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Xin Gen Lei - One of the best experts on this subject based on the ideXlab platform.
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avian selenogenome response to dietary se and vitamin e deficiency and supplementation
Poultry Science, 2019Co-Authors: Lvhui Sun, Jia-qiang Huang, Xin Gen Lei, Jiang DengAbstract:Selenium (Se) is an essential nutrient for humans and all food-producing animal species. Nutritional deficiencies of Se and (or) vitamin E induce exudative diathesis, Nutritional pancreatic atrophy, and Nutritional Muscular Dystrophy in chicks. Although these diseases are presumably associated with the need of Se for the synthesis of the 21st amino acid, selenocysteine (Sec, U) in selenoproteins, metabolic functions of the 25 selenoproteins identified in avian species remain largely unknown. This paper reviews regulations of the whole selenogenome and selected selenoproteins by different concentrations and chemical forms of dietary Se and (or) vitamin E in various affected tissues. The avian selenogenome may be divided into 2 groups: responders and non-responders, based on its response to dietary Se and vitamin E changes. Mechanisms for the gene-, tissue-, and age-dependent responses and the correlation with the stress and cell death signaling are explored. Overall, this review intends to link the novel regulation and function of avian selenogenome to the protection by Se against oxidative insults associated with the classical Se/vitamin E deficiency diseases in chicks.
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selenoproteins protect against avian Nutritional Muscular Dystrophy by metabolizing peroxides and regulating redox apoptotic signaling
Free Radical Biology and Medicine, 2015Co-Authors: Jia-qiang Huang, Xin Gen Lei, Chen Xiao, Fazheng Ren, Yunyun JiangAbstract:Abstract Nutritional Muscular Dystrophy (NMD) of chicks is induced by dietary selenium (Se)/vitamin E (Vit. E) deficiencies and may be associated with oxidative cell damage. To reveal the underlying mechanisms related to the presumed oxidative cell damage, we fed four groups of 1-day-old broiler chicks ( n = 40/group) with a basal diet (BD; 10 μg Se/kg; no Vit. E added, −Se −Vit. E) or the BD plus all-rac-α-tocopheryl acetate at 50 mg/kg (−Se +Vit. E), Se (as sodium selenite) at 0.3 mg/kg (+Se −Vit. E), or both of these nutrients (+Se +Vit. E) for 6 weeks. High incidences of NMD (93%) and mortality (36%) of the chicks were induced by the BD, starting at week 3. Dietary Se deficiency alone also induced muscle fiber rupture and coagulation necrosis in the pectoral muscle of chicks at week 3 and thereafter, with increased ( P P P 0.05) glutathione peroxidase activities in the muscle. To link these oxidative damages of the muscle cells to the Se-deficiency-induced NMD, we first determined gene expression of the potential 26 selenoproteins in the muscle of the chicks at week 2 before the onset of symptoms. Compared with the +Se chicks, the −Se chicks had lower ( P Gpx1, Gpx3, Gpx4, Sepp1, Selo, Selk, Selu, Selh, Selm, Sepw1, and Sep15 . The −Se chicks also had decreased ( P P P P
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selenoproteins protect against avian Nutritional Muscular Dystrophy by metabolizing peroxides and regulating redox apoptotic signaling
