Vitamin C

Properties and Metabolism

Vitamin C occurs in two forms, namely L-ascorbic acid (reduced form) and dehydro-L-ascorbic acid (oxidized form). Although in nature the vitamin is primarily present as ascorbic acid, both forms are biologically active. The L-isomer of ascorbic acid is biologically active; the D-isomer is not. In nature, the reduced form of ascorbic acid may reversibly oxidize to the dehydroxidized form, the dehydroascorbic acid is irreversibly oxidized to the inactive diketogulonic acid. Since this change takes place readily, vitamin C is very susceptible to destruction through oxidation, which is accelerated by heat and light. Reversible oxidation-reduction of ascorbic acid with dehydroascorbic acid is the most important chemical property of vitamin C and the basis for its known physiological activities and stabilities (Moser and Bendich, 1991). Vitamin C is the least stable and, therefore, most easily destroyed of all the vitamins. 

Properties and Metabolism

Vitamin C is a white to yellow-tinged crystalline powder. It crystallizes out of water as square or oblong crystals (Illus. 6-1), slightly soluble in acetone and lower alcohols. A 0.5% solution of ascorbic acid in water is strongly acid with a pH of 3. The vitamin is more stable in an acid than an alkaline medium. A number of chemical substances, such as air pollutants, industrial toxins, heavy metals and tobacco smoke, as well as several pharmacologically active compounds, among them some antidepressants and diuretics, are antagonistic to vitamin C and can lead to increased requirements for the vitamin.

Illustration 6-1

The metabolic need for ascorbic acid is a general one among species, but a dietary need is limited to humans, subhuman primates, guinea pigs, fruit-eating bats, some birds (including the red-vented bulbul and related Passeriformesspecies), insects, fish (such as coho salmon, rainbow trout, and carp), and perhaps certain reptiles (McDowell, 2000). Under normal conditions, poultry can synthesize vitamin C within their body.Vitamin C is absorbed in a manner similar to carbohydrates (monosaccharides). Intestinal absorption in vitamin C-dependent animals appears to require a sodium-dependent active transport system (Johnston, 2006). It is assumed that those species that are not scurvy prone do have an absorption mechanism by diffusion (Spencer et al., 1963). Ascorbic acid is readily absorbed when quantities ingested are small, but limited intestinal absorption occurs when excess amounts of ascorbic acid are ingested. Bioavailability of vitamin C in feeds is limited, but apparently 80% to 90% appears to be absorbed (Kallner et al., 1977). Site of absorption in the guinea pig is in the duodenal and proximal small intestine, whereas the rat showed highest absorption in the ileum (Hornig et al., 1984).

In its metabolism, ascorbic acid is first converted to dehydroascorbate by several enzymes or nonenzymatic processes and can then be reduced back to ascorbic acid in cells (Johnston et al., 2007). Absorbed vitamin C readily equilibrates with the body pool of the vitamin. No specific binding proteins for ascorbic acid have been reported, and it is suggested that the vitamin is retained by binding to subcellular structures.

Ascorbic acid is widely distributed throughout the tissues, both in animals capable of synthesizing vitamin C as well as in those dependent on an adequate dietary amount of the vitamin. In experimental animals, highest concentrations of vitamin C are found in the pituitary and adrenal glands, and high levels are also found in the liver, spleen, brain and pancreas. Vitamin C also tends to localize around healing wounds. Tissue levels are decreased by virtually all forms of stress, which also stimulates the biosynthesis of the vitamin in those animals capable of synthesis.

Ascorbic acid is excreted mainly in urine, with small amounts in sweat and feces. In guinea pigs, rats, and rabbits, CO2is the major excretory mechanism for vitamin C. Primates do not normally utilize the CO2 catabolic pathway, with the main loss occurring in the urine. Urinary excretion of vitamin C depends on body stores, intake and renal function.


