The purpose of this 42-day study was to investigate the effects of methionine deficiency on spleen by determining the relative weight, morphological changes of spleen, cell cycle and apoptosis of splenocytes, and oxid...The purpose of this 42-day study was to investigate the effects of methionine deficiency on spleen by determining the relative weight, morphological changes of spleen, cell cycle and apoptosis of splenocytes, and oxidative markers of serum and spleen. One hundred and twenty one-day-old avian broilers were randomly divided into two groups and fed on a control diet (starter diet, methionine 0.50%;grower diet, methionine 0.40%) and methionine deficient diet (starter diet, methionine 0.26%;grower diet, methionine 0.28%) for 6 weeks. The relative weight of spleen was lighter in methionine deficiency than control group. Histopathologically, lymphopenia and congestion were observed. Ultrastructurally, there were more apoptosis lymphocytes in spleen and the mitochondria of lymphocytes were swelled in methionine deficiency. By flow cytometry, the G0/G1 phase of the cell cycle of the spleen was much higher (P < 0.01), and the S, G2+M phases and proliferating index were lower (P < 0.01) in methionine deficiency than in control group. And the percentage of apoptotic cells in the spleen was significantly increased in methionine deficiency (P < 0.01).The superoxide dismutase and glutathione peroxidase activities, and abilities to inhibit hydroxyl radicals were greatly decreased while the malondialdehyde contents were markedly increased in methionine deficiency. It was concluded that methionine deficiency could restraine the development of the spleen by cell cycle arrest and increased apoptosis, cause splenic lesions and reduce splenic antioxidant function. The splenic function should be finally impaired and then the immune function could be impacted in chickens.展开更多
The objective of this study was to determine the effects of dietary vanadium on small intestinal morphology of broilers by the methods of light microscopy (LM) and transmission electron microscopy (TEM). A total of 42...The objective of this study was to determine the effects of dietary vanadium on small intestinal morphology of broilers by the methods of light microscopy (LM) and transmission electron microscopy (TEM). 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 a control diet or the same diet supplemented with 5, 15, 30, 45 and 60 mg/kg vanadium in the form of ammonium metavanadate for 42 days. In comparison with those in the control group, the intestinal villus heights were decreased (P < 0.05 or P < 0.01) in the 30, 45 and 60 mg/kg groups, and crypt depths and villus height/crypt depth ratio were decreased in the 45 and 60 mg/kg groups. Ultrastructurally, the microvilli were apparently sparse and short, and the numbers of lysosomes were increased in abovementioned three intestines in the 45 and 60 mg/kg groups at 42 days of age. In conclusion, dietary vanadium in excess of 30 mg/kg could alter the villus height, crypt depth, villus height/crypt depth ratio and ultrastructure, which might impact the development of small intestines in broilers.展开更多
The aims of this study were to clarify the effects of high vanadium on the renal cell cycle and apoptosis in broilers. 420 one-day-old avian broilers were divided into six groups and fed on a control diet (vanadium 0....The aims of this study were to clarify the effects of high vanadium on the renal cell cycle and apoptosis in broilers. 420 one-day-old avian broilers were divided into six groups and fed on a 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;60 mg/kg, high vanadium group V) throughout the experimental period of 42 days. As tested by flow cytometry, the percentage of apoptotic renal cells was increased in high vanadium group II, III, IV and V when compared with that of control group. The Proliferating index (PI) of renal cell and the ratio of S, G2 + M phase cells were markedly decreased and population of G0/G1 cells was increased in high vanadium group II, III, IV and V. The results showed that dietary vanadium in excess of 15 mg/kg was toxic to kidney by the renal cells cycle arrest and increased apoptosis, which caused the growth depression of the kidney in broilers.展开更多
The aim of this study was to investigate the effects of high dietary fluoride (F) on serum biochemistry and oxidative damage in broiler chickens. 280 one-day-old healthy avian broiler chickens were randomly allotted i...The aim of this study was to investigate the effects of high dietary fluoride (F) on serum biochemistry and oxidative damage in broiler chickens. 