Free Radical Biology and Medicine, 2015Co-Authors: Jia-qiang Huang, Xin Gen Lei, Chen Xiao, Fazheng Ren, Yunyun JiangAbstract:Nutritional Muscular Dystrophy (NMD) of chicks is induced by dietary selenium (Se)/vitamin E (Vit. E) deficiencies and may be associated with oxidative cell damage. To reveal the underlying mechanisms related to the presumed oxidative cell damage, we fed four groups of 1-day-old broiler chicks (n = 40/group) with a basal diet (BD; 10 μg Se/kg; no Vit. E added, -Se -Vit. E) or the BD plus all-rac-α-tocopheryl acetate at 50mg/kg (-Se +Vit. E), Se (as sodium selenite) at 0.3mg/kg (+Se -Vit. E), or both of these nutrients (+Se +Vit. E) for 6 weeks. High incidences of NMD (93%) and mortality (36%) of the chicks were induced by the BD, starting at week 3. Dietary Se deficiency alone also induced muscle fiber rupture and coagulation necrosis in the pectoral muscle of chicks at week 3 and thereafter, with increased (P < 0.05) malondialdehyde, decreased (P < 0.05) total antioxidant capacity, and diminished (P < 0.05) glutathione peroxidase activities in the muscle. To link these oxidative damages of the muscle cells to the Se-deficiency-induced NMD, we first determined gene expression of the potential 26 selenoproteins in the muscle of the chicks at week 2 before the onset of symptoms. Compared with the +Se chicks, the -Se chicks had lower (P < 0.05) muscle mRNA levels of Gpx1, Gpx3, Gpx4, Sepp1, Selo, Selk, Selu, Selh, Selm, Sepw1, and Sep15. The -Se chicks also had decreased (P < 0.05) production of 6 selenoproteins (long-form selenoprotein P (SelP-L), GPx1, GPx4, Sep15, SelW, and SelN), but increased levels (P < 0.05) of the short-form selenoprotein P in muscle at weeks 2 and 4. Dietary Se deficiency elevated (P < 0.05) muscle p53, cleaved caspase 3, cleaved caspase 9, cyclooxygenase 2 (COX2), focal adhesion kinase (FAK), phosphatidylinositol 3-kinase (PI3K), phospho-Akt, nuclear factor-κB (NF-κB), p38 mitogen-activated protein kinase (p38 MAPK), phospho-p38 MAPK, phospho-JNK, and phospho-ERK and decreased (P < 0.05) muscle procaspase 3, procaspase 9, and NF-κB inhibitor α. In conclusion, the downregulation of SelP-L, GPx1, GPx4, Sep15, SelW, and SelN by dietary Se deficiency might account for induced oxidative stress and the subsequent peroxidative damage of chick muscle cells via the activation of the p53/caspase 9/caspase 3, COX2/FAK/PI3K/Akt/NF-κB, and p38 MAPK/JNK/ERK signaling pathways. Metabolism of peroxides and redox regulation are likely to be the mechanisms whereby these selenoproteins prevented the onset of NMD in chicks.
Jia-qiang Huang - One of the best experts on this subject based on the ideXlab platform.
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avian selenogenome response to dietary se and vitamin e deficiency and supplementation
Poultry Science, 2019Co-Authors: Lvhui Sun, Jia-qiang Huang, Xin Gen Lei, Jiang DengAbstract:Selenium (Se) is an essential nutrient for humans and all food-producing animal species. Nutritional deficiencies of Se and (or) vitamin E induce exudative diathesis, Nutritional pancreatic atrophy, and Nutritional Muscular Dystrophy in chicks. Although these diseases are presumably associated with the need of Se for the synthesis of the 21st amino acid, selenocysteine (Sec, U) in selenoproteins, metabolic functions of the 25 selenoproteins identified in avian species remain largely unknown. This paper reviews regulations of the whole selenogenome and selected selenoproteins by different concentrations and chemical forms of dietary Se and (or) vitamin E in various affected tissues. The avian selenogenome may be divided into 2 groups: responders and non-responders, based on its response to dietary Se and vitamin E changes. Mechanisms for the gene-, tissue-, and age-dependent responses and the correlation with the stress and cell death signaling are explored. Overall, this review intends to link the novel regulation and function of avian selenogenome to the protection by Se against oxidative insults associated with the classical Se/vitamin E deficiency diseases in chicks.
