Effect of Dietary Vanadium on the Ileac T Cells and Contents of Cytokines in Broilers

The purpose of this 42-day study was to examine the effect of dietary vanadium on the ileac T cells and contents of cytokines including interleukin-2 (IL-2), interleukin-6 (IL-6), and interferon-gamma (IFN-γ) in broilers by flow cytometry and enzyme-linked immunosorbent assay. A total of 420 one-day-old avian broilers were divided into six groups (seven replicates in each group and ten broilers in each replicate) and fed on control diet or the same diet supplemented with 5, 15, 30, 45, and 60 mg/kg vanadium in the form of ammonium metavanadate. The results showed that the percentages of CD3(+), CD3(+)CD4(+), and CD3(+)CD8(+) T cells in both ileac lamina propria lymphocytes (LPLs) and intraepithelial lymphocytes (IELs) were significantly lower (P < 0.05 or P < 0.01) in the 45- and 60-mg/kg groups than in the control group from 14 to 42 days of age. The CD4(+)/CD8(+) ratio was increased in ileac LPLs in the 60-mg/kg group at 28 days of age, and in ileac IELs in the 60-mg/kg group at 28 days of age and in the 45-mg/kg group at 42 days of age. Meanwhile, the ileac IL-2, IL-6 contents were decreased (P < 0.05 or P < 0.01) in the 60-mg/kg group from 14 to 42 days of age and in the 45-mg/kg group from 28 to 42 days of age in comparison with those of the control group. It was concluded that dietary vanadium in excess of 30 mg/kg reduced the ileac T cell population and percentages of T cell subsets, and IL-2, IL-6, and IFN-γ contents, implying that the immune function of local intestinal mucosa in broilers could be affected by the dietary vanadium.     

Changes of Relative Weight and Cell Cycle,and Lesions of Bursa of Fabricius Induced by Dietary Excess Vanadium in Broilers

The purpose of this 42-day study was to investigate the effects of dietary excess vanadium on immune function by determining the morphological changes and cell cycle of bursa of Fabricius, and the serum Ig contents. A total of 420 one-day-old avian broilers were divided into six groups and fed on a corn–soybean basal diet as control diet, or the same diet amended to contain 5, 15, 30, 45, and 60 ppm vanadium supplied as ammonium metavanadate. When compared with that of control group, the relative weight of bursa was significantly increased in the 15 ppm group from 14 to 35 days of age and increased in the 5 ppm group at 42 days of age, and significantly decreased in the 60 ppm group from 14 to 42 days of age and decreased in 30 and 45 ppm groups from 35 to 42 days of age. Pathological lesions progressed as the dietary vanadium increased. The gross lesions of bursa showed obvious atrophy with decreased volume and pale color in 45 and 60 ppm groups. Histopathologically, widened cortex and increased number of lymphocytes appeared in 5 and 15 ppm groups, and reduced lymphocytes and connective tissue hyperplasia appeared in 45 and 60 ppm groups. The bursal cells in static phase (G₀/G₁) were decreased, and those in the mitotic phase (G₂ + M) and the proliferating index (PI) were increased in 5 and 15 ppm groups. However, bursal cells in the G₀/G₁ phase were increased, and those in G₂ + M phase, synthesis phase (S) and the PI were decreased in 45 and 60 ppm groups. Also, the serum IgG and IgA contents were increased in 5 and 15 ppm groups, and the serum IgG, IgA, and IgM contents were decreased in 45 and 60 ppm groups. These results suggested that dietary excess vanadium (45 and 60 ppm) could inhibit growth of bursa of Fabricius and impair humoral immunity in chicken.     

The Cell Cycle Arrest and Apoptosis of Bursa of Fabricius Induced by Low Selenium in Chickens

The purpose of this 42-day study was to investigate the effects of low selenium (Se) on immune function by determining cell cycle and apoptosis of bursa of Fabricius. One hundred twenty 1-day-old avian broilers were randomly assigned to two groups of 60 each and were fed on a low Se diet (0.0342 mg/kg Se) or a control diet (0.2 mg/kg Se), respectively. The relative weight of bursa was significantly decreased in low Se group from 28 days of age in time-dependent manner when compared with that of control group. Cell cycle analysis by flow cytometry showed that low Se caused an increase in G₀G₁ phase cells that corresponded to a decrease in S phase cells in bursa of Fabricius. Ultrastructurally, mitochondria injury and increased apoptotic cells with condensed nuclei were observed. Low Se increased the percentage of Annexin V-positive cells, as measured by flow cytometry, in comparison with that of control group. These data suggested that low Se diet restrained the development of bursa of Fabricius by cell cycle arrest and apoptosis.     

