Dietary Vanadium Induces Lymphocyte Apoptosis in the Bursa of Fabricius of Broilers

The purpose of this 42-day study was to investigate the apoptosis in the bursa of Fabricius induced by different levels of dietary vanadium. A total of 420 1-day-old avian broilers were divided into 6 groups in which there were 7 replicates in each group and 10 broilers in each replicate and fed on a corn–soybean basal diet as control diet (vanadium 0.073 mg/kg) or the same diet amended to contain 5, 15, 30, 45, and 60 mg/kg vanadium supplied as ammonium metavanadate (NH₄VO₃). Ultrastructurally, mitochondrial injury and increased numbers of apoptotic cells with condensed nuclei were observed in the 30, 45, and 60 mg/kg groups. As measured by flow cytometry, the percentages of apoptotic lymphocytes were significantly increased in the 15-, 30-, 45-, and 60-mg/kg groups when compared with those of control group. Meanwhile, the terminal deoxynucleotidyl transferase 2′-deoxyuridine 5′-triphosphate nick end-labeling assay showed that there were increased numbers of apoptotic cells in the 30-, 45-, and 60-mg/kg groups. Immunohistochemical tests showed increased numbers of positive cells under Bax and caspase-3 protein detection and decreased Bcl-2 protein in the 15-, 30-, 45-, and 60-mg/kg groups. The vanadium content of the bursa was found to be significantly increased in the 30-, 45-, and 60-mg/kg groups. These results suggested that dietary vanadium in excess of 15 mg/kg could cause lymphocyte apoptosis in the bursa of Fabricius and impact humoral immunity in broilers. Lymphocyte apoptosis in the bursa induced by high levels of dietary vanadium is associated with mitochondrial injury and changes in levels of apoptogenic proteins, such as Bcl-2, Bax, and caspase-3.     

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 High Fluorine on the Cell Cycle and Apoptosis of Renal Cells in Chickens

The experiment was conducted with the objective of evaluating the effect of dietary high fluorine (F) on cell cycle and apoptosis of kidney in chickens by the methods of flow cytometry. Three hundred 1-day-old Avian broilers were divided into four groups and fed on control diet (F 23 mg/kg) and high F diets (400 mg/kg, high F group I; 800 mg/kg, high F group II; 1,200 mg/kg, high F group III) for 6 weeks. As tested by flow cytometry, the percentage of renal cell apoptosis was increased with increasing of dietary F, and it obviously rose in three high F groups when compared with that of control group. Renal cells in G₀/G₁ phase were much higher, and renal cells in S phase, G₂+M phase, and proliferation index value were much lower in high F groups I, II, and III than in control group. The results showed that excess dietary F in the range of 400–1,200 mg/kg caused G₀/G₁ arrest and increased cellular apoptosis in the kidney, which might finally interfere with the excretion and retention of fluoride in chickens.     

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.     

Low Dietary Selenium Induce Increased Apoptotic Thymic Cells and Alter Peripheral Blood T Cell Subsets in Chicken

The purpose of this 42-day study was to investigate the effects of low selenium (Se) on immune function by determining histopathological changes of thymus, apoptosis of thymic cells, and subpopulation of peripheral blood T cells. 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 thymus was significantly decreased in low Se group from 21 days of age in time-dependent manner when compared with that of control group. Histopathologically, lymphopenia in the cortex and medulla of thymus was observed in low Se group. In comparison with those of control group, the percentage of Annexin-V positive cells was increased, and the percentages of CD3⁺ and CD3⁺CD8⁺ T cells of the peripheral blood were decreased in low Se group, as measured by flow cytometry. These data suggested that low dietary Se induced histological lesions of thymus, increased apoptosis of thymic cells, and decreased T cell subsets. The cellular immune function was finally impaired in broilers.     

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.     

