Studies have been conducted in our laboratory to assess differences in mitochondrial function and biochemistry in male broilers with high and low feed efficiency (FE) from the same genetic line and fed the same diet. Mitochondria obtained from broilers with low FE exhibited greater uncoupling of the electron transport chain (ETC) that was apparently due to site-specific defects in electron transport resulting in higher amounts of reactive oxygen species (ROS) compared with high FE mitochondria. Higher amounts of ROS production in Low FE mitochondria were likely responsible for higher protein carbonyl levels, indicative of higher protein oxidation compared with High FE mitochondria and tissue. In turn, higher protein damage in Low FE mitochondria may have contributed to lower activity of electron transport chain complexes relative to values observed in high FE mitochondria. Low FE mitochondria did not exhibit a compromised ability to carryout oxidative phosphorylation, and although there were differences in expression of certain electron transport chain proteins, there was nothing that would indicate that differences in coupling and respiratory chain activity could be due to a general decrease in protein expression between low and high FE mitochondria. The results of these studies provide insight into understanding cellular mechanisms associated with the phenotypic expression of feed efficiency in broilers.

Experiments were designed to determine the effects of aflatoxicosis on avian renal function, calcium (CA), inorganic phosphorous (Pi), and vitamin D metabolism, and to determine if the effects of aflatoxin are reversible upon discontinuation of toxin administration. Three-week-old male broiler chickens (n = 12 per treatment) received aflatoxin (AF; 2 mg/kg po) or an equal volume of corn oil, the AF carrier vehicle, for 10 consecutive days. After 10 d of treatment, half of the birds from each treatment group were anesthetized and prepared for renal function analysis, which included a 2-h phosphate loading period. Ten days after discontinuation of AF treatment, the remaining birds in each treatment group were anesthetized and prepared for renal function analysis. AF decreased plasma 25-hydroxy vitamin D [25(OH)D] and 1,25-dihydroxy vitamin D [1,25(OH)2D] levels after 5 d of treatment. After 10 d of treatment, urine flow rate (V), fractional sodium excretion (FENa), and fractional potassium excretion (FEK) were lower in AF-treated birds. In addition, total plasma Ca tended to be lower (p = .10) and fractional Ca excretion (FECa) tended to be higher (p = .10) in the AF-treated birds. Intravenous phosphate loading produced a sharp increase in urine hydrogen ion concentration ([H+]) in the AF-treated birds. Glomerular filtration rate (GFR) was reduced and plasma osmolality was increased in AF-treated birds 10 d after discontinuation of toxin administration. The results indicate that AF directly or indirectly affects Ca and Pi metabolism in avians. At the present time, the effects may be related to altered vitamin D and parathyroid hormone (PTH) metabolism. Aflatoxicosis may decrease endogenous PTH synthesis and the renal sensitivity to PTH. The AF-related increase in urine [H+] during phosphate loading is probably due to increased Na+/H+ counterport, suggesting that AF stimulates sodium reabsorption. Also, the decrease in GFR exhibited 10 d after toxin removal indicates that AF may cause prolonged alteration in renal function.

Vitamin E (VE) is known for its antioxidant properties and has been shown to modulate immune system functions in various species. This study examined the influence of different levels of dietary VE (alpha-tocopherol acetate) on phagocytic functions of macrophages (abdominal exudate cells) in broiler chickens at 3, 5, and 7 wk. Birds were fed commercial diets containing 16 (control), 110, or 220 mg of VE/kg of feed. Macrophages were elicited into the abdominal cavity by injecting a 3% Sephadex solution prepared in PBS (G50-50, 1 mL/100 g of BW) 42 h prior to harvest. The percentage of phagocytically active macrophages and the number of SRBC phagocytosed per macrophage for unopsonized and antibody-opsonized SRBC were determined. These aspects of macrophage function were assessed based on 900 macrophages per sample. When unopsonized SRBC were used, dietary VE supplementation above control level did not affect phagocytic function of macrophages at wk 3, 5, or 7. With antibody-opsonized SRBC, the percentage of phagocytically active macrophages and the number of SRBC phagocytosed per macrophage were higher (P = 0.08 and P = 0.01, respectively) in 3-wk-old birds fed 110 and 220 mg of VE/kg of feed compared with age-matched controls. This enhancing effect of VE supplementation on macrophage function was not observed in 5- and 7-wk-old broilers. It appears from this study that supplemental VE enhances Fc-receptor-mediated macrophage phagocytic activity at early stages of broiler growth.

To gain insight into the immunomodulatory effects of vitamin E (VE), immune cell population analyses were conducted using thymus and spleen from male broilers fed diets with various levels of VE supplementation (0, 17, 46, and 87 mg dl-alpha-tocopherol acetate/kg of feed). At 2 and 7 wk of age, the percentages of B cells, macrophages, and T cell subsets, delineated by the expression of CD4, CD8, and T cell receptor (TCR) isotype, in thymus and spleen were determined by flow cytometry. The percentages of thymic and splenic B cells and macrophages from 2- and 7-wk-old chickens, as well as the percentage of thymic T cells in 2-wk-old chickens, were unaffected by VE treatment. However, 7-wk-old broilers maintained on 87 mg VE/kg feed had a higher percentage of CD4+CD8- thymocytes, a higher CD4+CD8- to CD4-CD8+ thymocyte ratio, and a lower percentage of CD4+CD8+ thymocytes than chickens receiving no dietary VE supplementation. The VE-induced increase in the percentage of CD4+CD8- thymocytes was due to an increase in the TCR2+CD4+CD8- thymocyte subset, whereas the decrease in the percentage of CD4+CD8+ thymocytes involved all TCR defined T cell subsets. In the spleen, the percentage of CD4+CD8- T cells was lower in 2-wk-old chickens and higher in 7-wk-old chickens maintained on 87 mg/kg feed than in chickens receiving no dietary VE supplementation. The decrease in CD4+CD8- splenocytes at 2 wk of age was due to a decline in the percentage of TCR2+CD4+CD8- splenocytes, whereas the increase in CD4+CD8- splenocytes in 7-wk-old chicks was due to an increase in the percentages of all TCR defined CD4+CD8- T cell subsets. These data support an immunomodulatory effect of VE on CD4+CD8- T cells.

Fractional rates of liver, muscle, plasma and acute phase portein synthesis were measured in chickens injected with saline or E. coli lipopolysaccharide (LPS). Male Single Comb White Leghorns were infused with a primed constant infusion of 15N-L-methionine and 2H5-L-phenylalanine into the portal vein for 2 h. Changes in plasma amino acid enrichment were similar for both amino acids reaching an apparent plateau by the 30 min sampling time. The enrichment of plasma protein-bound amino acid was measurable after 1 h of isotope infusion and increased linearly over 2h. LPS injection decreased free phenylalanine enrichment in the carotid artery (50%), and reduced tissue free methionine enrichment in the liver, pectoralis, and gastrocnemius by 16, 41, and 31% respectively. Isotopic enrichment of phenylalanine in liver protein, plasma protein and hemopexin increased in LPS injected birds relative to control birds. Fractional rates of muscle protein synthesis were not affected by LPS injection, however, liver protein, plasma protein, and hemopexin fractional synthesis rates increased 141, 161 and 266% respectively compared with untreated animals.