Dietary High Vanadium Causes Oxidative Damage-Induced Renal and Hepatic Toxicity in Broilers

The purpose of this study was to investigate the renal and hepatic oxidative damage and toxicity caused by dietary high vanadium in broilers. A total of 420 one-day-old avian broilers were divided into six groups and fed on a corn–soybean basal diet as control diet (vanadium 0.073 mg/kg), and five high vanadium diets (vanadium 5 mg/kg, high vanadium group I; 15 mg/kg, high vanadium group II; 30 mg/kg, high vanadium group III; 45 mg/kg, high vanadium group IV; and 60 mg/kg, high vanadium group V) throughout the experimental period of 42 days. The results showed that the renal and hepatic superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, ability to inhibit hydroxy radical, and malondialdehyde (MDA), glutathione, and vanadium contents were not significantly changed in high vanadium group I and II when compared with those of the control groups. However, the SOD and GSH-Px activities, ability to inhibit hydroxy radical, and GSH content were significantly decreased, and the MDA and vanadium contents were markedly increased in high vanadium groups III, IV, and V. At the same time, the lesions were also observed in the kidney and liver of high vanadium groups III, IV, and V. The renal tubular epithelial cells showed granular degeneration and vacuolar degeneration, and hepatocytes showed granular degeneration, vacuolar degeneration, and fatty degeneration. It was concluded that dietary vanadium in the range of 30–60 mg/kg could cause oxidative damage and vanadium accumulation, which induced renal and hepatic toxicity and lesions. The renal and hepatic function was finally impaired in boilers.     

Effect of Dietary Vanadium on Intestinal Microbiota in Broiler

The purpose of this 42-day study was to examine the effect of dietary vanadium on intestinal microorganism diversity in the duodenum, ileum, cecum, and rectum segments of broilers by the plate count and polymerase chain reaction?Cdenaturing gradient gel electrophoresis (DGGE). A total of 420 1-day-old avian broilers were divided into six groups and fed on a control diet or the same diet supplemented with vanadium at the doses of 5, 15, 30, 45, and 60?mg/kg in the form of ammonium metavanadate. In comparison with control group, the dietary vanadium at the doses of 45 and 60?mg/kg could decrease the counts of Bifidobacterium spp. in the intestinal tract at 21 and 42?days of age. With increasing level in dietary vanadium, the counts of Escherichia coli were significantly increased in the ileum, cecum, and rectum and were decreased in the duodenum at 21 and 42?days of age. However, the counts of Lactobacilli were decreased in the cecum and rectum and increased in the ileum of 45 and 60?mg/kg groups. The colonization of these three bacteria could be affected by dietary vanadium. DGGE analysis showed that the number of bands in duodenum, ileum, cecum, and rectum were obviously decreased in the 30, 45, and 60?mg/kg groups at 21 and 42?days of age. In conclusion, the dietary vanadium in excess of 30?mg/kg could alter the amount and diversity of intestinal bacteria in broilers, implying that the structure and initial balance in the intestinal microbiota were disrupted.     

The Effect of Dietary Vanadium on Cell Cycle and Apoptosis of Liver in Broilers

The objective of this study was to clarify the effects of dietary vanadium on cell cycle and apoptosis of liver in broilers. Four hundred and twenty one-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet as control diet or the same diet amended to contain 5, 15, 30, 45, and 60?mg/kg vanadium supplied as ammonium metavanadate for 42?days. As tested by flow cytometry, hepatocytes in G (0)/G (1) phase were significantly increased in number in 45 and 60?mg/kg groups, and hepatocytes in S, G (2)?+?M phases in 45 and 60?mg/kg groups and the proliferation index of hepatocytes in 30, 45, and 60?mg/kg were markedly decreased when compared with those of control group. At the same time, the percentage of hepatocyte apoptosis was markedly increased in both 45 and 60?mg/kg groups. The results showed that dietary vanadium in the range of 45?～?60?mg/kg caused cell cycle arrest and apoptosis of hepatocytes in broilers.     

