Effect of chronic oxidative/corticosterone-induced stress on ascorbic acid metabolism and total antioxidant capacity in chickens (Gallus gallus domesticus).

The consequences of chronic corticosterone-induced stress (CCIS) on ascorbic acid (AsA) metabolism in chickens, an animal that syntheses the vitamin, are not known. This study was conducted to determine whether CCIS alters AsA synthesis, as measured by l-gulonolactone oxidase (GLO) activity, tissue AsA, lipid peroxides and tissue total antioxidant capacity (TAC). Stress was induced by dietary administration of corticosterone from 2 to 4 weeks of age and measurements were made at 0, 7 and 14 days post-treatment. Ascorbic acid synthesis was not influenced by CCIS but hepatic, cardiac, renal, bursal and duodenal AsA concentrations were significantly decreased and plasma TAC and uric acid concentrations were significantly elevated. Stress caused significant hepatomegaly and hepatic lipidosis but hepatic peroxides were not elevated despite the slight decrease in hepatic TAC. Tissue TAC varied in different organs. It was markedly elevated in the kidney, reduced by 49% in the spleen, and changes were not detected in the heart and duodenum even though AsA concentration was significantly decreased in all tissues. We conclude that CCIS caused a significant reduction in tissue AsA concentration but did not inhibit GLO activity. The change in AsA concentration was associated with increase, decrease or no change in TAC in tissues examined. The findings suggest that CCIS may alter AsA recycling, influx or turnover in different tissues of chickens.

Ascorbic acid biosynthesis in hens producing strong and weak eggshells.

1. An experiment was conducted with two strains of layers to ascertain whether the reduction in eggshell strength occurring at the end of the production cycle is the result of reduced ascorbic acid biosynthesis. 2. Hens producing strong and weak eggshells were identified within each strain and egg production, egg weight, per cent shell, shell surface density, plasma, adrenal and hepatic ascorbic acid and renal L-gulonolactone oxidase activity were measured. 3. The strains differed in ascorbic acid synthesis, as measured by L-gulonolactone oxidase activity, and tissue ascorbic acid concentration. 4. Comparison of results from birds producing eggs of similar weight but markedly different in shell strength detected neither a shell strength group x strain interaction nor an effect of shell strength group on plasma and hepatic ascorbic acid and activity of L-gulonolactone oxidase. 5. The results did not support the hypothesis that tissue ascorbate and ascorbic acid biosynthesis are reduced in old hens producing weak eggshells.

Factors affecting ascorbic acid (AsA) biosynthesis in chickens. II. Effect of dietary AsA and strain of chicken.

The present study examined the effect of supplemental ascorbic acid (AsA) and ascertained if genotype is a determinant of biosynthesis and the response of strains to dietary AsA. Slow- (Ottawa Meat Control; OMC) and fast-growing (Peterson Enhanced x Hubbard; PEH) chicks were fed 1000 mg/kg AsA from 1 to 10 weeks of age. The activity of l-gulonolactone oxidase (GLO) was used to measure biosynthesis and estimated synthetic capacity (ESC) computed. Body weight was not affected by diets and relative kidney weight decreased with age. In 1 week, dietary AsA increased plasma AsA and inhibited GLO activity with a greater reduction in OMC birds. At 10 weeks, GLO activity was depressed almost uniformly in both strains. Strain by age and diet by age interactions were detected for GLO activity and ESC with significantly greater decline in PEH birds and birds fed supplemental AsA. The results demonstrated that dietary AsA inhibited biosynthesis in meat type chickens and the response at 10 weeks was not influenced by growth rate; and the age dependent decline in biosynthesis was more pronounced in the commercial PEH birds. The result suggests that such strains may be compromised in some situations. Research using multiple dietary levels of AsA, commercial strains, and defined stressors is warranted.

Factors affecting ascorbic acid biosynthesis in chickens: III. Effect of dietary fluoride on L-gulonolactone oxidase activity and tissue ascorbic acid (AsA) concentration.

The inconsistent beneficial responses to dietary ascorbic acid (AsA) may be due to dietary factors that alter biosynthesis or tissue turnover of AsA. It has been suggested on the basis of altered tissue AsA that dietary fluoride is a determinant of biosynthesis in chickens. Fluoride may enter the food chain of poultry via industrial contamination, feed ingredients and drinking water. The goal of this study was to ascertain whether dietary fluoride at 300 mg/kg influences l-gulonolactone oxidase (GLO) activity in commercial meat-type chickens. The experimental diet was fed from day-old to 3 weeks and responses measured. Growth and feed conversion were not affected by fluoride in the diet. Dietary fluoride neither inhibited nor enhanced GLO activity nor did it increase or decrease AsA concentration in plasma, liver, kidney, adrenal gland and muscle (pectoralis major). Tissue AsA concentration in ascending order was adrenal > liver > kidney > pectoralis major > plasma. The results are consistent with that reported for the rat and calculations based on the results eliminate fluorine contamination for the inconsistent responses of immature chickens to dietary AsA.

