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.
For heat-stressed chickens, supplemental vitamin C provided definite improvements in egg production, egg shell strength, and interior egg quality (El-Boushy and Van Albada, 1970; Cheng et al., 1988, 1990). Peebles and Brake (1984) also reported that supplemental ascorbic acid holds promise for increased production during high environmental temperatures or 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 associated with the stress. 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 while it had no effect on performance parameters (Ladmakhi et al., 1997).
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 infection (Takahashi et al., 1991).
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 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 superoxide anion in the phagocytic cells.