Ascorbic acid has been found to be involved in a number of biochemical processes. Function of vitamin C is related to its reversible oxidation and reduction characteristics. However, the exact role of this vitamin in the living system is not completely understood, since a coenzyme form has not yet been reported. In addition to the relationship of ascorbic acid to hydroxylase enzymes, Franceschi (1992) suggests that vitamin C is required for differentiation of connective tissue such as muscle, cartilage and bone derived from mesenchyme (embryonic cells capable of developing into connective tissue). It is proposed that the collagen matrix produced by ascorbic acid-treated cells provides a permissive environment for tissue-specific gene expression. A common finding in all studies is that vitamin C can alter the expression of multiple genes as cells progress through specific differentiation programs (Ikeda et al., 1997). The most clearly established functional role for vitamin C involves collagen biosynthesis. Beneficial effects result from ascorbic acid in the synthesis of “repair” collagen. Alteration of basement membrane collagen synthesis and its integrity in mucosal epithelium during vitamin C restriction might explain the mechanism by which the capillary fragility is induced in scurvy as well as the increased incidences of periodontal disease under vitamin C deprivation. Failure of wounds to heal and gum and bone changes, resulting from vitamin C undernutrition, are direct consequences of reduction of insoluble collagen fibers. Biochemical and physiological functions of vitamin C have been reviewed (Moser and Bendich, 1991; Padh, 1991; Gershoff, 1993; Johnston, 2006; Johnston et al., 2007). The functional importance of vitamin C, other than the previously mentioned role in collagen synthesis, includes the following:

  • (a) Due to the ease with which ascorbic acid can be oxidized and reversibly reduced, it is probable that it plays an important role in reactions involving electron transfer in the cell. Almost all terminal oxidases in plant and animal tissues are capable of directly or indirectly catalyzing the oxidation of L-ascorbic acid. Such enzymes include ascorbic acid oxidase, cytochrome oxidase, phenolase, and peroxidase. In addition, its oxidation is readily induced under aerobic conditions by many metal ions and quinones.
  • (b) Metabolic oxidation of certain amino acids, including tyrosine.
  • (c) Ascorbic acid has a role in metal ion metabolism due to its reducing and chelating properties. This results in enhanced absorption of minerals from the diet and their mobilization and distribution throughout the body. Ascorbic acid promotes non-heme iron absorption from food (Olivares et al., 1997) and acts by reducing the ferric iron at the acid pH in the stomach and by forming complexes with iron ions that stay in solution at alkaline conditions in the duodenum. Also, a sufficient vitamin C status is the prerequisite for the C-1 hydroxylation of vitamin D3 and its storage form 25(OH)D to the active form 1,25(OH)2D (Suter, 1990).
  • (d) Carnitine is synthesized from lysine and methionine and is dependent on two hydroxylases, both containing ferrous iron and L-ascorbic acid. Vitamin C deficiency can reduce the formation of carnitine, which can result in accumulation of triglycerides in blood and the physical fatigue and lassitude associated with scurvy (Ha et al., 1994). About 98% of total body carnitine is in muscle; skeletal and heart muscle carnitine concentrations are reduced by 50% in vitamin C-deficient guinea pigs compared with controls (Johnston, 2006).
  • (e) Interrelationships of vitamin C to B vitamins are known, as tissue levels and urinary excretion of vitamin C are affected in animals with deficiencies of thiamin, riboflavin, pantothenic acid, folic acid and biotin.
  • (f) Vitamin C has been demonstrated to inhibit nitrosamines, which are potent carcinogens. The vitamin is effective in detoxifying high nitrate diets for ruminants (Aseltine, 1990).
  • (g) Vitamin C is involved in controlling synthesis of glucocorticoids (corticosteroids) in the adrenal gland. The protective effects of vitamin C (also vitamin E) on health may partially be a result of reducing circulating levels of glucocorticoids (Nockels, 1990). During stress, glucocorticoids, which suppress the immune response, are elevated. Vitamin C reduces adrenal glucocorticoid synthesis, helping to maintain immunocompetence. In addition, ascorbate can regenerate the reduced form of alpha-tocopherol, perhaps accounting for the observed sparing effect on this vitamin (Jacob, 1995). In the process of sparing fatty acid oxidation, tocopherol is oxidized to the tocopheryl free radical. Ascorbic acid can donate an electron to the tocopheryl free radical, regenerating the reduced antioxidant form of tocopherol.
  • (h) Ascorbic acid is found in up to a ten-fold concentration in seminal fluid as compared to serum levels. Decreasing levels have caused nonspecific sperm agglutination. In a review of ascorbic acid and fertility, Luck et al. (1995) suggest how three of ascorbic acid’s principal functions, namely its promotion of collagen synthesis, its role in hormone production, and its ability to protect cells from free radicals, may explain its reproductive actions.
  • (i) Vitamin C has a biological role in keratinocytes. Because skin must provide the first line of defense against environmental free radical attack (e.g., sunburn, skin aging and skin cancer), it has developed a complex antioxidant network that includes enzymatic and non-enzymatic components. The epidermis is composed of several layers of keratinocytes supplied with enzymes (superoxide dismutase, catalase, thioredoxin reductase, and glutathione reductase) and low-molecular-weight antioxidant molecules (tocopherol, glutathione, and ascorbic acid) (Podda and Grundmann-Kollmann, 2001).
  • In keratinocytes, vitamin C contributes to counteract oxidative stress via transcriptional and post-translational mechanisms. Vitamin C can: 1) act directly by scavenging reactive oxygen species (ROS) generated by stressors; 2) prevent ROS-mediated cell damage by modulating gene expression; 3) regulate keratinocyte differentiation maintaining a balanced redox state; and 4) promote cell cycle arrest and apoptosis in response to DNA damage (Cataniet al., 2005).
  • (j) Ascorbic acid is reported to have a stimulating effect on phagocytic activity of leukocytes, function of the reticuloendothelial system and formation of antibodies. Tissue defense mechanisms against free-radical damage generally include vitamin C, vitamin E, and beta-carotene as the major vitamin antioxidant sources. In addition, several metalloenzymes that include glutathione peroxidase (selenium), catalase (iron), and superoxide dismutase (copper, zinc and manganese) are also critical in protecting the internal cellular constituents from oxidative damage. The dietary and tissue balance of all these nutrients is important in protecting tissue against free radical damage. Bothin vitro and in vivo studies showed that the antioxidant vitamins generally enhance different aspects of cellular and noncellular immunity. The antioxidant function of these vitamins could, at least in part, enhance immunity by maintaining the functional and structural integrity of important immune cells. A compromised immune system will result in reduced animal production efficiency through increased susceptibility to diseases, thereby leading to increased animal morbidity and mortality.

