K1.
The compound originally isolated from putrified fishmeal and designated vitamin K2 is now known to be only one of a series of K vitamins with unsaturated side chains synthesised by bacteria and referred to as menaquinones. The predominant vitamins of the menaquinone series contain six to ten isoprenoid (CH2:CCH3: CH:CH2) side-chain units. Menadione is the synthetic form of the vitamin and is designated as vitamin K3.
Vitamins K are relatively stable at ordinary temperatures but are rapidly destroyed on exposure to sunlight.
SourcesPhylloquinone is present in most green leafy materials, with lucerne, cabbage and kale being good sources. The amounts present in foods of animal origin are usually related to the diet, but egg yolk, liver and fishmeal are generally good sources.
Menaquinones are synthesised by bacteria in the digestive tract of animals.
MetabolismVitamin K is necessary for the synthesis of prothrombin in the liver. In the blood-clotting process, prothrombin is the inactive precursor of thrombin, an enzyme that converts the protein fibrinogen in blood plasma into fibrin, the insoluble fibrous protein that holds blood clots together. Prothrombin normally must bind to calcium ions before it can be activated. If the supply of vitamin K is inadequate, then the prothrombin molecule is deficient in ␥-carboxyglutamic acid, a specific amino acid responsible for calcium binding. Proteins containing ␥-carboxyglutamic acid, dependent on vitamin K
for their formation, are also present in bone, kidney and other tissues.
Deficiency symptomsSymptoms of vitamin K deficiency have not been reported in ruminants, horses and pigs under normal conditions, and it is generally considered that bacterial synthesis in the digestive tract supplies sufficient vitamin for the animal’s needs. A number of microorganisms are known to synthesise vitamin K, including Escherichia coli. Medicines that affect the bacteria in the gut may depress the production of vitamin K. A disease of cattle called ‘sweet clover disease’ is associated with vitamin K. Sweet clover (Melilotus albus) naturally contains compounds called coumarins which, when the crop is preserved as hay or silage, may be converted by a variety of fungi, such as the Aspergillus species, to dicoumarol. This compound lowers the prothrombin content of the blood and thereby impairs the blood-clotting process. The disease can be overcome by administering vitamin K to the animals. For this reason dicoumarol is sometimes referred to as an ‘anti-vitamin’.
The symptoms of vitamin K deficiency in chicks are anaemia and a delayed clotting time of the blood; birds are easily injured and may bleed to death. It is doubtful whether, in birds, microbially synthesised vitamin K is available by direct absorption from the digestive tract, because the site of its formation is too distal to permit absorption of adequate amounts except by ingestion of faecal material (coprophagy).
THE VITAMIN B COMPLEXThe vitamins included under this heading are all soluble in water and most of them are components of coenzymes (see Table 5.3). Although the mechanism of action in this role is known, the connection between the observed deficiency symptoms and the failure of the metabolic pathways is not always clear. Unlike the fat-soluble vitamins, members of the vitamin B complex, with the exception of cyanocobalamin, are not stored in the tissues in appreciable amounts and a regular exogenous supply is essential. In ruminants, all the vitamins in this group can be synthesised by microbial action in the rumen and generally this will provide satisfactory amounts for normal metabolism in the host and secretion of adequate quantities into milk. For example, it has been estimated that the amount of thiamin synthesised in the rumen is equal to the thiamin requirement. However, under certain conditions, deficiencies of thiamin and cyanocobalamin can occur in ruminants. In horses, the B vitamins synthesised by the microbial population of the gut plus those vitamins occurring in the food can meet the requirements of most adult animals.
Some coenzymes and enzyme prosthetic groups involving the B vitamins 
ThiaminChemical natureThiamin (vitamin B1) is a complex nitrogenous base containing a pyrimidine ring joined to a thiazole ring. Because of the presence of a hydroxyl group at the end of the side chain, thiamin can form esters.The main form of thiamin in animal tissues is the diphosphate ester, commonly known as thiamin pyrophosphate (TPP). The vitamin is very soluble in water and is fairly stable in mildly acidic solution but readily decomposes in neutral solutions.
