Vitamin C occurs in two forms, L-ascorbic acid (reduced form) and dehydro-L-ascorbic acid (oxidized form). Although in nature, ascorbic acid is the predominant form, both forms are biologically active. The L-isomer of ascorbic acid is biologically active, while the D-isomer is not. In biological systems, L-ascorbic acid can be reversibly oxidized to dehydro-L-ascorbic acid. Dehydroascorbic acid is irreversibly oxidized to the inactive diketogulonic acid. Since this change takes place readily, vitamin C is very susceptible to destruction by 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 (Jaffe, 1984). Vitamin C is the least stable, and therefore most easily destroyed, of all the vitamins. Vitamin C is a white to yellow 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% aqueous solution of ascorbic acid is strongly acid, with a pH of 3. Ascorbic acid is more stable in an acidic than an alkaline medium. Vitamin C is structurally similar to glucose.
Vitamin C is efficiently absorbed in a manner similar to monosaccharides. Absorption occurs by both a sodium-dependent, active transport system at low concentrations and by diffusion at higher concentrations (Tsukaguchi et al., 1999; Johnson, 2006). Absorption occurs in the small intestine with an apparent 80% to 90% absorption rate (Kallneret 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). High levels of dietary iron, zinc, copper and pectin reduce the utilization of ascorbic acid, either by direct oxidation of vitamin C or by reducing its absorption (Sauberlich, 1990). Considerable quantities of ascorbic acid are secreted into the gastrointestinal tract and then re-absorbed as dehydroascorbate (Dabrowski, 1990). Endogenous production of vitamin C is dependent on the presence or absence of the liver microsomal enzyme L-gluconolactone oxidase, which imparts the ability to synthesize ascorbic acid from monosaccharides (Lehninger, 1982). Humans, other primates, guinea pigs, invertebrates, some insects, fish, bats and birds lack this enzyme and cannot synthesize vitamin C (Sauberlich, 1990). Ruminants synthesize vitamin C.
A second important feature of vitamin C metabolism is the interconversion of L-ascorbic acid and dehydro-L-ascorbic acid. In its metabolism, ascorbic acid is converted to dehydroascorbate by enzymatic or nonenzymatic means and can be enzymatically reduced back to ascorbic acid in cells in a glutathione-dependent reaction (Johnson et al., 2007; Sauberlich, 1990; Vethanayagam et al., 1999). Dehydroascorbic acid is the preferred form of vitamin C for uptake by erythrocytes, lymphocytes and neutrophils (Sauberlich, 1990). Recycling between dehydroascorbate and ascorbate is a prominent feature of vitamin C metabolism in erythrocytes and white blood cells, and appears to aid in maintaining antioxidant reserves (Mendiratta et al., 1998). The selenium enzyme glutathione peroxidase is involved in the regeneration of ascorbic acid from dehydroascorbic acid in bovine erythrocytes (Washburn and Wells, 1999). Ascorbic acid is also stabilized by the antioxidant enzymes superoxide dismutase and catalase (Miyake et al., 1999), which require copper, zinc, manganese and iron.
Ascorbic acid is widely distributed throughout the tissues. The highest concentrations are found in the adrenal glands, pituitary gland, pancreas, spleen and white blood cells, quantitatively the largest pools of vitamin C are found in skeletal muscle, the lungs, brain and liver (Sauberlich, 1990). Vitamin C tends to be concentrated in tissues during wound healing. In calves the major reservoirs of ascorbic acid are in the lungs, liver and muscle tissue (Toutain et al., 1997). Based on radioisotope measurements of ascorbic acid kinetics, the lungs appear to be a smaller but rapidly mobilized vitamin C pool, while the liver and muscle are larger, more slowly mobilized reserves (Toutain et al., 1997).
Ascorbic acid is metabolized to 2,3-diketogulonic acid and oxalate and excreted in the urine (Sauberlich, 1990). When vitamin C intake far exceeds requirements, ascorbic acid is excreted in urine unchanged (Sauberlich, 1990). Urinary excretion of vitamin C depends on vitamin C status and renal function.
The primary enzymatic role of ascorbic acid in metabolism is that of a reducing agent for hydroxylation reactions (Sauberlich, 1990). Synthesis of collagen and other connective tissue involves several of these reactions (Table 6-1). The other major role of vitamin C is that of water-soluble antioxidant, where its function is linked to that of the antioxidant enzymes, such as glutathione peroxidase, and to vitamin E.