Dietary Vanadium Induces Oxidative Stress in the Intestine of Broilers

The purpose of this study was to examine oxidative stress induced by dietary vanadium in the mucosa of different parts of intestine including duodenum, jejunum, ileum, and cecal tonsil. A total of 420 1-day-old avian broilers were divided into six groups and fed on a corn–soybean basal diet as control diet or the same basal diet supplemented with 5, 15, 30, 45, and 60 mg/kg vanadium as ammonium metavanadate. During the experimental period of 42 days, oxidative stress parameters were determined for both control and experimental groups. The results showed that malondialdehyde content was significantly higher (p < 0.05 or p < 0.01) in 30, 45, and 60 mg/kg groups than in control group. In contrast, the activities of superoxide dismutase, catalase, and glutathione peroxidase, and ability to inhibit hydroxyl radical, and glutathione hormone content were significantly decreased (p < 0.05 or p < 0.01) mainly in 45 and 60 mg/kg groups in comparison with those of control group. However, the abovementioned oxidative stress parameters were not significantly changed (p > 0.05) in 5 and 15 mg/kg groups. It was concluded that dietary vanadium in excess of 30 mg/kg could cause obvious oxidative stress in the intestinal mucosa, which could impact the antioxidant function of intestinal tract in broilers.     

Effect of High Dietary Manganese on the Immune Responses of Broilers Following Oral Salmonella typhimurium Inoculation

Manganese (Mn) is an essential nutrient for both host and pathogen. Recent studies have demonstrated the nutritional immunity of Mn against Salmonella infection in mammals. To investigate the effect of high dietary Mn on immune responses of broilers following Salmonella challenge, 144 1-day-old male broilers were fed a basal diet (containing 20.04 mg Mn/kg) plus an additional 40 (the control group) or 400 mg Mn/kg (the H-Mn group) for 7 days. The 72 broilers in each group were then orally inoculated with 5 × 10⁷ CFUs of Salmonella typhimurium (ATCC#14028) or phosphate-buffered saline. Peripheral blood, spleens, cecal tonsils, and bursa of Fabricius were collected from Salmonella-inoculated and Salmonella-noninoculated broilers (n = 6) at 2 days post inoculation (2 DPI) and 7 days post inoculation (7 DPI). Peripheral blood lymphocyte subpopulations were determined by flow cytometry. The messenger RNA (mRNA) abundance of genes was determined by quantitative real-time polymerase chain reaction. Salmonella counts were higher (P < 0.05) in the H-Mn group than that in the control group at 2 DPI in the cecal contents of Salmonella-inoculated broilers. High dietary Mn increased CD3⁺CD4⁺ and CD3⁺CD8⁺ percentages in the peripheral blood of Salmonella-inoculated broilers at 2 DPI. Salmonella inoculation increased interleukin (IL)-6 mRNA expression in spleens and bursa of Fabricius at 2 DPI and increased IL-1β and IL-6 mRNA expression in cecal tonsils at 7 DPI in the H-Mn group. These changes were not observed in the control group. High dietary Mn increased interferon-γ (IFN-γ) in spleens and decreased IFN-γ and IL-12 mRNA expression in cecal tonsils of Salmonella-inoculated broilers at 2 DPI. High dietary Mn decreased IL-17 mRNA expression in the bursa of Fabricius at 7 DPI, but increased this expression in cecal tonsils at 2 and 7 DPI in Salmonella-inoculated broilers. These results suggested that dietary Mn level affected T helper (Th) 1-cytokine reaction in spleens and cecal tonsils, and Th17-mediated immunity in cecal tonsils and the bursa of Fabricius of broilers when challenged with Salmonella.