SourcesThiamin is widely distributed in foods. It is concentrated in the outer layers of seeds, the germ, and in the growing areas of roots, leaves and shoots. Fermentation products, such as brewer’s yeast, are rich sources.Animal products rich in thiamin include egg yolk, liver, kidney and pork muscle. The synthetic vitamin is available, usually marketed as the hydrochloride.
MetabolismThiamin pyrophosphate (or thiamin diphosphate) is a coenzyme involved in (1) the oxidative decarboxylation of pyruvate to acetyl coenzyme A (enzyme: pyruvate dehydrogenase), (2) the oxidative decarboxylation of ␣-ketoglutarate to succinyl coenzyme A (␣-ketoglutarate dehydrogenase) in the tricarboxylic acid cycle, (3) the pentose phosphate pathway (transketolase) and (4) the synthesis of branched-chain amino acids such as valine (branched-chain ketoacid dehydrogenase) in bacteria, yeasts and plants. Thiamin triphosphate is involved in the activation of the chloride ion channel in the membranes of nerves, possibly by phosphorylation of the channel protein.
Deficiency symptomsEarly signs of thiamin deficiency in most species include loss of appetite, emaciation, muscular weakness and a progressive dysfunction of the nervous system. In pigs, appetite and growth are adversely affected and the animals may vomit and have respiratory troubles.
Chicks reared on thiamin-deficient diets have poor appetites and consequently are emaciated.After about 10 days they develop polyneuritis, which is characterised by head retraction, nerve degeneratio paralysis.
Many of these deficiency conditions in animals can be explained in terms of the role of TPP in the oxidative decarboxylation of pyruvic acid. On a thiamin-deficient diet animals accumulate pyruvic acid and its reduction product lactic acid in their tissues, which leads to muscular weakness. Nerve cells are particularly dependent on the utilisation of carbohydrate and for this reason a deficiency of the vitamin has a particularly serious effect on nervous tissue. Since acetyl coenzyme A is an important metabolite in the synthesis of fatty acids (see p. 220), lipogenesis is reduced.The pentose phosphate pathway is also impaired by a deficiency of thiamin but there is little effect on the activity of the citric acid cycle.
Because thiamin is fairly widely distributed in foods and, in particular, because cereal grains are rich sources of the vitamin, pigs and poultry are in practice unlikely to suffer from thiamin deficiency.
In ruminants, microbial synthesis of the vitamin in the digestive tract, together with that present in the diet, will normally provide adequate amounts of thiamin to satisfy the animal’s requirements. However, under certain conditions, bacterial thiaminases can be produced in the rumen, which destroy the vitamin, thereby causing the deficiency condition known as cerebrocortical necrosis (CCN). This condition is characterised by circling movements, head pressing, blindness and muscular tremors. There are two types of thiaminase: one splits the molecule in two and the other substitutes an N-containing ring for the thiazole ring.The resulting compound is absorbed and blocks the reactions involving thiamin. It has been suggested that lactic acidosis caused by feeding with rapidly fermentable foods may be an important factor in the
production of thiaminases. Young animals appear to be the most susceptible.
Thiaminase is present in bracken (Pteridium aquilinum), and thiamin deficiency symptoms have been reported in horses consuming this material. Raw fish also contains the enzyme, which destroys the thiamin in foods with which the fish is mixed. The activity of the thiaminase is, however, destroyed by cooking.
RiboflavinChemical natureRiboflavin (vitamin B2) consists of a dimethyl-isoalloxazine nucleus combined with ribitol. Its structure is shown here:
It is a yellow crystalline compound, which has a yellowish-green fluorescence in aqueous solution. Riboflavin is only sparingly soluble in water; it is heat-stable in acid or neutral solutions, but it is destroyed by alkali. It is unstable to light, particularly ultraviolet light.
SourcesRiboflavin occurs in all biological materials. The vitamin can be synthesised by all green plants, yeasts, fungi and most bacteria, although the lactobacilli are a notable exception and require an exogenous source. Rich sources are yeast, liver, milk (especially whey) and green leafy crops. Cereal grains are poor sources.