Effect of Dietary High Molybdenum on the Cell Cycle and Apoptosis of Kidney in Broilers

The experiment was conducted with the objective of examining the effects of high molybdenum on the cell cycle and apoptosis of kidney in broilers by the methods of flow cytometry. Three hundred 1-day-old Avian broilers were randomly divided into four groups, and fed on diets as follows: control diet (Mo 13 mg/kg) and high molybdenum diets (Mo 500 mg/kg, high molybdenum group I; Mo 1,000 mg/kg, high molybdenum group II; Mo 1,500 mg/kg, high molybdenum group III) for 6 weeks. The results showed that the relative weight of kidney were higher (P?<?0.05 or P?<?0.01), and the cellular percentages of G₀/G₁ phase were lower, and cellular percentages of S phase and the proliferating index were higher in high molybdenum groups II and III than in control group (P?<?0.01). The percentage of renal cell apoptosis was increased in high molybdenum groups II and III when compared with that of control group (P?<?0.01). Immunohistochemical test showed that there were increased frequencies of positive cells containing Bax protein and decreased frequencies of positive cells containing Bcl-2 protein in high molybdenum groups II and III. It was concluded that dietary high molybdenum (1,000 mg/kg and 1,500 mg/kg) impaired the progression of renal cells from S phase to G₂M phase obviously and induced renal cell apoptosis.     

The Molecular Mechanisms of Protective Role of Se on the G<Subscript>2</Subscript>/M Phase Arrest of Jejunum Caused by AFB<Subscript>1</Subscript>

Aflatoxin B₁ (AFB₁) is the most toxic among the mycotoxins and causes detrimental health effects on human and animals. Selenium (Se) plays an important role in chemopreventive, antioxidant, anticarcinogen, and detoxification and involved in cell cycle regulation. The aim of this study was to explore the molecular mechanisms of selenium involved in inhibition of G₂/M cell cycle arrest of broiler’s jejunum. A total of 240 one-day-old healthy Cobb broilers were randomly divided into four groups and fed with basal diet (control group), 0.6 mg/kg AFB₁ (AFB₁ group), 0.4 mg/kg Se (+Se group), and 0.6 mg/kg AFB₁ + 0.4 mg/kg Se (AFB₁ + Se group) for 21 days, respectively. The histological observation and morphological analysis revealed that 0.4 mg/kg Se prevented the AFB₁-associated lesions of jejunum including the shedding of the apical region of villi, the decreased villus height, and villus height/crypt ratio. The cell cycle analysis by flow cytometry showed that 0.4 mg/kg Se ameliorated the AFB₁-induced G₂/M phase arrest in jejunal cells. Moreover, the expressions of ATM, Chk2, p53, Mdm2, p21, PCNA, Cdc25, cyclin B, and Cdc2 analyzed by immunohistochemistry and qRT-PCR demonstrated that 0.4 mg/kg Se restored these parameters to be close to those in the control group. In conclusion, Se promoted cell cycle recovery from the AFB₁-induced G₂/M phase arrest by the molecular regulation of ATM pathway in the jejunum of broilers. The outcomes from the present study may lead to a better understanding of the nature of selenium’s essentiality and its protective roles against AFB₁.     

Low Selenium Diet Alters Cell Cycle Phase, Apoptotic Population and Modifies Oxidative Stress Markers of Spleens in Broilers

The purpose of this 42-day study was to investigate the effects of low selenium (Se) on histopathological changes of spleen, cell cycle and apoptosis of splenocytes, and oxidative status of the spleen. One hundred twenty 1-day-old avian broilers were randomly divided into 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 weight and relative weight of the spleen were significantly decreased in the low Se group when compared with those of the control group. Histopathologically, splenic lesions in low-Se chicken were characterized by lymphocyte depletion and congestion of red pulp. As measured by flow cytometry, splenocytes in G(0)/G(1) phase were significantly increased, while splenocytes in S phase and G(2) + M phase were obviously decreased in the low Se group. The percentage of apoptotic splenocytes was greatly increased in the low Se group when compared with that of control group. At the same time, the occurrence frequencies of apoptotic splenocytes was markedly increased in the low Se group with the appearance of condensed nucleus ultrastructurally. Oxidative stress in the spleens of the low Se group was evidenced by decrease in glutathione peroxidase and catalase activities and increase in malondialdehyde contents. The results showed that low Se diet intake caused increased apoptosis, arrested cell cycle, and obvious oxidative stress, which provided a possible pathway for the injured structure and immune function of the spleen in chickens.     