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selenoproteins protect against avian Nutritional Muscular Dystrophy by metabolizing peroxides and regulating redox apoptotic signaling
Free Radical Biology and Medicine, 2015Co-Authors: Jia-qiang Huang, Xin Gen Lei, Chen Xiao, Fazheng Ren, Yunyun JiangAbstract:Abstract Nutritional Muscular Dystrophy (NMD) of chicks is induced by dietary selenium (Se)/vitamin E (Vit. E) deficiencies and may be associated with oxidative cell damage. To reveal the underlying mechanisms related to the presumed oxidative cell damage, we fed four groups of 1-day-old broiler chicks ( n = 40/group) with a basal diet (BD; 10 μg Se/kg; no Vit. E added, −Se −Vit. E) or the BD plus all-rac-α-tocopheryl acetate at 50 mg/kg (−Se +Vit. E), Se (as sodium selenite) at 0.3 mg/kg (+Se −Vit. E), or both of these nutrients (+Se +Vit. E) for 6 weeks. High incidences of NMD (93%) and mortality (36%) of the chicks were induced by the BD, starting at week 3. Dietary Se deficiency alone also induced muscle fiber rupture and coagulation necrosis in the pectoral muscle of chicks at week 3 and thereafter, with increased ( P P P 0.05) glutathione peroxidase activities in the muscle. To link these oxidative damages of the muscle cells to the Se-deficiency-induced NMD, we first determined gene expression of the potential 26 selenoproteins in the muscle of the chicks at week 2 before the onset of symptoms. Compared with the +Se chicks, the −Se chicks had lower ( P Gpx1, Gpx3, Gpx4, Sepp1, Selo, Selk, Selu, Selh, Selm, Sepw1, and Sep15 . The −Se chicks also had decreased ( P P P P
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selenoproteins protect against avian Nutritional Muscular Dystrophy by metabolizing peroxides and regulating redox apoptotic signaling
Free Radical Biology and Medicine, 2015Co-Authors: Jia-qiang Huang, Xin Gen Lei, Chen Xiao, Fazheng Ren, Yunyun JiangAbstract:Nutritional Muscular Dystrophy (NMD) of chicks is induced by dietary selenium (Se)/vitamin E (Vit. E) deficiencies and may be associated with oxidative cell damage. To reveal the underlying mechanisms related to the presumed oxidative cell damage, we fed four groups of 1-day-old broiler chicks (n = 40/group) with a basal diet (BD; 10 μg Se/kg; no Vit. E added, -Se -Vit. E) or the BD plus all-rac-α-tocopheryl acetate at 50mg/kg (-Se +Vit. E), Se (as sodium selenite) at 0.3mg/kg (+Se -Vit. E), or both of these nutrients (+Se +Vit. E) for 6 weeks. High incidences of NMD (93%) and mortality (36%) of the chicks were induced by the BD, starting at week 3. Dietary Se deficiency alone also induced muscle fiber rupture and coagulation necrosis in the pectoral muscle of chicks at week 3 and thereafter, with increased (P < 0.05) malondialdehyde, decreased (P < 0.05) total antioxidant capacity, and diminished (P < 0.05) glutathione peroxidase activities in the muscle. To link these oxidative damages of the muscle cells to the Se-deficiency-induced NMD, we first determined gene expression of the potential 26 selenoproteins in the muscle of the chicks at week 2 before the onset of symptoms. Compared with the +Se chicks, the -Se chicks had lower (P < 0.05) muscle mRNA levels of Gpx1, Gpx3, Gpx4, Sepp1, Selo, Selk, Selu, Selh, Selm, Sepw1, and Sep15. The -Se chicks also had decreased (P < 0.05) production of 6 selenoproteins (long-form selenoprotein P (SelP-L), GPx1, GPx4, Sep15, SelW, and SelN), but increased levels (P < 0.05) of the short-form selenoprotein P in muscle at weeks 2 and 4. Dietary Se deficiency elevated (P < 0.05) muscle p53, cleaved caspase 3, cleaved caspase 9, cyclooxygenase 2 (COX2), focal adhesion kinase (FAK), phosphatidylinositol 3-kinase (PI3K), phospho-Akt, nuclear factor-κB (NF-κB), p38 mitogen-activated protein kinase (p38 MAPK), phospho-p38 MAPK, phospho-JNK, and phospho-ERK and decreased (P < 0.05) muscle procaspase 3, procaspase 9, and NF-κB inhibitor α. In conclusion, the downregulation of SelP-L, GPx1, GPx4, Sep15, SelW, and SelN by dietary Se deficiency might account for induced oxidative stress and the subsequent peroxidative damage of chick muscle cells via the activation of the p53/caspase 9/caspase 3, COX2/FAK/PI3K/Akt/NF-κB, and p38 MAPK/JNK/ERK signaling pathways. Metabolism of peroxides and redox regulation are likely to be the mechanisms whereby these selenoproteins prevented the onset of NMD in chicks.
Romero Pérez Atmir - One of the best experts on this subject based on the ideXlab platform.