As an effective scavenger of reactive oxygen species, ascorbic acid minimizes the oxidative stress associated with the respiratory burst of activated phagocytic leukocytes, thereby functioning to control the inflammation and tissue damage associated with immune responses (Chien et al., 2004). Ascorbic acid levels are very high in phagocytic cells, with these cells using free radicals and other highly reactive oxygen containing molecules to help kill pathogens that invade the body. In the process, however, cells and tissues may be damaged by these reactive species. Ascorbic acid helps to protect these cells from oxidative damage (McDowell, 2006).


A wide variety of plant and animal species can synthesize vitamin C (ascorbic acid) from carbohydrate precursors including glucose and galactose. The missing step in the pathway of ascorbic acid biosynthesis in all vitamin C-dependent species has been traced to inability to convert L-gulonolactone to 2-keto-L-gulonate, which is transformed into L-ascorbic acid. Vitamin C dietary-dependent species, including poultry, therefore lack the enzyme L-gulonolactone oxidase. Domestic animals such as poultry have the ability to biosynthesize ascorbic acid within their body. However, biosynthesis of vitamin C is limited in very young birds and increases with age up to about 60 days of age (Leeson and Summers, 2001). Strains of birds differ in ascorbic acid synthesis as measured by L-gulonolactone oxidase activity and tissue ascorbic acid concentration (Maurice et al., 2004). It seems that broiler chicks with higher growth rates have a high demand for antioxidant defense and thus a higher vitamin C requirement (Surai et al., 2002).

In general, research studies have shown that healthy animals under ordinary conditions do not respond to supplemental vitamin C and hence there is no recommended requirement established by the NRC. However, Marks (1975) proposed vitamin C requirements (mg per kg; mg per lb of diet) for poultry and swine as follows: poultry (50 to 60; 23 to 27), starting pigs (300; 136), and finishing pigs (150; 68).