Low-Selenium Diet Induces Cell Cycle Arrest of Thymocytes and Alters Serum IL-2 Content in Chickens

The purpose of this 42-day study was to investigate the effects of low selenium (Se) on cellular immune function by determining cell cycle of thymus, serum IL-2 content, and mitogenesis of peripheral blood T-lymphocytes. 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. Cell cycle analysis by flow cytometry showed that low-Se diet caused an increase in G(0)G(1) phase cells that corresponded to a decrease in S-phase cells in thymus. Ultrastructurally, mitochondria injury and increased apoptotic cells with condensed nuclei were observed. Low-Se diet decreased the serum IL-2 contents and mitogenesis of peripheral blood lymphocytes to concanavalin A in comparison with those of control group. These data indicate that low-Se diet inhibits the development of thymus by arresting the cell cycle and decreasing the IL-2 content.     

Effects of Aflatoxin B1 Exposure and Sodium Selenite Supplementation on the Histology,Cell Proliferation,and Cell Cycle of Jejunum in Broilers

The aim of this study was to investigate the effects of aflatoxin B₁ (AFB₁) exposure and sodium selenite supplementation on the histology, cell proliferation and cell cycle of jejunum in broilers. A total of 240 1-day-old male AA broilers were divided into four groups of 60 each, fed with basal diet (control group), 0.3 mg/kg AFB₁ (AFB₁ group), 0.4 mg/kg supplement Se (Se group), and 0.3 mg/kg AFB₁?+?0.4 mg/kg supplement Se (AFB₁ + Se group) for 21 days, respectively. Compared with the control group, decreased jejunal villus height, villus height/crypt ratio, and proliferation cell nuclear antigen (PCNA)-positive cells, and G₂/M phase arrest and shedded epithelial cells on the tip of jejunal villus were observed in AFB₁ groups at 7 and 14 days of age. However, the villus/crypt ratio, PCNA-positive cells and cell percentage of G₀/G₁, S, and G₂/M phases had no significant differences between AFB₁ group and control group at 21 days. Simultaneous supplementation with sodium selenite restored these parameters to be close to those in control group. In conclusion, 0.3 mg/kg AFB₁ in the diet inhibits the development of broiler’s jejunum by reducing cellular proliferation and inducing G₂/M arrest during only the first 2 weeks after hatching. Supplementation of dietary sodium selenite at the concentration of 0.4 mg/kg Se had protective action against these toxic effects of AFB₁.     

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.

     

Selenoproteins and heat shock proteins play important roles in immunosuppression in the bursa of Fabricius of chickens with selenium deficiency