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Diseño y evaluación de nanoparticulas de selenito de sodio para su uso en rumiantes
Colegio de Postgraduados (COLPOS), 2012Co-Authors: Romero Pérez AtmirAbstract:El selenito de sodio, el suplemento de selenio mas usado en rumiantes en la prevención de la deficiencia del elemento y las enfermedades resultantes, fue encapsulado por nanoprecipitación y emulsión-evaporación en nanopartículas poliméricas. Fue evaluado el efecto del método de preparación de nanoparticulas, proporciones de polímeros (Eudragit RL 100 y RS 100) y solvente empleado (etanol y acetona), sobre las características fisicoquímicas (potencial z, índice de polidispersidad y porcentaje de encapsulación) y la morfología (tamaño de partícula y forma) de las nanopartículas. El tamaño de partícula obtenido presentó valores de 34.64 a 213.86 nm. Tanto el tamaño como el potencial z y el PDI se incrementaron (P < 0.05) cuando se utilizó el método de nanoprecipitación al igual que cuando se utilizó el solvente etanol. No se encontraron diferencias significativas (P > 0.05) para las diferentes proporciones de polímeros, probablemente porque las diferencias entre las proporciones no eran tan marcadas. Con el método de emulsión-evaporación se obtuvo un porcentaje de encapsulación de 26% mientras que con el método de nanoprecipitación la encapsulación fue de 78%. Las nanopartículas que se formaron con el método de nanoprecipitación presentaron una forma esférica con una gran variación en el tamaño, mientras que las observadas en el método emulsión-evaporación fueron tanto esféricas como irregulares con un tamaño de partícula más homogéneo. La liberación de selenio de las nanopartículas fue mayor en condiciones de pH acido. Esta condición puede representar una mejor disponibilidad del selenio a nivel intestinal. _________Sodium selenite, predominant selenium supplement for ruminants used in the prevention of selenium deficiency and the treatment of Nutritional Muscular Dystrophy (white muscle disease) and cardiac myopathy, was encapsulated by nanoprecipitation and emulsion-evaporation methods, within polymeric nanoparticles. The effect of methods, polymer proportion (Eudragit RL and RS) and solvent (ethanol and acetone) on the physicochemical (drug entrapment, polidispersity index (PDI) and z potential) and morphological characteristics (particle morphology and particle size) was evaluated. Particle size from each nanoparticle formulation ranged from 36.64 to 213.86 nm. Particle size, z potential and PDI increased when nanoprecipitation and ethanol were used. No significant differences were observed when different polymeric proportions were used. Selenium entrapment was 26% when emulsion-evaporation method was used and 78% with nanoprecipitation. Nanoparticles produced by nanoprecipitation were spherical and present a great variation in particle size, on the other hand, nanoparticles produced by emulsion-evaporation were spherical as well as amorphous and present a homogeneous nanopartcicle size distribution. The release of selenium from nanoparticles was higher in acid pH, this condition may represent a better availability of the mineral in the small intestine
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Diseño y evaluación de nanoparticulas de selenito de sodio para su uso en rumiantes
Colegio de Postgraduados (COLPOS), 2008Co-Authors: Romero Pérez AtmirAbstract:El selenito de sodio, el suplemento de selenio mas usado en rumiantes en la prevención de la deficiencia del elemento y las enfermedades resultantes, fue encapsulado por nanoprecipitación y emulsión-evaporación en nanopartículas poliméricas. Fue evaluado el efecto del método de preparación de nanoparticulas, proporciones de polímeros (Eudragit RL 100 y RS 100) y solvente empleado (etanol y acetona), sobre las características fisicoquímicas (potencial z, índice de polidispersidad y porcentaje de encapsulación) y la morfología (tamaño de partícula y forma) de las nanopartículas. El tamaño de partícula obtenido presentó valores de 34.64 a 213.86 nm. Tanto el tamaño como el potencial z y el PDI se incrementaron (P < 0.05) cuando se utilizó el método de