Vitamin C has a clearly established role in collagen biosynthesis, the lack of which leads to the symptoms of scurvy. Vitamin C is required for the synthesis of “repair” collagen and is specifically required for the incorporation and crosslinking of proline and lysine residues in collagen biosynthesis (Moser and Bendich, 1991). Impairment of collagen synthesis in basement membranes and subsequent reduction in the integrity of the mucosal epithelium may explain the capillary fragility and increased incidence of periodontal disease observed in vitamin C deficiency (Chatterjee, 1978). Failure of wound healing, gum lesions and abnormal bone development are other symptoms of vitamin C deficiency that are linked to impaired collagen synthesis. Biochemical functions of vitamin C have been reviewed (Sauberlich, 1994; Johnston, 2006; Johnston et al., 2007). Aside from its role in collagen synthesis and wound healing, some important known functions of vitamin C are:
Of these functions, those with antioxidant properties are of great interest to researchers. The antioxidant role of vitamin C appears to be a common link in its role in the function and integrity of various cell types in the body, in detoxification functions and in the normal functioning of the adrenal glands, lungs, brain, eye and immune system.
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 (Cantani et al., 2005).
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 Passeriformes species), insects, fish (such as coho salmon, rainbow trout, and carp), and perhaps certain reptiles (McDowell, 2000). Under normal conditions, ruminants can synthesize vitamin C within their body.
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 observed sparing effects of these vitamins (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. 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.
Ascorbic acid has a role in metal ion metabolism due to its reducing and chelating properties. It can result 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 a prerequisite for the C-1 hydroxylation of vitamin D3 and conversion of its storage form 25-(OH)D3 to the active form 1,25-(OH)2D3 (Suter, 1990).
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, thieoredoxin reductase, and glutathione reductase) and low-molecular-weight antioxidant molecules (tocopherol, glutathione, and ascorbic acid), (Podda and Grundmann-Kollmann, 2001).
Ascorbic acid and glutathione are the most plentiful soluble antioxidants in leukocytes and erythrocytes. Extensive recycling of vitamin C occurs in neutrophils, monocytes and macrophages (May et al., 1999; Washko et al., 1993), and this process is stimulated by the presence of bacteria (Wang et al., 1997). Vitamin C deficiency impairs the bactericidal activity of neutrophils (Goldschmidt, 1991). Chronic, low-grade skin infections in humans have been shown to respond to vitamin C supplementation (Levy et al., 1996). Ascorbic acid enhances macrophage production of nitric oxide, which is involved in bactericidal reactions (Mizutani et al., 1998). Supplementation with both vitamin C and E potentiates white blood cell function in healthy adults (Jeng et al., 1996).
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 are important in protecting tissue against free radical damage. Both in 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).
Vitamin C has an antihistamine effect (Johnston and Huang, 1991; Johnston et al., 1992), resulting in reduced plasma histamine levels and possible enhancement of neutrophil chemotaxis and improved bronchial dilation during infection (Gershoff, 1993). In related findings, vitamin C has been shown to attenuate the damaging effects of bacterial Escherichia coli endotoxin on the lungs of sheep (Dwenger et al., 1994) and guinea pigs (Benito and Bosch, 1997). Vitamin C has also been shown to impart protection against E. coli endotoxin (lipopolysaccharide) damage to the liver (Cadenas et al., 1998) and heart (Rojas et al., 1996), possibly by induction of the mixed-function oxidase system (Takahashi et al., 1997). High concentrations of endotoxin inhibit uptake of vitamin C by the adrenal cortical cells (Garcia and Municio, 1990).
In ruminants, limited evidence exists on the effect of vitamin C on immune function. Researchers at Auburn University reported both positive effects (Blair and Cummins, 1984) (Figure 6-1) and no effect (Cummins and Brunner, 1989) on plasma immunoglobulin concentration of colostrum-deprived dairy calves. Hidiroglou et al. (1995) reported no effect of vitamin C alone (0,1 or 2 g per day) on immunoglobulin concentrations or lymphocyte response to mitogen in dairy calves. However, the same authors reported a trend for increased immunoglobulin M (IgM) in plasma when calves received both vitamin C and vitamin E. Roth and Kaeberle (1985) reported that parenteral ascorbic acid (20 mg per kg or 9.1 mg per lb body weight) reversed the suppressive effects of dexamethasone on neutrophil function and tended to enhance neutrophil phagocytosis of S. aureus bacteria. Ascorbic acid supplementation reduced respiratory rate, rectal temperature and serum cortisol level and increased serum thyroid hormone (T4) in heat-stressed lambs (Kobeisy et al., 1997). High environmental temperature has been reported to reduce plasma vitamin C concentrations in Holstein cattle, especially above 80°F (26.6°C) (Singh, 1957). Given these limited data, it would appear that the role of supplemental vitamin C in ruminants deserves further study.