Selenium (Se) is necessary for the immune system in chicken and mediates its physiological functions through selenoproteins. Heat shock proteins (Hsps) are indispensable for maintaining normal cell function and for directing the immune response. The aim of the present study was to investigate the effects of Se deficiency on the messenger ribonucleic acid (mRNA) expression levels of selenoproteins and Hsps as well as immune functions in the chicken bursa of Fabricius. Two groups of chickens, namely the control and Se-deficient (L group) groups, were reared for 55 days. The chickens were offered a basal diet, which contained 0.15 mg Se/kg in the diet fed to the control group and 0.033 mg Se/kg in the diet fed to the L group. We performed real-time quantitative polymerase chain reactionto detect the mRNA expression levels of selenoproteins and Hsps on days 15, 25, 35, 45 and 55. Western blotting was used to determine the protein expression levels of Hsps on days 35, 45 and 55, and immune functions were assessed through an enzyme-linked immunosorbent assay on days 15, 35, and 55. The data showed that the mRNA expression levels of selenoproteins, such as Txnrd1, Txnrd2, Txnrd3, Dio1, Dio2, Dio3, GPx1, GPx2, GPx3 GPx4, Sepp1, Selo, Sel-15, Sepx1, Sels, Seli, Selu, Selh, and SPS2, were significantly lower (P < 0.05) in the L group compared with the control group. Additionally, the mRNA and protein expression levels of Hsps (Hsp27, Hsp40, Hsp60, Hsp70, and Hsp90) were also significantly higher (P < 0.05) in the L group. The expression levels of IL-2, IL-6, IL-8, IL-10, IL-17, IL-1β, IFN-α, IFN-β, and IFN-γ were significantly lower (P < 0.05) and TNF-α was significantly higher (P < 0.05) in the L group compared with the control group. Our results show that immunosuppression was accompanied by a downregulation of mRNA expression levels of selenoproteins and an upregulation of the Hsp mRNA expression levels. Thus, Se deficiency causes defects in the chicken bursa of Fabricius, and selenoproteins and Hsps play important roles in immunosuppression in the bursa of Fabricius of chickens with Se deficiency.     

Selenium Deficiency Induces Autophagy in Immune Organs of Chickens

The aim of the present study was to investigate the effects of selenium (Se) deficiency on autophagy-related genes and on ultrastructural changes in the spleen, bursa of Fabricius, and thymus of chickens. The Se deficiency group was fed a basal diet containing Se at 0.033 mg/kg and the control group was fed the same basal diet containing Se at 0.15 mg/kg. The messenger RNA (mRNA) levels of the autophagy genes microtubule-associated protein 1 light chain 3 (LC3)-I, LC3-II, Beclin 1, dynein, autophagy associated gene 5 (ATG5), and target of rapamycin complex 1 (TORC1) were assessed using real-time qPCR. The protein levels of LC3-II, Beclin 1, and dynein were investigated using western blot analysis. Furthermore, the ultrastructure was observed using an electron microscope. The results indicated that spleen mRNA levels of LC3-I, LC3-II, Beclin 1, dynein, ATG5, and TORC1 and the protein levels of LC3-II, Beclin 1, and dynein were increased in the Se deficiency group compared with the control group. In the bursa of Fabricius, the mRNA levels of LC3-I, LC3-II, Beclin 1, dynein, ATG5, and TORC1 and the protein levels of Beclin 1 and dynein were increased; furthermore, the protein level of LC3-II was decreased in the Se deficiency group compared to the control group. In the thymus, the mRNA levels of LC3-I, Beclin 1, and ATG5 increased; the levels of LC3-II, dynein, and TORC1 were decreased; the protein level of Beclin 1 increased; and the levels of LC3-II and dynein decreased in the Se deficiency group compared to those in the control group. Further cellular morphological changes, such as autophagy vacuoles, autolysosomes, and lysosomal degradation, were observed in the spleen, bursa of Fabricius, and thymus of the Se-deficiency group. In summary, Se deficiency caused changes in autophagy-related genes, which increased the autophagic process and also caused structural damages to the immune organs of chickens.     

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.     

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.     

Testicular toxicity induced by dietary cadmium in cocks and ameliorative effect by selenium