Effects of exposing broiler breeders to nicarbazin contaminated feed.

Ten-mo-old broiler feeds were fed nicarbazin (NCZ) at 0, 25, 50 and 100 ppm of their diet for 2, 4, or 6 days to simulate accidental contamination of their feed with the medicant. Reduced egg production was observed in all treatments except 25 and 50 ppm NCZ for 2 days. A consistent reduction in egg weight occurred only at the maximum treatment level of 100 ppm for 6 days. Reduction in hatchability was generally evident by Days 5 and 6 of the experiment except for the lowest treatment of 25 ppm NCZ for 2 days. Due partially to the low number of eggs set, no statistically significant reduction in hatchability was seen for the group receiving 50 ppm NCZ for 4 days, but hatchability had dropped over 17 percentage points (from 93.3 to 75.5%) by Days 5 and 6 of the experiment, and continued to drop to a low of 31% on Days 11 and 12 of the experiment. Shell pigmentation was the most sensitive characteristic measured, with significant depigmentation occurring after only 2 days of feeding 25 ppm NCZ. Generally, the severity and duration of effects were in proportion to medicant concentration and length of treatment time. Fertility was not influenced by the medicant.

Production and egg-quality responses of White Leghorn layers to anticoccidial agents.

Two studies were conducted to determine the effects of anticoccidial agents on the production and reproduction of White Leghorns. In Experiment 1, nicarbazin (NCZ) was fed at 0, 20, 50, and 100 ppm. Hen-day egg production, egg weight, the egg-yolk DNC (4-4'-dinitrocarbanilide) level, and egg-yolk mottling were affected by the treatments. When response was evidenced, the relationship between those variables and the level of NCZ was basically linear. Decreased egg production occurred from Days 5 and 6 of the treatment through Days 1 and 2 of withdrawal. On Days 9 and 10 of treatment, the control hens peaked at 92% hen-day production, while hens fed 20, 50, and 100 ppm of NCZ peaked late--at 90, 82, and 80%, respectively. Compared to the controls, egg weight was reduced linearly as the level of dietary NCZ increased. The egg-yolk DNC level increased from Days 3 and 4 of treatment through Days 9 and 10 of withdrawal. Egg yolk mottling generally increased along with the level and duration of feeding NCZ. If the NCZ was mistakenly fed to White Leghorn layers, ill effects would be alleviated within 10 days after drug withdrawal. In Experiment 2, halofuginone (3 ppm), maduramicin (5 ppm), monensin (100 ppm), narasin (70 ppm), nicarbazin (125 ppm), robenidine (33 ppm), and salinomycin (60 ppm) were fed to White Leghorn hens at the levels specified in parentheses. Nicarbazin reduced egg production, depressed egg weight, reduced shell thickness, and caused egg-yolk mottling; but internal egg quality, as measured by Haugh Units, was unaffected. Halofuginone, maduramicin, monensin, narasin, robenidine, and salinomycin did not have a meaningful effect on the variables measured when fed to White Leghorn layers.

Reproduction responses of broiler-breeders to anticoccidial agents.

Two experiments were conducted to determine the effects of anticoccidial agents on production and reproduction of broiler breeders. In Experiment 1, nicarbazin (NCZ) was fed at 20, 50, and 100 ppm. There was no depression in egg production, egg weight, or fertility from feeding these levels. As level of NCZ increased, there was a linear decrease in hatchability. The amount of 4,4'-dinitrocarbanilide (DNC) in the egg yolks increased linearly as the levels of NCZ went up; the degree of egg-shell depigmentation was directly related to the level of NCZ fed starting at 50 ppm. Experiment 2 utilized a different strain of broiler breeders. Halofuginone (3 ppm), maduramicin (5 ppm), monensin (100 ppm), narasin (70 ppm), NCZ (125 ppm), robenidine (33 ppm), and salinomycin (60 ppm) were fed to broiler breeders at the levels listed. Only NCZ reduced egg production. Narasin induced a reduction in egg weight. Both narasin and salinomycin caused a significant drop in hatchability. Feeding NCZ also induced a rapid and more severe decrease in hatchability. Monensin was the only anticoccidial agent that reduced fertility. Halofuginone, maduramicin, and robenidine had no biologically significant effect on henday production, egg weight, hatch of fertile eggs, or shell depigmentation. Feeding NCZ at 125 ppm caused a complete bleaching of brown-shell eggs by the 3rd consecutive day of treatment; but 7 days after NCZ was withdrawn from the feed, pigmentation returned to the pretreatment level.