A key aspect of vitamin C metabolism is its interaction with vitamin E. Vitamin C has been shown to partially reverse the effects of vitamin E deficiency in rats (Chen and Thacker, 1986). Vitamins C and E exert a sparing effect on each other in terms of controlling oxidative load (Tanaka et al., 1997). Vitamin C is also stabilized by the antioxidant enzymes glutathione peroxidase, superoxide dismutase and catalase (Miyake et al., 1999). Vitamin C has been shown to actively regenerate vitamin E from its oxidized state to its reduced state, and reduce the accumulation of the oxidized metabolite alpha-tocopherolquinone (Halpner et al., 1998). This interaction between the water-soluble (ascorbic acid) and lipid-soluble (alpha-tocopherol) antioxidant vitamins provides a strong network for protecting cell components and is nutritionally important. Other effects of vitamin C include induction of the gluconeogenic liver enzyme phosphoenolpyruvate carboxykinase (Maggini and Walter, 1997), and a repair function for DNA damaged by oxidation (Cooke, 2003).
A wide variety of plant and animal species synthesize vitamin C from monosaccharides, including glucose and galactose. Domestic livestock including ruminants have the ability to biosynthesize vitamin C, although young ruminants may not produce adequate endogenous ascorbic acid until four months of age. Plasma concentrations of ascorbic acid were lower in calves and growing steers reared under stressful conditions (i.e., slatted floors, cold stress) than animals housed in better environments (NRC, 2001). It has been suggested that calves less than four months of age may have a marginal vitamin C deficiency and that this deficiency may affect disease resistance early in life (Wegger and Moustgaard, 1982). A study with radio-labeled ascorbic acid was able to detect synthesis of vitamin C by seven days of age in calves (Toutain et al., 1997), but the quantity produced may be marginal.
There appears to be no microbial synthesis of vitamin C in the intestine (Miller and Kornegay, 1983). Due to the uncertainty of endogenous synthesis and high stress levels of young dairy calves, recommendations have been made to supplement with 200 to 2,000 mg per day (Kolb, 1962; Dvorak, 1964; Itze, 1984). Cummins (1992) references several published reports of vitamin C deficiency signs in calves.
Colostrum is a good source and milk a moderate source of ascorbic acid (Toutain et al., 1997) (Figure 6-2). Although the NRC makes no recommendation of vitamin C in calf nutrition, it may be prudent to supplement milk replacer with levels at least equal to those in whole milk (80 to 90 mg/kg or 36.3 to 40.8 mg/lb solids). Plasma vitamin C levels of calves decline over the first three weeks of life to levels below those observed in cows (Toutain et al., 1997). Radio-tracer data indicate the existence of several body storage pools of ascorbic acid, with varying rates of equilibration with plasma ascorbic acid (Toutain et al., 1997) (Figure 6-3). These findings led the authors to suggest that megadoses of vitamin C would not be well utilized in calves, and that supplementation should be aimed at raising plasma vitamin C to 8 µg/ml using a gradually released form of vitamin C. Schulze and Willy (1997) reported that plasma L-ascorbic acid concentrations peaked at 7.5 to 8.0 µg/ml, five to seven hours after oral dosing with either crystalline ascorbic acid or ascorbyl-2-monophosphate at the rate of 100 mg per kg (45.4 mg per lb) body weight. Plasma vitamin C of control calves averaged 4.3 µg/ml. Ascorbyl-2-monophosphate is significantly more stable during storage and in solution than crystalline vitamin C.
The main sources of vitamin C are fruits and green plants. Vitamin C occurs in significant quantities in organs, such as liver and kidney, but in only small quantities in meat. Vitamin C content is very low in grains and plant protein supplements.
L-ascorbic acid is the most important of several compounds that have vitamin C activity. Ascorbic acid is commercially available as pure crystalline vitamin C and various coated products, such as 97.5% ethylcellulose-coated vitamin C. The most stable form of vitamin C available to the feed industry is L-ascorbyl-monophosphate. Bioavailability of commercial vitamin C sources is similar. Stability during storage, feed processing and dissolution is the primary differentiating property among the forms.
