Hemolysis, tocopherol, and lipid oxidation in erythrocytes and muscle tissue in chickens, ducks, and turkeys.

Muscle from turkeys is more sensitive to lipid oxidation during post mortem storage compared with that of chicken and duck which may involve increased lysis of turkey erythrocytes that releases hemoglobin oxidant. Three separate experiments were conducted to study characteristics of chicken, duck, and turkey erythrocytes in which dietary tocopherols were standardized. In Experiment I, tocopherol, fatty acid composition, and lipid oxidation capacity were measured in erythrocytes from chickens, ducks, and turkeys. Tocopherol content was greater in chicken erythrocytes compared with that of duck and turkey (P < 0.05). Oleic and linoleic acid content was higher in chicken erythrocytes compared with that of turkey (P < 0.05). Lipid oxidation capacity of erythrocytes in washed turkey muscle (WTM) at pH 5.8 ranked chicken > duck > turkey (P < 0.05). In Experiment II, hemolysis was measured in erythrocytes from turkeys and chickens. Detergent-induced hemolysis (pH 7.4) was on average 12-fold greater for turkey erythrocytes compared with that of chicken (P < 0.05). In Experiment III, the ability of lysed and non-lysed erythrocytes to promote lipid oxidation was examined. Lysed erythrocytes promoted lipid oxidation in WTM more effectively than intact erythrocytes (P < 0.05). Reasons that turkey erythrocytes were more labile to detergent-induced hemolysis whereas chicken erythrocytes more effectively promoted lipid oxidation in the WTM model system are discussed. These studies describe variation in chemical and physical properties of erythrocytes from chickens, ducks, and turkeys that can influence progression of lipid oxidation in poultry muscle.

Effect of whole yeast cell product supplementation (CitriStim®) on immune responses and cecal microflora species in pullet and layer chickens during an experimental coccidial challenge.

Three separate experiments were conducted to study the effects of whole yeast cell product supplementation in pullets and layer hens. Body weight gain, fecal and intestinal coccidial oocyst counts, cecal microflora species, cytokine mRNA amounts, and CD4+ and CD8+ T-cell populations in the cecal tonsils were analyzed following an experimental coccidial infection. In Experiment I, day-old Leghorn layer chicks were fed 3 experimental diets with 0, 0.1, or 0.2% whole yeast cell product (CitriStim®, ADM, Decatur, IL). At 21 d of age, birds were challenged with 1 × 105 live coccidial oocysts. Supplementation with whole yeast cell product decreased the fecal coccidial oocyst count at 7 (P = 0.05) and 8 (P < 0.01) d post-challenge. In Experiment II, 27-week old Leghorn layer hens were fed 3 experimental diets with 0, 0.05 or 0.1% whole yeast cell product and challenged with 1 × 105 live coccidial oocysts on d 25 of whole yeast cell product feeding. Supplementation with whole yeast cell product decreased the coccidial oocyst count in the intestinal content (P < 0.01) at 5, 13, and 38 d post-coccidial challenge. Supplementation with whole yeast cell product increased relative proportion of Lactobacillus (P < 0.01) in the cecal tonsils 13 d post-coccidial challenge. Supplementation with whole yeast cell product decreased CD8+ T cell percentages (P < 0.05) in the cecal tonsils at 5 d post-coccidial challenge. In Experiment III, 32-week-old Leghorn layer hens were fed 3 experimental diets with 0, 0.1, or 0.2% whole yeast cell product and challenged with 1 × 105 live coccidial oocysts on d 66 of whole yeast cell product feeding. At 5 d post-coccidial challenge, whole yeast cell product supplementation down-regulated (P = 0.01) IL-10 mRNA amount. It could be concluded that supplementing whole yeast cell product can help minimize coccidial infection in both growing pullets and layer chickens.

Role of Cytochrome P450 Hydroxylase in the Decreased Accumulation of Vitamin E in Muscle from Turkeys Compared to that from Chickens.

Turkeys and chickens reared to 5 weeks of age and fed diets with feedstuffs low in endogenous tocopherols were examined. Treatments included feed supplemented with RRR (natural source vitamin E) alpha tocopheryl acetate (AcT, 35 mg/kg feed) and all-racemic (synthetic vitamin E) AcT (10 and 58 mg/kg feed). Alpha tocopherol hydroxylase activity was greater in liver microsomes prepared from turkeys compared to that from chickens (p < 0.01). Alpha and gamma tocopherol metabolites were higher in turkey bile than in chicken when assessing the RRR AcT diet and the all-racemic AcT diet at 58 mg/kg feed (p < 0.01). Turkey cytochrome P450 2C29 was increased relative to its chicken ortholog on the basis of RNA-Seq transcript abundance (p < 0.001) and activity-based protein profiling (p < 0.01) of liver tissue. Alpha tocopherol concentrations in plasma, liver, and muscle from turkey were lower than the respective tissues from chicken (p < 0.05). Lipid oxidation was greater in turkey thigh than in chicken (p < 0.05). These results suggest that elevated tocopherol metabolism by cytochrome P450 hydroxylase(s) in turkeys contributes to the decreased accumulation of alpha tocopherol in turkey tissues compared to that of chickens.

Effect of yeast cell product (CitriStim) supplementation on turkey performance and intestinal immune cell parameters during an experimental lipopolysaccharide injection.