     

The Decrease of Relative Weight,Lesions, and Apoptosis of Bursa of Fabricius Induced by Excess Dietary Selenium in Chickens

Selenium is an essential trace element possessing immune-stimulatory properties. The purpose of this 42-day study was to investigate the effects of excess dietary sodium selenite on immune function by determining morphological changes and apoptosis of bursa of Fabricius. Three hundred 1-day-old Avian broilers were fed on a basic diet (0.2 ppm selenium) or the same diet amended to contain 1, 5, 10, and 15 ppm selenium supplied as sodium selenite (n = 60/group). Relative weight of bursa was significantly decreased in the 1, 5, 10, and 15 ppm groups at 28 days of age, when compared with that of 0.2 ppm group. Pathological lesions were progressed with the dietary Se level increased. The gross lesions of bursa involved obvious atrophy with decreased volume and pale color. Histopathologically, decreased number of lymphocytes and loosely packed lymphocytes appeared in the medulla and cortex in the follicles. Ultrastructurally, mitochondria injury and increased apoptotic cells with condensed nuclei were observed. In comparison to that of control group, excess Se (5, 10, and 15 ppm) intake increased the percentage of Annexin V positive cells, as measured by flow cytometry. Terminal deoxynucleotidyl transferase 2′-deoxyuridine 5′-triphosphate nick end-labeling assay showed that there were increased frequencies of apoptotic cells in 10 and 15 ppm selenium groups. These data suggest that Se supplementation with sodium selenite should be carefully evaluated as excess selenium (more than 5 ppm) intake could cause profound immunologic inhibition.     

Changes of IgA+ Cells and Cytokines in the Cecal Tonsil of Broilers Fed on Diets Supplemented with Vanadium

The cecal tonsil of broiler is known as a secondary lymphoid tissue, which is involved in antigen-specific humoral immune responses. The purpose of this study was to investigate the effects of dietary vanadium on the tissue distribution and quantity of immunoglobulin A-positive (IgA(+)) cell in the cecal tonsil by immunohistochemistry. Simultaneously, the changes in interleukin-6 (IL-6), interleukin-10 (IL-10), interferon gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) contents in the cecal tonsil were also quantified by enzyme-linked immunosorbent assay (ELISA). A total of 420 one-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet (control diet) or the same diet supplemented respectively with 5, 15, 30, 45, and 60 mg/kg of vanadium in the form of ammonium metavanadate for 42 days. The results showed that the population of the IgA(+) cells in the cecal tonsil were significantly lower (p < 0.05 or p < 0.01) in the 45 and 60 mg/kg groups than that in the control group. Meanwhile, IL-10, IFN-γ and TNF-α contents in the cecal tonsil were significantly decreased (p < 0.05 or p < 0.01) in the 30, 45 and 60 mg/kg groups in comparison with those of the control group. However, IL-6 content in the cecal tonsil was only decreased (p < 0.05 or p < 0.01) in 60 mg/kg at 14 and 28 days of age. In conclusion, dietary vanadium in excess of 30 mg/kg reduced the numbers of the IgA(+) cells and changed the contents of the abovementioned cytokines in the cecal tonsil, which may finally impact the function of local mucosal humoral immunity in broilers.     

Effect of Dietary Vanadium on Cecal Tonsil T Cell Subsets and IL-2 Contents in Broilers

The purpose of this 42-day study was to investigate the effects of dietary excess vanadium on intestinal immune function by histopathological observation of cecal tonsil and changes of the cecal tonsil T cell subsets by method of flow cytometry. Four hundred twenty 1-day-old avian broilers were divided into six groups and fed on a corn-soybean basal diet as control diet or the same diet amended to contain 5, 15, 30, 45, and 60 mg/kg vanadium supplied as ammonium metavanadate. In comparison with those of control group, lymphocytes in the lymphatic nodule of cecal tonsil were apparently decreased in 45 and 60 mg/kg groups. The percentage of CD(3)(+) T cells was decreased (p?相似文献   

Dietary Excess Vanadium Induces Lesions and Changes of Cell Cycle of Spleen in Broilers