MacLeod et al., (1966) reported that ascorbyl-2 polyphosphate is more rumen-stable than crystalline vitamin C and is effective in elevating plasma ascorbic acid concentrations in ruminating dairy cattle. The average plasma ascorbic acid concentration was approximately 4.0 µg/ml and was increased by 22% in cattle supplemented with 20 g/d stabilized in vitamin C (MacLeod et al., 1996). The effect persisted over a 31-day experimental period indicating that endogenous synthesis was not reduced by vitamin C supplementation.
Hidiroglou (1999) reported that cows dosed orally with 40 g/d ethylcellulose-coated vitamin C had higher plasma vitamin C levels than when dosed with crystalline vitamin C. Interestingly, cows dosed with vitamin C via the abomasums had only slightly higher plasma vitamin C levels than cows dosed orally. In sheep, Hidiroglou et al., (1997a) found that duodenal administration of vitamin C did result in higher plasma levels than oral dosing. However, they found little difference among crystalline vitamin C, ethylcellulose-coated vitamin C, ascorbyl-2-polyphosphate and sodium ascorbate in the effect on plasma vitamin C and the level above basal plasma levels. These studies are in conflict with early experiments showing rapid and extensive ruminal destruction of crystalline vitamin C (Cappa, 1958; Itze, 1984). Garrett et al. (2007) evaluated encapsulation (rumen protected) of vitamin C as it related to fermentation by rumen bacteria. Raw ascorbic acid (unencapsulated) was extensively degraded by rumen bacteria in less than six hours. Two different encapsulation methods proved to be an effective means of protecting 50% or more of the ascorbic acid exposed to rumen bacterial fermentation through 24 hours. Padilla et al. (2007) supplemented cows with a vitamin C preparation coated with hydrogenated soybean oil. Cattle likely absorbed more than half of this protected product. Further studies are needed in this area. Black and Hidirogou (1996) reported that for parental vitamin C, intramuscular injection produced a greater level above basal plasma vitamin C compared to intravenous administration.
Classic symptoms of vitamin C deficiency, or scurvy, are marked deterioration of mucosal integrity and health and subsequent loss of disease resistance. Because ruminants possess the metabolic pathway to synthesize ascorbic acid, they are only likely to experience outright deficiency symptoms in the neonatal period, before synthesis reaches full capacity. Cummins (1992) cites several published reports of vitamin C deficiency signs in young calves. The signs included lesions of the oral cavity and skin, low plasma ascorbate levels, increased susceptibility to disease and evidence of muscle pain and subcutaneous hemorrhage. In other species, vitamin C deficiency results in impaired neutrophil and macrophage chemotaxis and depressed T-lymphocyte response to respiratory disease (Beisel, 1982; Sauberlich, 1994; Hemila and Douglas, 1999). Stress caused by housing, disease, weather changes, transport or other factors is the most likely cause of marginal vitamin C deficiency in ruminants (Cummins and Brunner, 1991; Mackenzie et al., 1997). However, studies to date have not established a clear basis for the level of vitamin C that may be required for optimal health and performance of calves, lambs or goat kids. Supplementation of milk replacer with vitamin C at levels similar to whole milk would appear advisable.
Death of cows and calves due to scurvy was characterized by changes in the oral cavity mucosa, muzzle and skin, accompanied by weight loss and general unthriftiness (Cole et al., 1944; Duncan, 1944). In calves, extensive dermatosis, accompanied by hair loss and thickening of skin, was observed in animals receiving insufficient milk. Blood ascorbic acid was low, and the condition was successfully treated with parenteral vitamin C administration. Martynjuk (1952) reported the incidence of scurvy and reduced blood ascorbic acid content in weaned calves. Studies of blood vitamin C concentrations in calves fed a common diet revealed large individual differences, with variations related to genetic background (Palludan and Wegger, 1984).
Positive effects of ascorbic acid supplementation on milk yield and milk quality has been reported (Kucmyj, 1955; Chaiyottwittayakun, 2002). Even though cows can synthesize vitamin C and vitamin C is not a required nutrient for dairy cows, data are accumulating that show a large reduction in plasma vitamin C for lactating cows with mastitis (Weiss et al., 2004; Kleczkowski et al., 2005) and in heat-stressed cows (Padilla et al., 2006). The severity of clinical signs of mastitis is correlated with the magnitude of the decrease in plasma vitamin C in concentration (Weisset al., 2004). Vitamin C supplementation stimulated recovery from acute mammary inflammation with reduced somatic cell counts (Chaiyotwittayaku et al., 2002; Weiss and Hogan, 2007).