Although vitamin C can be synthesized by poultry, the synthesis is reduced or the requirements for vitamin C are increased during times of stress. During times of environmental, nutritional or pathological stress, the addition of ascorbic acid to the birds’ feed or to their drinking water appears to alleviate many of the undesirable physical consequences of exposure (e.g., chronic adrenocortical activation, immunosuppression, weight loss and reduced egg production) to single or multiple concurrent stressful stimuli such as high environmental temperature, beak trimming, coccidiosis challenge and transportation (Pardue and Thaxton, 1986; Satterlee et al., 1989; Kutlu and Forbes, 1993; McKee and Harrison, 1995; Jones, 1996; Whitehead and Keller, 2003, Roussan et al., 2008). Thyroid status may be a factor affecting the ascorbic acid requirement, with supplemental vitamin C improving chick performance from experimentally induced hypothyroidism (Takahashi et al., 1991).


The main sources of vitamin C are fruits and green plants, but some foods of animal origin contain more than traces of the vitamin. Vitamin C occurs in significant quantities in animal organs, such as liver and kidney, but in only small quantities in meat. Vitamin C is very low in the predominant feedstuffs for poultry (i.e., grains and plant protein supplements). Postharvest storage values vary with time, temperature, damage and enzyme content (Zee et al., 1991).

Of animals raised for food production, sources of vitamin C would be most important for fish and next for stressed animals. L-ascorbic acid is commercially available as 100% crystalline, 50% fat-coated, and 97.5% ethylcellulose-coated products and their dilutions. The more soluble sodium salt of ascorbic acid (sodium ascorbate) is also commercially available. Various derivatives of ascorbic acid, which are more stable than the parent compound, have been shown to provide antiscorbutic activity. These include L-ascorbate-2-sulfate, L-ascorbyl-2-monophosphate, magnesium-L-ascorbyl-2-phosphate, and L-ascorbyl-2-polyphosphate. When providing supplemental ascorbic acid, it is advisable to use a stabilized form; a coating of ascorbic acids and crystals with ethylcellulose is a suitable stabilization method. In storage experiments, ascorbic acid protected in this manner was found to be four times more stable than untreated ascorbic acid crystals (Kolb, 1984).

Adams (1982) reported that coated (ethylcellulose) ascorbic acid showed higher retention after processing than the crystalline form, 84% versus 48%. Retention of ascorbic acid in mash feed was fairly good, but with elevated storage time and temperature, stability was poor in crumbled feeds. Although retention of vitamin C activity in feed containing the ethylcellulose-coated product was low, it was 19% to 32% better than that of the crystalline form.

Recent reports have evaluated polyphosphorylated L-ascorbic acid for fish (Chen and Chang, 1994; Matusiewicz et al., 1995), which has been found to be more stable against oxidation and extrusion. Approximately 50% of the supplemental ascorbic acid is destroyed during the manufacture of extruded catfish feeds (Lovell and Lim, 1978) and excess ascorbic acid is added to commercial formulations to ensure that an adequate concentration of the vitamin is retained during processing. The form of the vitamin selected depends on how the fish feed is manufactured and how long it is stored before being fed to the fish. It may be more economical to over fortify channel catfish feeds with ethycellulose-coated product than to use phosphate derivatives of ascorbic acid; price-to-benefit relationships must be considered. Crystalline L-ascorbic acid and L-ascorbyl-2-polyphosphate were of similar bioavailability for broiler chicks (Pardue et al., 1993). Magnesium-L-ascorbic-2-phosphate is a stable form of vitamin C that was shown to be available in swine diets (Mahan et al., 1994).


Poultry are able to synthesize vitamin C and thus it is assumed they do not require dietary sources of the vitamin. However, for newly hatched poultry there is a slow rate of ascorbic acid synthesis and this combined with encountered stress increases probability of vitamin C deficiency. The chick is subject to considerable stress conditions, including rapid growth, exposure to hot or cold temperatures, starvation, vaccination and disease conditions such as coccidiosis. Pardue and Williams (1990) reported that plasma ascorbic acid levels in poults were depressed significantly by cold stress, beak trimming, and injection at one and 14 days of age. Supplemental vitamin C (150 mg per kg or 68.2 mg per lb diet) enhanced performance of broiler chicks exposed to multiple concurrent environmental stressors (McKee and Harrison, 1995).For both stressed mature and newly hatched poultry, several reports have documented a beneficial effect of supplementing the diet with ascorbic acid on growth rate, egg production, egg shell strength and thickness, fertility and spermatozoa production, on counteracting unfavorable climate and housing conditions and in case of intoxication or disease (McDonald et al., 1981; Pardue, 1987; Bashir et al.,1998). On the contrary, some researchers have found no beneficial effect of vitamin C supplementation under any conditions. Heat stress is one of the major stressors in poultry production and produces a wide range of physiological changes. The nature and magnitude of these changes depend upon the degree of heat stress imposed. Typical responses include elevation in plasma concentrations of corticosteroids (five-fold increase), protein, glucose, and sodium as well as decreases in potassium and the relative weights of adrenal, bursa, spleen and thyroid. To minimize its heat load, the bird will reduce food intake and production will fall as a result. The bird will also pant to increase evaporative heat loss, and this results in loss of C02 and an increase in blood pH. As the heat load on the bird increases, the rise in body temperature will result in tissue damage and release of intracellular components into the circulation (Whitehead and Keller, 2003).