280 one-day-old healthy avian broiler chickens were randomly allotted into four equal groups and fed with a corn-soybean basal diet containing 22.6 mg·F/kg (control group) or same basal diets supplemented with 400, 800, and 1200 mg·F/kg (high F groups I, II, and III) in the form of sodium fluoride for 42 days. At 42 days of age, the serum F content was markedly higher in the three high F groups than that in the control group. From 28 to 42 days of age, the contents of serum total protein (TP) and albumin (ALB) were significantly lower in the three high F groups. From 14 to 42 days of age, the activities of alkaline phosphatase (ALP), alanine aminotransferase (ALT) and the creatinine (Crea) contents in the serum showed a marked increase in the three high F groups;aspartate aminotransferase (AST) activity and uric acid (Ua) content were significantly increased, and a significant increase in the content of malondialdehyde (MDA) along with marked decreases in the activities of total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), catalase (CAT), the glutathione (GSH) content and the ability to inhibit hydroxyl radical were observed in the high F groups II and III. In conclusion, F has accumulated in the blood circulatory system and dietary F in the range of 800 - 1200 mg/kg could significantly induce abnormalities of bone, liver and kidney, inhibit the synthesis of protein, enhance lipid peroxidation and disturb the antioxidative system of broiler chickens.展开更多
The purpose of this study was to observe the histopathological lesions and oxidative damage induced by dietary nickel chloride (NiCl2) in the thymus. A total of 280 one-day-old avian broilers were divided into four gr...The purpose of this study was to observe the histopathological lesions and oxidative damage induced by dietary nickel chloride (NiCl2) in the thymus. A total of 280 one-day-old avian broilers were divided into four groups and fed on a corn-soybean basal diet as the control diet or the same basal diet supplemented with 300, 600, and 900 mg/kg of NiCl2 for 42 days. In the NiCl2-treated groups, the broiler weight and thymic relative weight were significantly (P P < 0.01) decreased. Histopathologically, thymic corpuscles were increased and enlarged;the reticular cells were degenerate and necrotic, and lymphocytes were slightly decreased and loosely arranged in the medulla of thymus in the 600 mg/kg and 900 mg/kg groups. The activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), and the ability to inhibit hydroxy radical and glutathione (GSH) content were significantly (P P < 0.01) lower in the NiCl2-treated groups than those in the control group, while MDA content was higher. The above-mentioned results demonstrated that dietary NiCl2 in excess of 300 mg/kg could reduce the broiler weight and thymic relative weight, and cause histopathological lesions and oxidative damage in the thymus, which finally impaired the thymic function.展开更多
The purpose of this study was to investigate the serum oxidative stress induced by dietary nickel chloride (NiCl2) in broilers. A total of 240 one-day-old avian broilers were divided into four groups and fed on a corn...The purpose of this study was to investigate the serum oxidative stress induced by dietary nickel chloride (NiCl2) in broilers. A total of 240 one-day-old avian broilers were divided into four groups and fed on a cornsoybean basal diet as control diet or the same basal diet supplemented with 300 mg/kg, 600 mg/kg and 900 mg/kg NiCl2. During the experimental period of 42 days, oxidative stress parameters were determined for both control and experimental groups. The results showed that malondialdehyde (MDA) content was significantly higher (p < 0.05 or p < 0.01) in the 300 mg/kg, 600 mg/kg and 900 mg/kg groups than that in the control group. In contrast, the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione per- oxidase (GSH-Px), and the ability to inhibit hydroxy radical, and glutathione hormone (GSH) content were significantly decreased (p < 0.05 or p < 0.01) in the 300 mg/kg, 600 mg/kg and 900 mg/kg groups in comparison with those of the control group. It was concluded that dietary NiCl2 in excess of 300 mg/kg could cause oxidative stress, which could finally impaired the antioxidant function in broilers.展开更多
文摘The purpose of this 42-day study was to investigate the effects of methionine deficiency on spleen by determining the relative weight, morphological changes of spleen, cell cycle and apoptosis of splenocytes, and oxidative markers of serum and spleen. One hundred and twenty one-day-old avian broilers were randomly divided into two groups and fed on a control diet (starter diet, methionine 0.50%;grower diet, methionine 0.40%) and methionine deficient diet (starter diet, methionine 0.26%;grower diet, methionine 0.28%) for 6 weeks. The relative weight of spleen was lighter in methionine deficiency than control group. Histopathologically, lymphopenia and congestion were observed. Ultrastructurally, there were more apoptosis lymphocytes in spleen and the mitochondria of lymphocytes were swelled in methionine deficiency. By flow cytometry, the G0/G1 phase of the cell cycle of the spleen was much higher (P < 0.01), and the S, G2+M phases and proliferating index were lower (P < 0.01) in methionine deficiency than in control group. And the percentage of apoptotic cells in the spleen was significantly increased in methionine deficiency (P < 0.01).The superoxide dismutase and glutathione peroxidase activities, and abilities to inhibit hydroxyl radicals were greatly decreased while the malondialdehyde contents were markedly increased in methionine deficiency. It was concluded that methionine deficiency could restraine the development of the spleen by cell cycle arrest and increased apoptosis, cause splenic lesions and reduce splenic antioxidant function. The splenic function should be finally impaired and then the immune function could be impacted in chickens.