MetabolismRiboflavin is an important constituent of the flavoproteins. The prosthetic group of these compound proteins contains riboflavin in the form of the phosphate (flavin mononucleotide, FMN) or in a more complex form as flavin adenine dinucleotide (FAD). There are several flavoproteins that function in the animal body; they are all concerned with chemical reactions involving the transport of hydrogen. Further details of the importance of flavoproteins in carbohydrate and amino
acid metabolism are discussed in Chapter 9. Flavin adenine dinucleotide plays a role in the oxidative phosphorylation system and forms the prosthetic group of the enzyme succinic dehydrogenase, which converts succinic acid to fumaric acid in the citric acid cycle. It is also the coenzyme for acyl-CoA dehydrogenase.
Deficiency symptomsIn pigs, deficiency symptoms include poor appetite, with consequent retardation in growth, vomiting, skin eruptions and eye abnormalities. Riboflavin is essential in the diet of sows to maintain normal oestrus activity and prevent premature parturition. Chicks reared on a riboflavin-deficient diet grow slowly and develop ‘curled toe paralysis’, a specific symptom caused by peripheral nerve degeneration, in which the chicks walk on their hocks with the toes curled inwards. In breeding hens, a deficiency reduces hatchability. Embryonic abnormalities occur, including the characteristic ‘clubbed down’ condition in which the down feather continues to grow inside the follicle, resulting in a coiled feather.
The vitamin is synthesised in the rumen and deficiencies in animals with functional rumens are unlikely to occur. However, riboflavin deficiencies have been demonstrated in young calves and lambs. Symptoms include loss of appetite, diarrhoea and lesions in the corners of the mouth.
NicotinamideChemical natureAnother member of the B vitamin complex, nicotinamide is the amide derivative of nicotinic acid (pyridine 3-carboxylic acid) and is the form in which it functions in the body.The relationship between nicotinic acid, nicotinamide and the amino acid tryptophan, which can act as a precursor, is shown here:
Nicotinamide is a stable vitamin and is not easily destroyed by heat, acids, alkalis or oxidation.
SourcesNicotinic acid can be synthesised from tryptophan in the body tissues; since animals can convert the acid to the amidecontaining coenzyme (see below), it follows that if the diet is adequately supplied with proteins rich in tryptophan, then the dietary requirement for the vitamin itself should be low. However, the efficiency of conversion of tryptophan into nicotinamide is poor. Studies with chicks have shown that the amino acid was converted into the vitamin at a ratio of only
45 : 1 on a weight basis and with some foods, such as soya bean meal, the conversion ratio may be even greater. Because of this it is generally considered that an exogenous source of the vitamin is also necessary. Although cats possess the
enzymes for the conversion of tryptophan to nicotinic acid, the activity of an enzyme in a competing pathway is very high and no nicotinic acid is synthesised. Cats do not need to produce nicotinic acid because their natural diet is well supplied with NAD and NADH. Rich sources of the vitamin are liver, yeast, groundnut and sunflower meals. Although cereal grains contain the vitamin, much of it is present in a bound form that is not readily available to pigs and poultry. Milk and eggs are almost devoid of the vitamin, although they contain the precursor tryptophan.
MetabolismNicotinamide functions in the animal body as the active group of two important coenzymes: nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP).These coenzymes are involved in the mechanism of hydrogen transfer in living cells NAD is involved in the oxidative phosphorylation system, the tricyclic acid (TCA) cycle and the metabolism of many molecules, including pyruvate, acetate, -hydroxy-butyrate, glycerol, fatty acids and glutamate; NADPH is the hydrogen acceptor in the pentose phosphate pathway.
Deficiency symptomsIn pigs, deficiency symptoms include poor growth, anorexia, enteritis, vomiting and dermatitis. In fowls, a deficiency of the vitamin causes bone disorders, feathering abnormalities, and inflammation of the mouth and upper part of the oesophagus.