An experiment was conducted to identify the effect of whole yeast cell product supplementation in turkeys following an experimental inflammatory challenge. A total of 105 one-day-old turkey tom poults were fed basal diets supplemented with 0, 0.1, and 0.2% whole yeast cell product (CitriStim, ADM, Quincy, IL). At 6 wk of age and 16 wk of age, turkeys were injected with lipopolysaccharide (LPS) at 0 or 0.25 mg/kg of BW in a 3 × 2 factorial arrangement. BW gain (P = 0.31) and feed conversion ratio (P = 0.53; 3.13, 2.94, and 2.98 for the 0, 0.10, and 0.20% CitriStim treatments, respectively) at 15 wk of age were not significantly affected by the treatment diets. Yeast cell wall product supplementation had no effect on growth in control-injected turkeys but decreased growth in LPS-injected turkeys (yeast × LPS, P < 0.05). Splenic macrophages from birds fed whole yeast cell product and injected with LPS produced higher (P < 0.01) nitric oxide than the control group injected with LPS at both 6 and 16 wk of age. At 6 and 16 wk of age, birds injected with LPS (P < 0.01; P < 0.01) and supplemented with whole yeast cell product (P = 0.05; P = 0.10) showed increased IL-1 mRNA amounts in cecal tonsils. In birds not injected with LPS, whole yeast cell supplementation increased regulatory T cell percentage and IL-10 mRNA amounts, whereas in birds injected with LPS, whole yeast cell supplementation decreased IL-10 mRNA amounts at both 6 (P < 0.01) and 16 wk (P = 0.01) of age in cecal tonsils. Whole yeast cell product supplementation increased Lactobacillus (P < 0.01 and P = 0.01) and Bifidobacteria (P < 0.01 and P = 0.01) population at 6 and 16 wk of age. In conclusion, the effect of feeding whole yeast cell product on turkeys was dependent on the inflammatory status of the bird.

Effect of yeast cell product supplementation on broiler cecal microflora species and immune responses during an experimental coccidial infection.

This experiment was conducted to study the effects of whole yeast (Pichia guilliermondii; CitriStim, ADM, Quincy, IL) cell product supplementation on cecal microflora population and intestinal immune parameters in broilers. In the first experiment, birds were fed 0, 0.1, or 0.2% yeast cell wall product for 42 d. Feeding yeast cell wall products decreased (P = 0.03) the proportion of Escherichia coli in the ceca by 31% compared with the control group. The group fed 0.2% yeast cell wall product had a 20% decrease (P = 0.23) in Salmonella population compared with the control group. In the second experiment, birds were fed yeast cell wall product for 21 d and challenged or not challenged with coccidial oocysts, thus resulting in a 2 (0 and 0.2% whole yeast product) × 2 (coccidial challenge and no coccidial challenge) factorial model. Supplementing whole yeast cell wall product prevented a coccidial infection-induced decrease in the Lactobacillus population (P = 0.09) at 12 d postchallenge. Supplementing yeast cell wall product prevented a coccidial infection-induced increase in the Salmonella population (P = 0.08) and E. coli (P = 0.12) at 12 d postchallenge. At 5 d (P < 0.01) and 12 d (P < 0.01) postcoccidial infection, yeast cell wall product supplementation or coccidial infection increased the regulatory T cell (Treg) percentage in the cecal tonsils, whereas yeast cell wall product supplementation in the coccidial-infected group decreased the increase in Treg percentage. At 5 d postcoccidial infection, coccidial infection increased (P = 0.01) the relative amounts of cecal interferon (IFN)γ mRNA. In addition, the yeast cell wall product supplementation in the coccidial-infected groups further increased (P = 0.15) the IFNγ mRNA. It could be concluded that yeast cell wall product supplementation decreased coccidial-infection-induced increase in E. coli and Salmonella colonization and improved IFNγ mRNA amounts after coccidial infection.

Effect of yeast cell product (CitriStim) supplementation on broiler performance and intestinal immune cell parameters during an experimental coccidial infection.

This experiment studied the effects of whole yeast cell product supplementation on broiler production parameters, fecal coccidial oocyst counts, and local and systemic immune parameters following an experimental coccidial infection. Birds were fed 0, 0.1, or 0.2% whole yeast cell product (CitriStim). At 21 d of age, birds were challenged with live coccidial oocysts. Supplementation with whole yeast cell product increased BW gain between 0 and 12 d (P = 0.01) postcoccidial challenge. Birds supplemented with 0.2% Citristim had better (P = 0.01) feed efficiency between 0 and 12 d postcoccidial infection. Supplementation with whole yeast cell product decreased (P = 0.01) the fecal coccidial oocyst count at 7 d postcoccidial challenge. Citristim supplementation at 0.2% increased (P < 0.01) macrophage nitric oxide production by 93 and 193% at 5 and 12 d postcoccidial challenge. Supplementation with whole yeast cell product at 0.2% increased cecal tonsil interleukin-1 mRNA amounts approximately 4.5- and 3.7-fold at 5 and 12 d postcoccidial challenge, respectively, over the group with no whole yeast cell product supplementation. Citristim supplementation downregulated cecal tonsil interleukin-10 mRNA amounts compared with the unsupplemented groups at both 5 (P = 0.01) and 12 d (P < 0.01) postcoccidial challenge. Supplementation with whole yeast cell product did not alter (P > 0.05) serum anticoccidial IgG contents or cecal tonsil CD4(+) and CD8(+) cell percentages at 5 and 12 d postcoccidial infection. It could be concluded that supplementing whole yeast cell product (CitriStim) to broiler diets can improve production parameters, decrease fecal oocyst count, and increase inflammatory cytokine production postcoccidial infection.