For heat-stressed chickens, supplemental vitamin C has provided definite improvements in growth, health, egg production, egg shell strength, and interior egg quality (El-Boushy and Van Albada, 1970; Cheng et al., 1988, 1990; Puthponsgsiriporn et al., 2001; Whitehead and Keller, 2003; Sahin et al., 2004; Balnave and Brake, 2005; Roussan et al., 2008). Dietary vitamin C and folic acid supplementation also increased performance and antioxidant status of Japanese quail under heat stress (34°C) (Sahin et al., 2003). Peebles and Brake (1984) also reported that supplemental ascorbic acid holds promise for increased production during high environmental temperatures and also for nutritionally marginal diets. When ascorbic acid was used at levels of 100 mg per kg (45 mg per lb) of diet or less for commercial layers, there was improvement in livability, egg production, and egg shell quality. Perek and Kendler (1963) carried out experiments in the Jordan Valley where hens were subjected to hot temperatures and reported an increase in egg production of 23% and 11.2% in two experiments with birds given supplemental ascorbic acid. They also reported increased egg weights and decreased culls and mortality, but there were no shell quality differences. Ascorbic acid also can alleviate nutritional stress. Balnave et al. (1994) showed that poor shell quality of hens given saline drinking water could be overcome by addition of ascorbic acid to the water (1 g per L). Other researchers were not able to confirm the positive effects of ascorbic acid supplementation.

Male reproduction is favored by vitamin C supplementation. Monsi and Onitchi (1991) supplemented the feed of heat-stressed broiler breeders with 0, 125, 250 or 500 ppm of ascorbic acid. Semen volume, total sperm per ejaculate, and motile sperm per ejaculate were significantly increased due to the addition of ascorbic acid. Semen volume and sperm concentration of tom turkeys were found to be increased by 28% by the supplementation of 150 mg per kg (68.2 mg per lb) of ascorbic acid to the breeder ration (Dobrescu, 1987). Noll (1993) supplemented the feed of male breeder turkeys with 200 mg per kg (90.0 mg per lb) of ascorbic acid for eight weeks; ascorbic acid supplementation improved semen volume 16% and increased sperm concentration 18%. More recently, Noll (1997) also reported improved sperm cell concentrations in males and more eggs per hen when turkey breeder diets were supplemented with 200 mg per kg (90.9 mg per lb) of vitamin C. This improved reproductive performance was noted in spite of environmental temperature fluctuations.

Vitamin C is necessary for bone development and egg shell quality. Supplementing ascorbic acid to molted laying hens was beneficial to egg production and egg shell quality (Zapata and Gernat, 1995). Orban et al. (1993) reported large doses of ascorbic acid (2,000 mg per kg or 909 mg per lb) in the diet influenced calcium metabolism, affecting bone and egg shell mineralization in chickens. Vitamin C is a necessary cofactor for the bioconversion of vitamin D3 to its active form 1,25-(OH)2D3. Weiser et al. (1990) reported that 100 mg per kg (45.5 mg per lb) of ascorbic acid in the diet of chicks increased plasma concentrations of 1,25-(OH)2D3, which led to elevated activities of duodenal calcium-binding protein and greater weights and breaking strength of bones. It is possible that the many cases of “field rickets” in poults may be due to stress-induced deficiency of vitamin C. Vitamin C has been shown to influence the developmental process in the growth plate for bone growth (Farquharson et al., 1998).