Deficiency symptoms are particularly likely in pigs and poultry if diets with a high maize content are used, since maize contains very little of the vitamin or of tryptophan.
It has been suggested that through its effects on (1) rumen fermentation (some experiments have shown increased microbial growth and increased propionic acid production) and (2) cell metabolism (increased utilisation of carbohydrate and reduced lipid mobilisation), nicotinic acid may be a useful supplement to dairy cows, particularly in situations of subclinical ketosis. However, the experimental evidence is not consistent. Nicotinic acid does not always give positive responses in the rumen and increases in blood concentrations were not observed in all experiments. Current
recommendations do not advocate the supplementation of dairy cow diets in order to increase milk yield and composition.
Vitamin B6Chemical natureThe vitamin exists in three forms, which are interconvertible in the body tissues. The parent substance is known as pyridoxine, the corresponding aldehyde derivative as pyridoxal and the amine as pyridoxamine. The term vitamin B6 is generally used to describe all three forms.
The amine and aldehyde derivatives are less stable than pyridoxine and are destroyed by heat.
SourcesThe vitamin is present in plants as pyridoxine, whereas animal products may also contain pyridoxal and pyridoxamine. Pyridoxine and its derivatives are widely distributed: yeast, pulses, cereal grains, liver and milk are rich sources.
MetabolismOf the three related compounds, the most actively functioning is pyridoxal in the form of the phosphate. Pyridoxal phosphate plays a central role as a coenzyme in the reactions by which a cell transforms nutrient amino acids into mixtures of amino acids and other nitrogenous compounds required for its own metabolism. These reactions involve the activities of transaminases and decarboxylases and over 50 pyridoxal phosphate-dependent enzymes have been identified. In transamination, pyridoxal phosphate accepts the ␣-amino group of the amino acid to form pyridoxamine phosphate and a keto acid. The amino group of pyridoxamine phosphate can be transferred to another keto acid, regenerating pyridoxal phosphate. The vitamin is believed to play a role in the absorption of amino acids from the intestine.
Deficiency symptomsBecause of the numerous enzymes requiring pyridoxal phosphate, a large variety of biochemical lesions are associated with vitamin B6 deficiency. These lesions are concerned primarily with amino acid metabolism, and a deficiency affects the animal’s growth rate. Convulsions may also occur, possibly because a reduction in the activity of glutamic acid decarboxylase results in an accumulation of glutamic acid. In addition, pigs reduce their food intake and may develop anaemia. Chicks on a deficient diet show jerky movements; in adult birds, hatchability and egg production are adversely affected. In practice, vitamin B6 deficiency is unlikely to occur in farm animals because of the vitamin’s wide distribution.
Pantothenic acidChemical naturePantothenic acid, another member of the vitamin B complex, is an amide of pantoic acid and -alanine and has the following formula:
SourcesThe vitamin is widely distributed; indeed, the name is derived from the Greek pantothen, ‘from everywhere’, indicating its ubiquitous distribution. Rich sources are liver, egg yolk, groundnuts, peas, yeast and molasses. Cereal grains and potatoes are also good sources of the vitamin. The free acid is unstable. The synthetically prepared calcium pantothenate is the commonest product used commercially.
MetabolismPantothenic acid is a constituent of coenzyme A, which is the important coenzyme in fatty acid oxidation, acetate metabolism, and cholesterol and steroid synthesis. It forms the prosthetic group of acyl carrier protein in fatty acid synthesis. Chemically, coenzyme A is 3-phospho-adenosine-5-diphospho-pantotheine.
Deficiency symptomsDeficiency of pantothenic acid in pigs causes slow growth, diarrhoea, loss of hair, scaliness of the skin and a characteristic ‘goose-stepping’ gait; in severe cases, animals are unable to stand. In the chick, growth is retarded and dermatitis occurs.
In mature birds, hatchability is reduced. Pantothenic acid, like all the B complex vitamins, can be synthesised by rumen microorganisms; Escherichia coli, for example, is known to produce this vitamin. Pantothenic acid deficiencies are consid-
ered to be rare in practice because of the wide distribution of the vitamin, although deficiency symptoms have been reported in commercial herds of Landrace pigs.
