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.     

Carnitine Supplementation Modulates High Dietary Copper-Induced Oxidative Toxicity and Reduced Performance in Laying Hens

This experiment was conducted to evaluate the effects of L-carnitine on performance, egg quality and certain biochemical parameters in laying hens fed a diet containing high levels of copper proteinate. Forty-eight 42-week-old laying hens were divided into four groups with four replicates. The laying hens were fed with a basal diet (control) or the basal diet supplemented with either 400 mg carnitine (Car)/kg diet, 800 mg copper proteinate (CuP)/kg diet or 400 mg carnitine + 800 mg copper (Car+CuP)/kg diet, for 6 weeks. Supplemental CuP decreased feed consumption (p?相似文献   

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.     

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.     

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.     

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.     

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   

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.     

Suppressive Effects of Dietary High Fluorine on the Intestinal Development in Broilers

Fluoride (F) is a well-recognized hazardous substance. Ingested F initially acts locally on the intestines. The small intestine plays a critical role in the digestion, absorption, and defense. In this study, therefore, we investigated the effects of fluorine on the intestinal development by light microscopy, transmission electron microscopy, and histochemistry. A total of 280 one-day-old avian broilers were randomly divided into four groups and fed on a corn-soybean basal diet as control diet (fluorine, 22.6 mg/kg) or the same basal diet supplemented with 400, 800, and 1,200 mg/kg fluorine (high fluorine groups I, II, and III) in the form of sodium fluoride for 42 days. The results showed that the intestinal gross, histological, and ultrastructural changes were observed in the high fluorine groups II and III. Meanwhile, the intestinal length, weight, viscera index, villus height, crypt depth, villus height to crypt depth ratio, diameter, muscle layer thickness, and goblet cell numbers were significantly lower (p?<?0.01 or p?<?0.05), and the intestinal diameter to villus height ratio was markedly higher (p?<?0.01 or p?<?0.05) in the high fluorine groups II and III than those in control group. In conclusion, dietary fluorine in the range of 800–1,200 mg/kg obviously altered the aforementioned parameters of the intestines, implying that the intestinal development was suppressed and the intestinal functions, such as digestion, absorption, defense, or osmoregulation were impaired in broilers.     

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.     

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.     

Effects of Dietary Supplementation with Vitamin C and Vitamin E and Their Combination on Growth Performance,Some Biochemical Parameters,and Oxidative Stress Induced by Copper Toxicity in Broilers

This study investigated effects of dietary supplementation with vitamin C, vitamin E on performance, biochemical parameters, and oxidative stress induced by copper toxicity in broilers. A total of 240, 1-day-old, broilers were assigned to eight groups with three replicates of 10 chicks each. The groups were fed on the following diets: control (basal diet), vitamin C (250 mg/kg diet), vitamin E (250 mg/kg diet), vitamin C + vitamin E (250 mg/kg?+?250 mg/kg diet), and copper (300 mg/kg diet) alone or in combination with the corresponding vitamins. At the 6th week, the body weights of broilers were decreased in copper, copper + vitamin E, and copper + vitamin C + vitamin E groups compared to control. The feed conversion ratio was poor in copper group. Plasma aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase activities, iron, copper concentrations, and erythrocyte malondialdehyde were increased; plasma vitamin A and C concentrations and erythrocyte superoxide dismutase were decreased in copper group compared to control. Glutathione peroxidase, vitamin C, and iron levels were increased; aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and copper levels were decreased in copper + vitamin C group, while superoxide dismutase, glutathione peroxidase, and vitamin E concentrations were increased; aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase were decreased in copper with vitamin E group compared to copper group. The vitamin C concentrations were increased; copper, uric acid, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and malondialdehyde were decreased in copper + vitamin C + vitamin E group compared to copper group. To conclude, copper caused oxidative stress in broilers. The combination of vitamin C and vitamin E addition might alleviate the harmful effects of copper as demonstrated by decreased lipid peroxidation and hepatic enzymes.     

Dietary Magnesium Sulfate Supplementation Protects Heat Stress-Induced Oxidative Damage by Restoring the Activities of Anti-oxidative Enzymes in Broilers

The purpose of this study was to investigate the effect of dietary magnesium sulfate supplementation on heat stress-induced oxidative damage in broilers. One hundred twenty 14-day-old broilers were randomly assigned into four treatment groups with three replicates of ten birds each. The broilers were reared under normal ambient temperature (24 ± 1°C) fed with a basal (control) diet or reared under high ambient temperature (35 ± 1°C between 1000 and 1800 h, 8 h each day) fed with a basal diet supplemented with magnesium sulfate (0, 2.5 or 5.0 mg/kg of diet) from 14 to 42 days of age. Growth performance and oxidative damage were evaluated in each treatment group. Our results demonstrated that dietary magnesium sulfate supplementation significantly prevented heat stress-induced oxidative damage and improved growth performance in broilers compared with that of control. Mechanistically, this beneficial effect was mediated, at least partly, by restoring the activity of anti-oxidative enzymes. This finding suggests that magnesium sulfate supplementation might be a potential strategy to attenuate heat stress-induced detrimental effects in broilers raised in summer season or tropical areas.     