Njoku (1986) concluded that during periods of heat stress in the tropics, dietary supplementation of broiler diets with 200 mg of ascorbic acid per kg (90 mg per lb) of feed was necessary and economically advantageous as body weight and feed:gain responses were improved. Other researchers have not been able to confirm the positive effects of ascorbic acid supplementation. In a study supplementing 2,600 mg per kg (1,182 mg per lb) of ascorbic acid, egg production, egg shell thickness, egg weight and mortality were not affected, but interior quality was improved (Nockels, 1988).

Pardue et al. (1985) were unable to find significant vitamin C effects on heat stress in broiler performance except heat-associated mortality was markedly reduced in females supplemented with vitamin C. When acute heat stress was imposed on broilers, vitamin C reduced adrenal corticosteroid concentration in the plasma of stressed birds. Apparently, high levels of ascorbic acid in the adrenal gland regulate glucocorticoid synthesis, thus limiting some of the deleterious responses associated with stress and delaying the depletion of steroid hormone precursors.

Disease conditions have been found to affect vitamin C metabolism in poultry. When chicks were infected with fowl typhoid, their plasma vitamin C concentrations were reduced (Hill and Garren, 1958). The vitamin C concentrations in plasma and tissue were also reduced in chicks infected with intestinal coccidiosis (Kechik and Sykes, 1979). Dietary ascorbate was shown to prevent this and contributed to intestinal repair. Ascites, a costly metabolic disease in chickens that is a consequence of pulmonary hypertension, can be modified by vitamin C. The addition of vitamin C to broiler diets significantly reduced the ascites mortality (Xiang et al., 2002; Broz and Ward 2007).

In addition to performance, evidence also suggests an association between ascorbic acid and the animal’s ability to tolerate or resist bacterial infection. In early work, chickens infected with fowl typhoid had reduced levels of ascorbic acid in the blood and the administration of ascorbic acid at 1,000 mg per kg (454 mg per lb) of feed resulted in reduced early mortality from typhoid infection (Satterfield et al., 1940). Chickens fed a diet containing supplemental ascorbic acid showed increased resistance to a combined Newcastle disease virus Mycoplasma gallissepticum infection and to a secondary E. coli infection, as well as to a primary E. coli challenge (Takahashi et al., 1991).

Lohakare et al. (2005a) studied the effect of supplemental ascorbic acid on immunity of commercial broilers. As dietary vitamin C increased the lymphocyte subpopulation showed higher CD4 and T-Cell receptor-II cells. The infectious bursal disease (IBD) and Newcastle disease (ND) titers measured postvaccination showed significantly higher IBD titers for birds supplemented with vitamin C at 200 mg per kg (90.9 mg per lb) feed. It can be concluded that supplementation of ascorbic acid was beneficial for improving the performance and immunity and for exploiting the full genetic potential of the commercial broilers. Both vitamin E (65 IU per kg and 30 IU per lb of diet) and vitamin C at 1,000 ppm enhanced in vitro lymphocyte proliferative responses of hens during heat stress (Puthpongsiriporn et al., 2001).

Six-week-old Leghorn-type chickens supplemented with 330 mg per kg (150 mg per lb) of vitamin C and exposed to air-sac challenge with E. coli had a 19% incidence of E. coli infection versus 76% in control chickens (Gross et al., 1988). These authors hypothesized that the response to ascorbic acid may be attributed to ascorbic acid increasing the synthesis of the superoxide anion, which kills phagocytized bacteria. Dietary level of ascorbic acid appears to be important since too little ascorbic acid results in too little superoxide anion production and excessive ascorbic acid may result in reduction of the superoxide anion in the phagocytic cells.