Folic acidChemical natureThis B complex vitamin was first discovered in the 1930s when it was found that a certain type of anaemia in human beings could be cured by treatment with yeast or liver extracts. The active component in the extracts, which was also shown to be
essential for the growth of chicks, was found to be present in large quantities in green leaves and was named folic acid (Latin folium, a leaf).
The chemical name for folic acid is pteroylmonoglutamic acid. It is made up of three moieties: p-aminobenzoic acid, glutamic acid and a pteridine nucleus.
Several active derivatives of the vitamin are known to occur, these containing up to 11 glutamate residues in the molecule. The monoglutamate form is readily absorbed from the digestive tract but the polyglutamates must be degraded by enzymes to the monoglutamate form before they can be absorbed.
SourcesFolic acid is widely distributed in nature; green leafy materials, cereals and extracted oilseed meals are good sources of the vitamin. Folic acid is reasonably stable in foods stored under dry conditions, but it is readily degraded by moisture, particularly at high temperatures. It is also destroyed by ultraviolet light.
MetabolismAfter absorption into the cell, folic acid is converted into tetrahydrofolic acid, which functions as a coenzyme in the mobilisation and utilisation of single-carbon groups (e.g. formyl, methyl) that are added to, or removed from, such metabolites as histidine, serine, glycine, methionine and purines. It is involved in the synthesis of RNA, DNA and neurotransmitters.
Deficiency symptomsA variety of deficiency symptoms in chicks and young turkeys have been reported, including poor growth, anaemia, poor bone development and poor egg hatchability. Folic acid deficiency symptoms rarely occur in other farm animals because of synthesis by intestinal bacteria. Injections of folic acid in sows has increased litter size. In one experiment, dietary supplements resulted in higher foetal survival, thought to be related to prostaglandin activity, but the response has not
been substantiated in other experiments, possibly because of the variable content of folic acid in foods. Its role in nucleic acid metabolism concurs with the view that supplements might be beneficial at times of growth and differentiation of embryonic tissue.
BiotinChemical natureA part of the vitamin B complex, biotin is chemically 2-keto-3,4-imidazolido-2-tetrahydrothiophene-n-valeric acid. Its structure is:
SourcesBiotin is widely distributed in foods: liver, milk, yeast, oilseeds and vegetables are rich sources. However, in some foods, much of the bound vitamin may not be released during digestion and hence may be unavailable. Studies with chicks and pigs have shown that the availability of biotin in barley and wheat is very low, whereas the biotin in maize and certain oilseed meals, such as soya bean meal, is completely available.
MetabolismBiotin serves as the prosthetic group of several enzymes that catalyse the transfer of carbon dioxide from one substrate to another. In animals there are three biotindependent enzymes of particular importance: pyruvate carboxylase (carbohydrate
synthesis from lactate), acetyl coenzyme A carboxylase (fatty acid synthesis) and propionyl coenzyme A carboxylase (the pathway of conversion of propionate to succinyl-CoA).
Deficiency symptomsIn pigs, biotin deficiency causes foot lesions, alopecia (hair loss) and dry scaly skin. In growing pigs, both growth rate and food utilisation are adversely affected. In breeding sows, a deficiency of the vitamin can adversely influence reproductive performance.
In poultry, biotin deficiency causes reduced growth, dermatitis, leg bone abnormalities, cracked feet, poor feathering, and fatty liver and kidney syndrome (FLKS).This last condition, which mainly affects 2- to 5-week-old chicks, is characterised by a lethargic state with death frequently following within a few hours. On autopsy, the liver and kidneys, which are pale and swollen, contain abnormal depositions of lipid.
Although ruminants and horses do not have a requirement for dietary biotin, microbial production in the gut normally being adequate, feeding biotin has improved hoof structure and strength.