The purpose of this 42-day study was to investigate the effects of dietary excess vanadium on spleen growth and lesions by determining morphological changes and cell cycle of spleen. Four hundred twenty 1-day-old avian broilers were divided into six groups and fed on a corn–soybean basal diet as control diet or the same diet amended to contain 5, 15, 30, 45, 60 ppm of vanadium supplied as ammonium metavanadate. When compared with that of control group, the relative weight of spleen was significantly raised in 5- and 15-ppm groups, but depressed in 45- and 60-ppm groups. The gross lesions of spleen showed obvious atrophy with decreased volume and pale color in 45- and 60-ppm groups. Histopathologically, lymphocytes in splenic corpuscle and periarterial lymphatic sheath were variously decreased in number in 30-, 45-, and 60-ppm groups. The percentage of static phase (G₀/G₁) was significantly decreased, and the percentage of synthesis period (S) phase and the proliferating index (PI) were significantly increased in 5- and 15-ppm groups. The percentage of G₀/G₁ phase was significantly increased, and the percentage of mitotic phase (G₂ + M), S phase, and PI significantly decreased in 45- and 60-ppm groups. These results suggested that dietary excess vanadium (45 and 60 ppm) could inhibit growth of spleen and induce lesions in spleen in chicken.     

Excess Dietary Vanadium Induces the Changes of Subsets and Proliferation of Splenic T Cells in Broilers

The purpose of this 42-day study was to investigate the effects of dietary excess vanadium on immune function by determining changes of the subsets and proliferation function of splenic T cells. Four hundred twenty 1-day-old avian broilers were divided into six groups and fed on a corn–soybean basal diet as control diet or the same diet amended to contain 5, 15, 30, 45, and 60 ppm of vanadium supplied as ammonium metavanadate. When compared with those of the control group, the percentage of CD3⁺, CD3⁺CD4⁺, and CD3⁺CD8⁺ of splenic T cells were decreased in the 45 and 60 ppm groups; however, the percentage of CD3⁺ and CD3⁺CD4⁺ were increased in the 5 ppm group, and the CD₄⁺/CD₈⁺ ratios were raised in the 5 and 15 ppm groups at 14 days of age. Meanwhile, the proliferation of splenic T cells were depressed in the 45 and 60 ppm groups but raised in the 5 and 15 ppm groups. Also, the serum interleukin-2 (IL-2) and interleukin-6 (IL-6) contents were decreased in the 45 and 60 ppm groups and increased in the 5 ppm group. It was concluded that dietary vanadium in excess of 30 ppm changed the percentages of splenic T cell subsets and inhibited the proliferation of splenic T cells and reduced the serum IL-2 and IL-6 contents. The cellular immune function was finally impaired in broilers.     

Excess Dietary Sodium Selenite Alters Apoptotic Population and Oxidative Stress Markers of Spleens in Broilers

Three hundred 1-day-old avian broilers were fed on a basic diet (0.2 mg/kg selenium) or the same diet amended to contain 1, 5, 10, and 15 mg/kg selenium supplied as sodium selenite (n = 60/group). In comparison with those of 0.2 mg/kg selenium group, the percentages of annexin V-positive splenocytes were increased in 5, 10, and 15 mg/kg selenium groups. TUNEL assay revealed that apoptotic cells with brown-stained nuclei distributed within the red pulp and white pulp of the spleens with increased frequency of occurrence in 10 and 15 mg/kg selenium groups in comparison with that of 0.2 mg/kg Se group. Sodium selenite-induced oxidative stress in spleens of chickens was evidenced by decrease in glutathione peroxidase, superoxide dismutase, and catalase activities and increase in malondialdehyde contents. The results indicate that excess dietary selenium in the range of 5–15 mg/kg of feed causes oxidative stress, which may be mainly responsible for the increased apoptosis of splenocytes in chickens.     

Influence of Dietary Copper Methionine Concentrations on Growth Performance,Digestibility of Nutrients,Serum Lipid Profiles,and Immune Defenses in Broilers