nanoprecipitación al igual que cuando se utilizó el solvente etanol. No se encontraron diferencias significativas (P > 0.05) para las diferentes proporciones de polímeros, probablemente porque las diferencias entre las proporciones no eran tan marcadas. Con el método de emulsión-evaporación se obtuvo un porcentaje de encapsulación de 26% mientras que con el método de nanoprecipitación la encapsulación fue de 78%. Las nanopartículas que se formaron con el método de nanoprecipitación presentaron una forma esférica con una gran variación en el tamaño, mientras que las observadas en el método emulsión-evaporación fueron tanto esféricas como irregulares con un tamaño de partícula más homogéneo. La liberación de selenio de las nanopartículas fue mayor en condiciones de pH acido. Esta condición puede representar una mejor disponibilidad del selenio a nivel intestinal. _________Sodium selenite, predominant selenium supplement for ruminants used in the prevention of selenium deficiency and the treatment of Nutritional Muscular Dystrophy (white muscle disease) and cardiac myopathy, was encapsulated by nanoprecipitation and emulsion-evaporation methods, within polymeric nanoparticles. The effect of methods, polymer proportion (Eudragit RL and RS) and solvent (ethanol and acetone) on the physicochemical (drug entrapment, polidispersity index (PDI) and z potential) and morphological characteristics (particle morphology and particle size) was evaluated. Particle size from each nanoparticle formulation ranged from 36.64 to 213.86 nm. Particle size, z potential and PDI increased when nanoprecipitation and ethanol were used. No significant differences were observed when different polymeric proportions were used. Selenium entrapment was 26% when emulsion-evaporation method was used and 78% with nanoprecipitation. Nanoparticles produced by nanoprecipitation were spherical and present a great variation in particle size, on the other hand, nanoparticles produced by emulsion-evaporation were spherical as well as amorphous and present a homogeneous nanopartcicle size distribution. The release of selenium from nanoparticles was higher in acid pH, this condition may represent a better availability of the mineral in the small intestine.Tesis (Maestría en Ciencias, especialista en Ganadería).- Colegio de Postgraduados, 2008.CONACY
Yunyun Jiang - One of the best experts on this subject based on the ideXlab platform.
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selenoproteins protect against avian Nutritional Muscular Dystrophy by metabolizing peroxides and regulating redox apoptotic signaling
Free Radical Biology and Medicine, 2015Co-Authors: Jia-qiang Huang, Xin Gen Lei, Chen Xiao, Fazheng Ren, Yunyun JiangAbstract:Abstract Nutritional Muscular Dystrophy (NMD) of chicks is induced by dietary selenium (Se)/vitamin E (Vit. E) deficiencies and may be associated with oxidative cell damage. To reveal the underlying mechanisms related to the presumed oxidative cell damage, we fed four groups of 1-day-old broiler chicks ( n = 40/group) with a basal diet (BD; 10 μg Se/kg; no Vit. E added, −Se −Vit. E) or the BD plus all-rac-α-tocopheryl acetate at 50 mg/kg (−Se +Vit. E), Se (as sodium selenite) at 0.3 mg/kg (+Se −Vit. E), or both of these nutrients (+Se +Vit. E) for 6 weeks. High incidences of NMD (93%) and mortality (36%) of the chicks were induced by the BD, starting at week 3. Dietary Se deficiency alone also induced muscle fiber rupture and coagulation necrosis in the pectoral muscle of chicks at week 3 and thereafter, with increased ( P P P 0.05) glutathione peroxidase activities in the muscle. To link these oxidative damages of the muscle cells to the Se-deficiency-induced NMD, we first determined gene expression of the potential 26 selenoproteins in the muscle of the chicks at week 2 before the onset of symptoms. Compared with the +Se chicks, the −Se chicks had lower ( P Gpx1, Gpx3, Gpx4, Sepp1, Selo, Selk, Selu, Selh, Selm, Sepw1, and Sep15 . The −Se chicks also had decreased ( P P P P
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selenoproteins protect against avian Nutritional Muscular Dystrophy by metabolizing peroxides and regulating redox apoptotic signaling