Biotin deficiency can be induced by giving animals avidin, a protein present in the raw white of eggs, which combines with the vitamin and prevents its absorption from the intestine. Certain bacteria of the Streptomyces spp. that are present in soil and manure produce streptavidin and stravidin, which have a similar action to the egg white protein. Heating inactivates these antagonist proteins.
CholineChemical natureThe chemical structure of choline is:
SourcesGreen leafy materials, yeast, egg yolk and cereals are rich sources of choline.
MetabolismUnlike the other B vitamins, choline is not a metabolic catalyst but forms an essential structural component of body tissues. It is a component of lecithins, which play a vital role in cellular structure and activity. It also plays an important part in lipid
metabolism in the liver, where it converts excess fat into lecithin or increases the utilisation of fatty acids, thereby preventing the accumulation of fat in the liver. Choline is a component of acetylcholine, which is responsible for the transmission of nerve impulses. Finally, choline serves as a donor of methyl groups in transmethylation reactions that involve folic acid or vitamin B12. Although other compounds, such as methionine and betaine, can also act as methyl donors, they cannot replace choline in its other functions.
Choline can be synthesised in the liver from methionine; the exogenous requirement for this vitamin is therefore influenced by the level of methionine in the diet.
Deficiency symptomsDeficiency symptoms, including slow growth and fatty infiltration of the liver, have been produced in chicks and pigs. Choline is also concerned with the prevention of perosis or slipped tendon in chicks.The choline requirement of animals is unusually large for a vitamin, but in spite of this, deficiency symptoms are not common in farm animals because of its wide distribution and its high concentrations in foods, and because it can be readily derived from methionine.
Vitamin B12Chemical natureVitamin B12 has the most complex structure of all the vitamins.The basic unit is a corrin nucleus, which consists of a ring structure comprising four five-membered rings containing nitrogen. In the active centre of the nucleus is a cobalt atom.A cyano group is usually attached to the cobalt as an artefact of isolation and, as this is the most stable form of the vitamin, it is the form in which the vitamin is commercially produced.
In the animal, the cyanide ion is replaced by a variety of ions, e.g. hydroxyl (hydroxocobalamin), methyl (methylcobalamin) and 5-deoxyadenosyl (5-deoxyadenosylcobalamin), the last two forms acting as coenzymes in animal metabolism.
SourcesVitamin B12 is considered to be synthesised exclusively by microorganisms and its presence in foods is thought to be ultimately of microbial origin.The main natural sources of the vitamin are foods of animal origin, liver being a particularly rich source. Its limited occurrence in higher plants is still controversial, since many think that its presence in trace amounts may result from contamination with bacteria or insect remains.
MetabolismBefore vitamin B12 can be absorbed from the intestine it must be bound to a highly specific glycoprotein, termed the intrinsic factor, which is secreted by the gastric mucosa. In humans, the intrinsic factor may be lacking, which leads to poor absorption of the vitamin and results in a condition known as pernicious anaemia.
The coenzymic forms of vitamin B12 function in several important enzyme systems. These include isomerases, dehydrases and enzymes involved in the biosynthesis of methionine from homocysteine. Of special interest in ruminant nutrition is the role of vitamin B12 in the metabolism of propionic acid into succinic acid. In this pathway, the vitamin is necessary for the conversion of methylmalonyl coenzyme A into succinyl coenzyme A.
Deficiency symptomsAdult animals are generally less affected by a vitamin B12 deficiency than are young growing animals, in which growth is severely retarded and mortality high.
In poultry, in addition to the effect on growth, feathering is poor and kidney damage may occur. Hens deprived of the vitamin remain healthy, but hatchability is adversely affected.
On vitamin B12-deficient diets, baby pigs grow poorly and show lack of coordination of the hind legs. In older pigs, dermatitis, a rough coat and suboptimal growth result. Intestinal synthesis of the vitamin occurs in pigs and poultry. Organisms that synthesise vitamin B12 have been isolated from poultry excreta; this fact has an important practical bearing on poultry housed with access to litter, where a majority, if not all, of the vitamin requirements can be obtained from the litter.