Management of Oxidative Stress by Heme Oxygenase-1 in Cisplatin-induced Toxicity in Renal Tubular Cells

Induction of heme oxygenase-1 (HO-1) may serve as an immediate protective response during treatment with the cytostatic drug cisplatin (CDDP). Oxidative pathways participate in the characteristic nephrotoxicity of CDDP. In the present study, cultured tubular cells (LLC-PK1) were used to investigate whether induction of HO provided protection against CDDP by maintaining the cellular redox balance. The antioxidants, &#102 -tocopherol (TOCO) and N -acetylcysteine (NAC), were used to demonstrate that elevation of ROS levels contribute to the development of CDDP-induced cytotoxicity. Chemical modulators of HO activity were used to investigate the role of HO herein. Hemin was used to specifically induce HO-1, while exposure of the cells to tin-protoporphyrin (SnPP) was shown to inhibit HO activity. Hemin treatment prior to CDDP-exposure significantly decreased the generation of ROS to control levels, while inhibition of HO increased the ROS levels beyond the levels measured in cells treated with CDDP alone. Furthermore, HO induction protected significantly against the cytotoxicity of CDDP, although this protection was limited. Similar results were obtained when the cells were preincubated with TOCO, suggesting that mechanisms other than impairment of the redox ratio are important in CDDP-induced loss of cell viability in vitro. In addition, SnPP treatment exacerbated the oxidative response and cytotoxicity of CDDP, especially at low CDDP concentrations. We therefore conclude that HO is able to directly limit the CDDP-induced oxidative stress response and thus serves as safeguard of the cellular redox balance.     

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.     

Beneficial Effects of an Alternating High- Fat Dietary Regimen on Systemic Insulin Resistance,Hepatic and Renal Inflammation and Renal Function

Background

An Alternating high- cholesterol dietary regimen has proven to be beneficial when compared to daily high- cholesterol feeding. In the current study we explored whether the same strategy is applicable to a high- fat dietary regimen.

Objective

To investigate whether an alternating high- fat dietary regimen can effectively diminish insulin resistance, hepatic and renal inflammation and renal dysfunction as compared to a continuous high- fat diet.

Design

Four groups of male ApoE*3Leiden mice (n = 15) were exposed to different diet regimens for 20 weeks as follows: Group 1: low- fat diet (10 kcal% fat); Group 2: intermediate- fat diet (25 kcal% fat); Group 3: high- fat diet (45 kcal% fat) and Group 4: alternating- fat diet (10 kcal% fat for 4 days and 45 kcal% fat for 3 days in a week).

Results

Compared to high fat diet feeding, the alternating and intermediate- fat diet groups had reduced body weight gain and did not develop insulin resistance or albuminuria. In addition, in the alternating and intermediate- fat diet groups, parameters of tissue inflammation were markedly reduced compared to high fat diet fed mice.

Conclusion

Both alternating and intermediate- fat feeding were beneficial in terms of reducing body weight gain, insulin resistance, hepatic and renal inflammation and renal dysfunction. Thus beneficial effects of alternating feeding regimens on cardiometabolic risk factors are not only applicable for cholesterol containing diets but can be extended to diets high in fat content.     

Dietary Squalene Increases High Density Lipoprotein-Cholesterol and Paraoxonase 1 and Decreases Oxidative Stress in Mice

Background and Purpose

Squalene, the main hydrocarbon in the unsaponifiable fraction of virgin olive oil, is involved in cholesterol synthesis and it has been reported to own antiatherosclerotic and antiesteatosic effects. However, the squalene''s role on lipid plasma parameters and the influence of genotype on this effect need to be addressed.

Experimental Approaches

Three male mouse models (wild-type, Apoa1- and Apoe- deficient) were fed chow semisynthetic diets enriched in squalene to provide a dose of 1 g/kg during 11 weeks. After this period, their plasma parameters and lipoprotein profiles were analyzed.

Key Results

Squalene administration at a dose of 1 g/kg showed decreased reactive oxygen species in lipoprotein fractions independently of the animal background and caused an specific increase in high density lipoprotein (HDL)-cholesterol levels, accompanied by an increase in phosphatidylcholine and paraoxonase 1 and no changes in apolipoproteins A1 and A4 in wild-type mice. In these mice, the cholesterol increase was due to its esterified form and associated with an increased hepatic expression of Lcat. These effects were not observed in absence of apolipoprotein A1. The increases in HDL- paraoxonase 1 were translated into decreased plasma malondialdehyde levels depending on the presence of Apolipoprotein A1.

Conclusions and Implications

Dietary squalene promotes changes in HDL- cholesterol and paraoxonase 1 and decreases reactive oxygen species in lipoproteins and plasma malondialdehyde levels, providing new benefits of its intake that might contribute to explain the properties of virgin olive oil, although the phenotype related to apolipoproteins A1 and E may be particularly relevant.