Fortification Considerations

Supplementation of vitamin C would not normally be recommended for common livestock species (ruminants, poultry, swine and horses) under normal management and feeding regimes. As previously mentioned, stress conditions do affect vitamin C synthesis and supplementation considerations must take this into account. Kolb (1984) has summarized various types of stress that apparently have increased demands while reducing animals’ capability to synthesize vitamin C: (1) dietary conditions: deficiencies of energy, protein, vitamin E, selenium, iron and starvation, etc.; (2) production or performance stress: high production or performance (e.g., rapid growth rates and high egg production); (3) transportation, animal handling and new environmental location stress: animals placed in new surroundings and stressful management practices (castration, debeaking, etc.); (4) temperature: high ambient temperature or cold trauma; (5) disease and parasite: fever and infection reduce blood ascorbic acid, while parasites, particularly in the liver, disturb ascorbic acid synthesis and increase requirements for the vitamin. Various studies have demonstrated beneficial effects of low supplemental levels of 50 to 100 mg per kg (23 to 45 mg per lb) of ascorbic acid in diets of broilers or laying hens exposed to heat stress (Kolb, 1984). Feeding layer hens 150 mg per kg (68.2 mg per lb) alleviated adverse effects of heat stress in live weight and egg quality profiles (Ajakaiye et al., 20ll a, b). Njoku (1986) reported that 200 mg of ascorbic acid per kg (90 mg per lb) of diet fed to broilers helped alleviate heat stress. Egg shell thickness increased for hens (El-Boushy et al., 1968), while livability, weight gain and immune response improved in broilers (Pardue and Thaxton, 1982) when heat-stressed birds received supplemental vitamin C. Peebles and Brake (1985) fed vitamin C to broiler breeders throughout a complete production cycle. They found fertility improved at dietary levels of 50 mg per kg (23 mg per lb) with improvement in hatch of fertile eggs due to a decrease in early embryonic mortality. There was no further benefit at 100 mg per kg (45 mg per lb) ascorbic acid. In turkeys, toms given 150 mg per kg (68 mg per lb) of dietary ascorbic acid increased semen volume by 28% and increased sperm concentration by 31% per ejaculate. It is thought that the ascorbic acid stimulates testicular activity by its involvement in the synthesis of steroid hormones (Dobrescu, 1987). Higher amounts of supplemental vitamin C have proved beneficial to poultry. Optimum responses in growth, feed efficiency and/or liveability in broilers under heat stress seem to occur with supplements of vitamin C. For laying hens under stress, there are improvements in livability, feed intake, egg production and egg quality with dietary vitamin C concentrations in the range of 250 to 400 mg per kg (114 to 182 mg per lb) (Whitehead and Keller, 2003). Production responses in poultry confirm that dietary supplementation with vitamin C generally only benefits birds under stress. Vitamin C supplementation of turkey breeder hen diets at a rate of 200 mg per kg (90.0 mg per lb) improved egg production 6.5% over a 24-week period (Noll et al., 1996b). Similarly, vitamin C supplemented at the rate of 330 mg per kg (136.4 mg per lb) reduced mortality and pericarditis in chicks infected with E. coli (Gross et al., 1988). The amount of vitamin C needed for this protective effect increased with higher environmental stress levels (Chew, 1994). Some commercial turkey operations have adopted the practice of feeding higher levels of vitamin C, riboflavin and vitamin E to prevent the pale, soft and exudative syndrome (PSE) in meat.

Large doses of ascorbic acid of 2,000 to 3,000 mg per kg (909 to 1,364 mg per lb) fed in granular coated form to White Leghorn hens increased egg weight up to 5% and also improved egg specific gravity (Orban et al., 1993). Improvement in egg specific gravity might be associated with thicker eggshells because the high level of ascorbic acid caused more calcium to be deposited on the shell. Levels of 250 and 500 mg per kg (114 or 227 mg per lb) of granular ascorbic acid in the diet of White Leghorns that have been force rested resulted in increased egg production an average of 5% over that of hens on lower levels, and egg shell quality was improved (Zapata and Gernat, 1995).

In another study, Noll et al. (1996a) reported improved feed intake and water consumption by poults when their drinking water was supplemented with a stabilized ascorbic acid product. Similar results were reported in broilers by McKee and Harrison (1995).

Ascorbic acid has been implicated in the fear response of poultry (Satterlee et al., 1994; Jones, 1996; Jones et al., 1996; Jones et al., 1999). This is an important consideration, since in a study involving 22 broiler farms, 28% of the variation in the feed:gain ratio could be attributed to fear of humans by the birds (Jones, 1996). Panic, hysteria and attempts to flee can have a negative effect on bird performance. In the 22-farm study, Jones (1996) determined that an improvement of 0.09 in F/G would be possible if fear levels at the farm with the most fearful birds were reduced to levels of the least fearful.