Vitamin B12 and a number of biologically inactive vitamin B12 analogues are synthesised by microorganisms in the rumen and, in spite of poor absorption of the vitamin from the intestine, the ruminant normally obtains an adequate amount of the vitamin from this source. However, if levels of cobalt in the diet are low, a deficiency of the vitamin can arise and cause reduced appetite, emaciation and anaemia. If cobalt levels are adequate, then except with very young ruminant animals, a dietary source of the vitamin is not essential. Horses also are supplied with sufficient B12 from microbial
fermentation when sufficient cobalt is supplied. Parasitised horses have responded to vitamin B12 supplementation, presumably as a result of impaired digestive activity.
Other growth factors included in the vitamin B complexA number of other chemical substances of an organic nature have been included in the vitamin B complex.These include inositol, orotic acid, lipoic acid, rutin, carnitine and pangamic acid, but it is doubtful whether these compounds have much practical significance in the nutrition of farm animals.
VITAMIN CChemical natureVitamin C is chemically known as L-ascorbic acid and has the following formula:
The vitamin is a colourless, crystalline, water-soluble compound with acidic and strong reducing properties. It is heat-stable in acid solution but is readily decomposed in the presence of alkali. The destruction of the vitamin is accelerated by
exposure to light.
SourcesWell-known sources of this vitamin are citrus fruits and green leafy vegetables. Synthetic ascorbic acid is available commercially.
MetabolismAscorbic acid plays an important part in various oxidation–reduction mechanisms in living cells.The vitamin is necessary for the maintenance of normal collagen metabolism. It also plays an important role in the transport of iron ions from transferrin, found in the plasma, to ferritin, which acts as a store of iron in the bone marrow, liver and spleen. As an antioxidant, ascorbic acid works in conjunction with vitamin E in protecting cells against oxidative damage caused by free radicals. The vitamin is required in the diet of only a few vertebrates – humans, other primates, guinea pigs, the red-vented bulbul bird and the fruit-eating bat (both native to India) and certain fishes. Some insects and other invertebrates also require a dietary source of vitamin C. Other species synthesise the vitamin from glucose, via glucuronic acid and gulonic acid lactone; the enzyme L-gulonolactone oxidase is required for the synthesis, and species requiring ascorbic acid are genetically deficient in this enzyme.
Deficiency symptomsThe classic condition in humans arising from a deficiency of vitamin C is scurvy, characterised by oedema, emaciation and diarrhoea. Failure in collagen formation results in structural defects in bone, teeth, cartilage, connective tissues and muscles. Resistance to infection is reduced.
Since farm animals can synthesise vitamin C, deficiency symptoms normally do not arise. However, it has been suggested that under certain conditions, e.g. climatic stress in poultry, the demand for ascorbic acid becomes greater than can be provided for by normal tissue synthesis, and a dietary supplement may then be beneficial.
HYPERVITAMINOSISHypervitaminosis is the name given to pathological conditions resulting from an overdose of vitamins. Under ‘natural’ conditions it is unlikely that farm animals will receive excessive doses of vitamins, although when synthetic vitamins are added to diets there is always the risk that abnormally large amounts may be ingested if errors are made during mixing. There is experimental evidence that toxic symptoms can occur if animals are given excessive quantities of vitamin A or D.
Clinical signs of hypervitaminosis A in young chicks kept under experimental conditions and given very high doses of vitamin A include loss of appetite, poor growth, diarrhoea, encrustation around the mouth and reddening of the eyelids. In pigs, toxic symptoms include rough coat, scaly skin, hyperirritability, haemorrhages over the limbs and abdomen, periodic tremors and death. Excessive intake of vitamin D causes abnormally high levels of calcium and phosphorus in the blood, which results in the deposition of calcium salts in the arteries and organs. Symptoms of hypervitaminosis D have been noted in cattle and calves. In the UK, the maximum amount of vitamin D supplement added to diets for farm
animals is controlled by legislation.
Depression in growth and anaemia caused by excessive doses of menadione (vitamin K) have been reported.