Cadmium (Cd) is an ubiquitous environmental pollutant that has been associated with male reproductive toxicity in animal models. However, little is known about the reproductive toxicity of Cd in birds. To investigate the toxicity of Cd on male reproduction in birds and the protective effects of selenium (Se) against subchronic exposure to dietary Cd, 100-day-old cocks received either Se (as 10 mg Na₂SeO₃ per kg of diet), Cd (as 150 mg CdCl₂ per kg of diet) or Cd + Se in their diets for 60 days. Histological and ultrastructural changes in the testis, the concentrations of Cd and Se, amount of lipid peroxidation (LPO), the activities of the antioxidants superoxide dismutase (SOD) and glutathione peroxidase (GPx), and apoptosis and serum testosterone levels were determined. Exposure to Cd significantly lowered SOD and GPx activity, Se content in the testicular tissue, and serum testosterone levels. It increased the amount of LPO, the numbers of apoptotic cells and Cd concentration and caused obvious histopathological changes in the testes. Concurrent treatment with Se reduced the Cd-induced histopathological changes in the testis, oxidative stress, endocrine disorder and apoptosis, suggesting that the toxic effects of cadmium on the testes is ameliorated by Se. Se supplementation also modified the distribution of Cd in the testis.     

Prediction of Selenoprotein T Structure and Its Response to Selenium Deficiency in Chicken Immune Organs

Selenoprotein T (SelT) is associated with the regulation of calcium homeostasis and neuroendocrine secretion. SelT can also change cell adhesion and is involved in redox regulation and cell fixation. However, the structure and function of chicken SelT and its response to selenium (Se) remains unclear. In the present study, 150 1-day-old chickens were randomly divided into a low Se group (L group, fed a Se-deficient diet containing 0.020 mg/kg Se) and a control group (C group, fed a diet containing sodium selenite at 0.2 mg/kg Se). The immune organs (spleen, thymus, and bursa of Fabricius) were collected at 15, 25, 35, 45, and 55 days of age. We performed a sequence analysis and predicted the structure and function of SelT. We also investigated the effects of Se deficiency on the expression of SelT, selenophosphate synthetase-1 (SPS1), and selenocysteine synthase (SecS) using RT-PCR and the oxidative stress in the chicken immune organs. The data showed that the coding sequence (CDS) and deduced amino acid sequence of SelT were highly similar to those of 17 other animals. Se deficiency induced lower (P?<?0.05) levels of SelT, SPS1, and SecS, reduced the catalase (CAT) activity, and increased the levels of hydrogen peroxide (H₂O₂) and hydroxyl radical (–OH) in immune organs. In conclusion, the CDS and deduced amino acid sequence of chicken SelT are highly homologous to those of various mammals. The redox function and response to the Se deficiency of chicken SelT may be conserved. A Se-deficient diet led to a decrease in SelT, SecS, and SPS1 and induced oxidative stress in the chicken immune organs. To our knowledge, this is the first report of predictions of chicken SelT structure and function. The present study demonstrated the relationship between the selenoprotein synthases (SPS1, SecS) and SelT expression in the chicken immune organs and further confirmed oxidative stress caused by Se deficiency. Thus, the information presented in this study is helpful to understand chicken SelT structure and function. Meanwhile, the present research also confirmed the negative effects of Se deficiency on chicken immune organs.     

Effects of Dietary Selenium on Selenoprotein W Gene Expression in the Chicken Immune Organs

Selenoprotein W (SelW) is expressed in the immune systems of mammals. However, its pattern of expression in the immune organs of birds is still unclear. To investigate the distribution of SelW and effects of dietary Se levels on the SelW mRNA expression in the immune organs of birds, 1-day-old male chickens were fed either a commercial diet or an Se-supplemented diet containing 0.601, 1.058, 1.514, or 2.427?mg Se per kilogram, and 1.0, 2.0, 3.0 or 5.0?mg sodium selenite per kilogram for 90?days. The immune organs (spleen, thymus, and bursa of Fabricius) were collected and examined for Se content and SelW mRNA levels. The mRNA expression of SelW was detected in all the tissues. Although Se content was the highest in the spleen, the remarkable stability of the SelW mRNA level was observed in this organ during different times of dietary Se supplementation. Se-supplemented diet can make the SelW expression levels higher within a certain range in thymus and bursa of Fabricius. The present study demonstrates that SelW is widely expressed in immune organs of birds and that Se-supplementation of the feed increases SelW expression in the thymus and the bursa of Fabricius.