Supplementation with ascorbic acid at 1,000 ppm in drinking water for 24 hours prior to stimuli resulted in a significant reduction in the length and intensity of fear responses in broilers (Satterlee et al., 1994). In a study with Japanese quail (Jones et al., 1999), ascorbic acid was tested in two genetic lines, which had been identified for either low or high innate fearfulness. Ascorbic acid at 1,000 ppm for 24 hours prior to stimuli significantly decreased timidity in both genetic lines by 20-25%. In an earlier study (Jones, 1996), ascorbic acid supplemented Japanese quail (1,000 ppm for 24 hrs prior to stimuli) were less likely (P < 0.05) to avoid strange objects in the feed trough and responded significantly faster to regain tonic movement after the induction of tonic immobility.

These responses could be explained if the metabolic requirements for this vitamin exceeds the capacity for biosynthesis during periods of stress (Satterlee et al., 1994). An alternative suggestion (Jones et al., 1999) is that ascorbic acid may modulate corticosteroid levels, which are elevated during stress (Satterlee et al., 1993).

L-ascorbic acid is the most important of the several compounds that have vitamin C activity. Ascorbic acid is commercially available as 100% crystalline, 50% fat-coated, and 97.5% ethylcellulose-coated products and their dilutions. The more soluble sodium salt of ascorbic acid (sodium ascorbate) is also commercially available. Various derivatives of ascorbic acid, which are more stable than the parent compound, have been shown to provide antiscorbutic activity. These include L-ascorbate-2-sulfate, L-ascorbyl-2-monophosphate, magnesium-L-ascorbyl-2-phosphate, and L-ascorbyl-2-polyphosphate. When providing supplemental ascorbic acid it is advisable to use a stabilized form, and coating of ascorbic acid crystals with ethylcellulose is a suitable stabilization method. In storage experiments, ascorbic acid protected in this manner was found to be four times more stable than untreated ascorbic acid crystals (Kolb, 1984).

The coated (ethylcellulose) ascorbic acid showed a higher retention after processing than the crystalline form, 84% versus 48%. Retention of ascorbic acid in mash feed was fairly good, but with elevated storage time and temperature the stability was poor in crumbled feeds. Although retention of vitamin C activity in feed containing the ethylcellulose-coated product was low, it was 19% to 32% better than that of the crystalline form.

Since ascorbic acid can be synthesized at the tissue level by domestic fowl, it has been held by many nutritionists that exogenous supplementation of ascorbic acid to poultry would be senseless. Over the past several decades, the relationship between stress and ascorbic acid in poultry has been recognized; however, research data have been inconsistent and conflicting, making it difficult to establish a requirement for this nutrient under all conditions.

The amount of ascorbic acid synthesized by the bird should be sufficient for normal growth and metabolism; however, there is evidence that ascorbic acid synthesis may not meet physiological needs under stressful conditions (Ferket, 1994). Pardue and Williams (1990) reported that plasma ascorbic acid levels in poults were depressed significantly by cold stress, beak trimming, and injection at one and 14 days of age. Stress causes a depletion of ascorbic acid at a faster rate than the bird’s natural capability to synthesize this vitamin (Pardue and Thaxton, 1986). The ability of poultry to synthesize ascorbic acid and the amount needed or used changes with age, management, environment, disease and stress. Pardue and Williams (1990) reported that serum ascorbic acid concentration in poults increased 170% from hatch to 49 days of age.

Research data indicate that supplementation with ascorbic acid should be considered as a management alternative to prevent vitamin C deficiencies when poultry are stressed (Quarles and Adrian, 1989; Quarles et al., 1989; Cheng et al., 1990; Ferket, 1994; Jones, 1996; Whitehead and Keller, 2003; Sahin et al., 2004). Vitamin C supplementation can modify the detrimental effects of environmental, nutritional or pathological stress (Jones, 1996; Jones et al., 1996; Balnave and Brake, 2005).

Vitamin Safety

In general, high intakes of vitamin C are considered to be of low toxicity. A number of studies with chickens and turkeys have shown no effect when birds were fed high levels of ascorbic acid (NRC, 1987). Dietary supplementation of ascorbic acid even at levels as high as 3% had no appreciable effects on body weight gain, feed intake and feed efficiency of growing chicks (Nakaya et al., 1986). Leeson and Summers (2001) note that toxic levels of vitamin C interfere with oxidase systems in the liver. One sign is excess accumulation of iron in the liver.

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