Neutrophils are a primary host defense mechanism against mastitis and responsiveness of neutrophils is related to the incidence and severity of mastitis in dairy cows. Vitamin C concentrations in neutrophils isolated from milk were about three times greater than concentrations in blood neutrophils (Weiss and Hogan, 2007). The duration of clinical mastitis, peak body temperature, number of colony-forming units of E. coli isolated from the infected gland, and loss in milk yield were associated with a change in concentration of vitamin C in milk from the challenged quarter (Weiss et al., 2004).
Studies with bulls indicated reduced vitamin C status during cold stress (Hidiroglou et al., 1977). Hypovitaminosis C has been observed primarily in winter and early spring, and most commonly in calves (Soldatenkov and Suganova, 1966). Jagos et al. (1977) found considerably lower plasma vitamin C content in calves with bronchopneumonia than in healthy animals. A relationship has been reported between hypovitaminosis C and skeletal muscle pain and subcutaneous hemorrhages in calves (Pribyl, 1963). Dobsinska et al. (1981) studied the relationship between ascorbic acid status and body weight gain of calves in a large commercial facility and found a negative correlation between the two parameters in two- to 22-week-old bull calves. Calves from herds characterized by poor health status generally had reduced ascorbic acid status during the critical period from birth to two weeks of age. Supplementation with 1.25 to 2.5 g of vitamin C per day reportedly reduced the incidence of respiratory disease (Itze, 1984; Palludan and Wegger, 1984; Hemingway, 1991).
In conclusion, it appears that young ruminants are susceptible to vitamin C deficiency during the first few weeks of life, particularly when subjected to stress, disease exposure or limited colostrum intake. Vitamin C is not an essential dietary nutrient for adult ruminants, however benefits have been shown for supplemental vitamin C for animals under stress or disease conditions, such as mastitis.
Kolb (1984) summarized various types of stress conditions that apparently increase vitamin C requirements for optimal health and performance:
Under these conditions, supplementation with 1 to 2 g of vitamin C per day has been beneficial. Lower levels would be typical of whole milk (e.g., 100 mg per calf per day). Colostrum contains several times the level of vitamin C found in whole milk, and therefore adequate colostrum intake is critical to provide short-term stores of vitamin C for the neonate. Young calves supplemented with vitamin C have experienced improved health as reflected by decreased naval infections, peritonitis, pneumonia, enteritis, respiration disease, scouring and mortality (Cummins and Brunner, 1989; McDowell, 2000).
Vitamin C is the least stable of all vitamins and is particularly susceptible to destruction by oxidation, which is accelerated by heat and light. Choline chloride is especially destructive of vitamin C. Gadient (1986) reported that vitamin C is almost completely destroyed in a vitamin premix with choline, with an average monthly loss of 40.0%. Some of the discrepancies in experimental results with calves fed vitamin C may be explained by the loss of vitamin C activity due to its low stability.
Supplemental dietary vitamin C is readily destroyed by rumen bacteria. Therefore,when providing supplemental ascorbic acid, it is advisable to use a stabilized form. In feed-storage experiments, coated ascorbic acid was four times more stable than crystalline vitamin C (Kolb, 1984). Adams (1978) reported that coated (ethylcellulose) ascorbic acid showed a higher retention after processing than the crystalline form, 84% versus 48%, respectively. Although retention of vitamin C activity in feed containing the ethylcellulose-coated product was low, it was 19% to 32% greater than the crystalline form. The ascorbyl-2-monophosphate form of vitamin C was developed for aquaculture applications and is significantly more stable than ethylcellulose-coated vitamin C.
Successful vitamin C products for dairy cows have been ascorbyl-2-polyphosphate (Weiss, 2001; Weiss and Hogan, 2007), vitamin C coated with hydrogenated soybean oil (Padilla et al., 2007) and lipid encapusulation (Garrett et al., 2007). Intravenously administered vitamin C, which bypassed rumenal bacteria, can be used (Chaiyotwittayakun et al., 2002).
In general, vitamin C is nontoxic. Oral ascorbic acid may be administered to most laboratory animals at doses of several grams per kilogram of body weight without any obvious general effect on health (NRC, 1987). Male guinea pigs fed 8.7% ascorbic acid for six weeks had decreased bone density and decreased urinary hydroxyproline compared to controls (Bray and Briggs, 1984). Leeson and Summers (2001) note toxicity of vitamin C to interfere with oxidase systems in the liver. One sign is excess accumulation of iron in the liver. Data are unavailable on tolerance and toxicity of ascorbic acid for ruminants. It would appear to be extremely difficult to produce vitamin C toxicity from dietary sources in ruminants, due to the apparent rumen destruction of the vitamin.
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