A 42-day experiment was conducted to evaluate the influence of dietary copper (Cu) concentrations on growth performance, nutrient digestibility, and serum parameters in broilers aged from 1 to 42 days. Five hundred forty 1-day-old broilers were randomly assigned into 1 of the following 6 dietary treatments: (1) control (basal diet without supplemental Cu), (2) 15 mg/kg supplemental Cu (Cu15), (3) 30 mg/kg supplemental Cu (Cu30), (4) 60 mg/kg supplemental Cu (Cu60), (5) 120 mg/kg supplemental Cu (Cu120), and (6) 240 mg/kg supplemental Cu (Cu240), Cu as copper methionine. A 4-day metabolism trial was conducted during the last week of the experiment feeding. The results showed that dietary Cu supplementation increased the average daily gain and the average daily feed intake (P < 0.01). The feed gain ratio, however, was not affected by dietary Cu (P > 0.10). Additionally, dietary Cu supplementation increased the digestibility of fat and energy (P < 0.05). The concentration of serum cholesterol, triglycerides, and high-density lipoprotein cholesterol decreased with dietary Cu supplementation (P < 0.05). The activities of serum Cu-Zn superoxide dismutase (P < 0.05), glutathione peroxidase (P < 0.05), and ceruloplasmin (P = 0.09), on the contrary, were increased by Cu addition. For immune indexes, dietary Cu supplementation increased serum IgA and IgM (P < 0.05). In addition, the activities of serum ALT increased with increasing dietary Cu supplementation (P < 0.05). In conclusion, our data suggest that Cu supplementation can increase fat digestibility and promote growth. Additionally, dietary Cu supplementation can reduce serum cholesterol and enhance antioxidant capacity in broilers.

     

Effect of Dietary High Molybdenum on Peripheral Blood T-Cell Subsets and Serum IL-2 Contents in Broilers

The objectives of this study were to investigate the effects of dietary high molybdenum (Mo) on immune function by determining changes of the subsets of peripheral blood T-cells and serum interleukin (IL)-2 contents. 300 1-day-old avian broilers were divided into four groups and fed on a corn–soybean basal diet as control diet or the same diet amended to contain 500; 1,000; and 1,500 mg/kg of Mo supplied as sodium molybdate dihydrate. In comparison with those of the control group, the percentages of CD3⁺, CD3⁺CD4⁺ and CD3⁺CD8⁺ were decreased in 1,000 and 1,500 mg/kg of Mo intake groups from 14 days of age to 42 days of age. Also, the serum IL-2 contents were decreased in 1,000 and 1,500 mg/kg of Mo intake groups from 14 days of age to 42 days of age. Histopathologically, hypocellularity appeared in the thymus in 1,000 and 1,500 mg/kg of Mo intake groups. It was concluded that dietary high-Mo (1,000 mg/kg and 1,500 mg/kg) reduced the percentages of peripheral blood T-cell subsets and serum IL-2 contents and caused thymic lesions. The cellular immune function was finally injured in broilers.     

Increased Apoptotic Lymphocyte Population in the Spleen of Young Chickens Fed on Diets High in Molybdenum

The experiment was conducted with the objective of examining the effects of high molybdenum (Mo) on the apoptosis of splenic lymphocytes in broilers by the methods of experimental pathology and flow cytometry (FCM). Three hundred 1-day-old avian broilers were divided into four groups of 75 each and were fed on control diet (Mo 13 mg/kg) and high Mo diets (Mo 500 mg/kg, high Mo group I; Mo 1,000 mg/kg, high Mo group II; and Mo 1,500 mg/kg, high Mo group III) for 42 days. The results showed that the relative weight of spleen was decreased, and lymphocytes were histopathologically decreased in high Mo groups II and III. Ultrastructurally, the apoptotic cells showed typical condensed nuclei with dark-round, petal-like, and horseshoe-like shapes. The mitochondria were swelled, and the endoplasmic reticulum and the Golgi apparatus were dilated in high Mo groups II and III. The statistical analyses by FCM indicated that the percentage of cellular apoptosis was higher in high Mo groups II and III than in control group. Also, the TUNEL staining was consistent with the results of FCM. It was concluded that dietary molybdenum in 1,000 and 1,500 mg/kg caused splenic lesions and lymphocyte apoptosis, which could inhibit the development of spleen and could impair immune function in broilers.     