文摘The objective of this study was to determine the effects of dietary vanadium on small intestinal morphology of broilers by the methods of light microscopy (LM) and transmission electron microscopy (TEM). 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 a control diet or the same diet supplemented with 5, 15, 30, 45 and 60 mg/kg vanadium in the form of ammonium metavanadate for 42 days. In comparison with those in the control group, the intestinal villus heights were decreased (P < 0.05 or P < 0.01) in the 30, 45 and 60 mg/kg groups, and crypt depths and villus height/crypt depth ratio were decreased in the 45 and 60 mg/kg groups. Ultrastructurally, the microvilli were apparently sparse and short, and the numbers of lysosomes were increased in abovementioned three intestines in the 45 and 60 mg/kg groups at 42 days of age. In conclusion, dietary vanadium in excess of 30 mg/kg could alter the villus height, crypt depth, villus height/crypt depth ratio and ultrastructure, which might impact the development of small intestines in broilers.
文摘The aims of this study were to clarify the effects of high vanadium on the renal cell cycle and apoptosis in broilers. 420 one-day-old avian broilers were divided into six groups and fed on a 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;60 mg/kg, high vanadium group V) throughout the experimental period of 42 days. As tested by flow cytometry, the percentage of apoptotic renal cells was increased in high vanadium group II, III, IV and V when compared with that of control group. The Proliferating index (PI) of renal cell and the ratio of S, G2 + M phase cells were markedly decreased and population of G0/G1 cells was increased in high vanadium group II, III, IV and V. The results showed that dietary vanadium in excess of 15 mg/kg was toxic to kidney by the renal cells cycle arrest and increased apoptosis, which caused the growth depression of the kidney in broilers.
文摘The aim of this study was to investigate the effects of high dietary fluoride (F) on serum biochemistry and oxidative damage in broiler chickens. 280 one-day-old healthy avian broiler chickens were randomly allotted into four equal groups and fed with a corn-soybean basal diet containing 22.6 mg·F/kg (control group) or same basal diets supplemented with 400, 800, and 1200 mg·F/kg (high F groups I, II, and III) in the form of sodium fluoride for 42 days. At 42 days of age, the serum F content was markedly higher in the three high F groups than that in the control group. From 28 to 42 days of age, the contents of serum total protein (TP) and albumin (ALB) were significantly lower in the three high F groups. From 14 to 42 days of age, the activities of alkaline phosphatase (ALP), alanine aminotransferase (ALT) and the creatinine (Crea) contents in the serum showed a marked increase in the three high F groups;aspartate aminotransferase (AST) activity and uric acid (Ua) content were significantly increased, and a significant increase in the content of malondialdehyde (MDA) along with marked decreases in the activities of total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), catalase (CAT), the glutathione (GSH) content and the ability to inhibit hydroxyl radical were observed in the high F groups II and III. In conclusion, F has accumulated in the blood circulatory system and dietary F in the range of 800 - 1200 mg/kg could significantly induce abnormalities of bone, liver and kidney, inhibit the synthesis of protein, enhance lipid peroxidation and disturb the antioxidative system of broiler chickens.
文摘The purpose of this study was to observe the histopathological lesions and oxidative damage induced by dietary nickel chloride (NiCl2) in the thymus. A total of 280 one-day-old avian broilers were divided into four groups and fed on a corn-soybean basal diet as the control diet or the same basal diet supplemented with 300, 600, and 900 mg/kg of NiCl2 for 42 days. In the NiCl2-treated groups, the broiler weight and thymic relative weight were significantly (P P < 0.01) decreased. Histopathologically, thymic corpuscles were increased and enlarged;the reticular cells were degenerate and necrotic, and lymphocytes were slightly decreased and loosely arranged in the medulla of thymus in the 600 mg/kg and 900 mg/kg groups. The activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), and the ability to inhibit hydroxy radical and glutathione (GSH) content were significantly (P P < 0.01) lower in the NiCl2-treated groups than those in the control group, while MDA content was higher. The above-mentioned results demonstrated that dietary NiCl2 in excess of 300 mg/kg could reduce the broiler weight and thymic relative weight, and cause histopathological lesions and oxidative damage in the thymus, which finally impaired the thymic function.
文摘The purpose of this study was to investigate the serum oxidative stress induced by dietary nickel chloride (NiCl2) in broilers. A total of 240 one-day-old avian broilers were divided into four groups and fed on a cornsoybean basal diet as control diet or the same basal diet supplemented with 300 mg/kg, 600 mg/kg and 900 mg/kg NiCl2. During the experimental period of 42 days, oxidative stress parameters were determined for both control and experimental groups. The results showed that malondialdehyde (MDA) content was significantly higher (p < 0.05 or p < 0.01) in the 300 mg/kg, 600 mg/kg and 900 mg/kg groups than that in the control group. In contrast, the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione per- oxidase (GSH-Px), and the ability to inhibit hydroxy radical, and glutathione hormone (GSH) content were significantly decreased (p < 0.05 or p < 0.01) in the 300 mg/kg, 600 mg/kg and 900 mg/kg groups in comparison with those of the control group. It was concluded that dietary NiCl2 in excess of 300 mg/kg could cause oxidative stress, which could finally impaired the antioxidant function in broilers.