Effects of Zinc Glycine Chelate on Oxidative Stress,Contents of Trace Elements,and Intestinal Morphology in Broilers

Three hundred and sixty healthy Ross × Ross 1-day-old broilers were used to study the effects of zinc glycine chelate (Zn-Gly) on oxidative stress, contents of trace elements, and intestinal morphology. All broilers were randomly assigned to six treatment groups, which replicates three times. Diets were as follows: (1) control (containing 29.3 mg zinc (Zn)/kg basic diet (0–21 days) and 27.8 mg Zn/kg (22–42 days)); (2) basic diet plus 30 mg Zn/kg from Zn-Gly; (3) basic diet plus 60 mg Zn/kg from Zn-Gly; (4) basic diet plus 90 mg Zn/kg from Zn-Gly; (5) basic diet plus 120 mg Zn/kg from Zn-Gly; and (6) positive control, basic diet plus 120 mg Zn/kg from zinc sulfate (ZnSO₄). The results showed that the addition of 90 or 120 mg/kg Zn-Gly led to an improvement of activity of Cu/Zn superoxide dismutase and glutathione peroxidase and a reduction of malondialdehyde content in livers at 21 and 42 days. With 90 mg/kg Zn-Gly, the content of sera zinc increased by 17.55% (P < 0.05) in 21-day broilers and 10.77% (P > 0.05) in 42-day broilers compared with that of the control. Adding 120 mg/kg Zn-Gly or ZnSO₄ to broilers' diets greatly enhanced the content of zinc in feces at 21 days (P < 0.05) and at 42 days (P < 0.05). For 42-day chickens, increased villus height and decreased crypt depth of the jejunum could be observed in the second growth stage of broilers fed with 90 mg/kg Zn-Gly. Also, intestinal wall thickness decreased (P < 0.05). In addition, adding 90 mg/kg Zn-Gly to the diet markedly elevated villus length of duodenum and decreased crypt depth of ileum (P < 0.05) in 42-day broilers.     

Histological Lesion of Spleen and Inhibition of Splenocyte Proliferation in Broilers Fed on Diets Excess in Selenium

The purpose of this 42-day study was to investigate the effects of excess dietary selenium on immune function by determining morphological changes of spleen and cell cycle of splenocyte. Three hundred 1-day-old avian broilers were fed on a basic diet (0.2 mg/kg selenium) or the same diet amended to contain 1, 5, 10, and 15 mg/kg selenium (Se) supplied as sodium selenite (n = 60/group). Anatomically, the spleens were shrinked in volume with pallecent color. Histopathologically, lymphopenia in splenic nodules and periarterial lymphatic sheaths and congestion of the red pulp were observed in 5, 10, and 15 mg/kg Se group. By flow cytometry method, the percentage of G₀/G₁ phase splenocytes was significantly increased, whereas the percentages of S phase and G₂+M phase splenocytes and the proliferation index were markedly decreased in 5, 10, and 15 mg/kg Se groups when compared with those of 0.2 mg/kg group. The results confirmed that excess dietary Se as sodium selenite in the range of 5∼15 mg/kg caused growth retardation of spleen by cell cycle blockage in young chickens.     

Effect of Dietary Nickel Chloride on Splenic Immune Function in Broilers

This study was designed to evaluate the effects of dietary nickel chloride (NiCl₂) on the splenic immunity in broilers by observing changes of cytokine mRNA expression and protein levels, immunoglobulin (IgA, IgG, and IgM) contents, and IgA⁺ B cell and T-cell numbers using the methods of qRT-PCR, flow cytometry (FCM), and ELISA. A total of 240 1-day-old avian broilers were equally allocated into four groups and fed on a corn–soybean basal diet as the control diet or the same diet supplemented with 300, 600, and 900 mg/kg NiCl₂ for 42 days. The mRNA expression and protein levels of IL-2, IL-6, IL-10, IL-12, TNF-α/LITAF, IFN-γ, and IgA, IgG, and IgM contents were significantly decreased (p?<?0.05 or p?<?0.01) in the 300-, 600-, and 900-mg/kg NiCl₂ groups when compared with those of the control group, which was consistent with the reduction of T-cell subset percentages and IgA⁺ B cell numbers in the 300-, 600-, and 900-mg/kg NiCl₂ groups. The abovementioned results showed that dietary NiCl₂ in excess of 300 mg/kg caused damage on splenocytes and splenic immune function. The results of the present study provided new experimental evidences for further study on the effect mechanism of NiCl₂ on splenic immunity.