Free Radical Biology and Medicine, 2015Co-Authors: Jia-qiang Huang, Xin Gen Lei, Chen Xiao, Fazheng Ren, Yunyun JiangAbstract:Nutritional Muscular Dystrophy (NMD) of chicks is induced by dietary selenium (Se)/vitamin E (Vit. E) deficiencies and may be associated with oxidative cell damage. To reveal the underlying mechanisms related to the presumed oxidative cell damage, we fed four groups of 1-day-old broiler chicks (n = 40/group) with a basal diet (BD; 10 μg Se/kg; no Vit. E added, -Se -Vit. E) or the BD plus all-rac-α-tocopheryl acetate at 50mg/kg (-Se +Vit. E), Se (as sodium selenite) at 0.3mg/kg (+Se -Vit. E), or both of these nutrients (+Se +Vit. E) for 6 weeks. High incidences of NMD (93%) and mortality (36%) of the chicks were induced by the BD, starting at week 3. Dietary Se deficiency alone also induced muscle fiber rupture and coagulation necrosis in the pectoral muscle of chicks at week 3 and thereafter, with increased (P < 0.05) malondialdehyde, decreased (P < 0.05) total antioxidant capacity, and diminished (P < 0.05) glutathione peroxidase activities in the muscle. To link these oxidative damages of the muscle cells to the Se-deficiency-induced NMD, we first determined gene expression of the potential 26 selenoproteins in the muscle of the chicks at week 2 before the onset of symptoms. Compared with the +Se chicks, the -Se chicks had lower (P < 0.05) muscle mRNA levels of Gpx1, Gpx3, Gpx4, Sepp1, Selo, Selk, Selu, Selh, Selm, Sepw1, and Sep15. The -Se chicks also had decreased (P < 0.05) production of 6 selenoproteins (long-form selenoprotein P (SelP-L), GPx1, GPx4, Sep15, SelW, and SelN), but increased levels (P < 0.05) of the short-form selenoprotein P in muscle at weeks 2 and 4. Dietary Se deficiency elevated (P < 0.05) muscle p53, cleaved caspase 3, cleaved caspase 9, cyclooxygenase 2 (COX2), focal adhesion kinase (FAK), phosphatidylinositol 3-kinase (PI3K), phospho-Akt, nuclear factor-κB (NF-κB), p38 mitogen-activated protein kinase (p38 MAPK), phospho-p38 MAPK, phospho-JNK, and phospho-ERK and decreased (P < 0.05) muscle procaspase 3, procaspase 9, and NF-κB inhibitor α. In conclusion, the downregulation of SelP-L, GPx1, GPx4, Sep15, SelW, and SelN by dietary Se deficiency might account for induced oxidative stress and the subsequent peroxidative damage of chick muscle cells via the activation of the p53/caspase 9/caspase 3, COX2/FAK/PI3K/Akt/NF-κB, and p38 MAPK/JNK/ERK signaling pathways. Metabolism of peroxides and redox regulation are likely to be the mechanisms whereby these selenoproteins prevented the onset of NMD in chicks.
Chen Xiao - One of the best experts on this subject based on the ideXlab platform.
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selenoproteins protect against avian Nutritional Muscular Dystrophy by metabolizing peroxides and regulating redox apoptotic signaling
Free Radical Biology and Medicine, 2015Co-Authors: Jia-qiang Huang, Xin Gen Lei, Chen Xiao, Fazheng Ren, Yunyun JiangAbstract:Abstract Nutritional Muscular Dystrophy (NMD) of chicks is induced by dietary selenium (Se)/vitamin E (Vit. E) deficiencies and may be associated with oxidative cell damage. To reveal the underlying mechanisms related to the presumed oxidative cell damage, we fed four groups of 1-day-old broiler chicks ( n = 40/group) with a basal diet (BD; 10 μg Se/kg; no Vit. E added, −Se −Vit. E) or the BD plus all-rac-α-tocopheryl acetate at 50 mg/kg (−Se +Vit. E), Se (as sodium selenite) at 0.3 mg/kg (+Se −Vit. E), or both of these nutrients (+Se +Vit. E) for 6 weeks. High incidences of NMD (93%) and mortality (36%) of the chicks were induced by the BD, starting at week 3. Dietary Se deficiency alone also induced muscle fiber rupture and coagulation necrosis in the pectoral muscle of chicks at week 3 and thereafter, with increased ( P P P 0.05) glutathione peroxidase activities in the muscle. To link these oxidative damages of the muscle cells to the Se-deficiency-induced NMD, we first determined gene expression of the potential 26 selenoproteins in the muscle of the chicks at week 2 before the onset of symptoms. Compared with the +Se chicks, the −Se chicks had lower ( P Gpx1, Gpx3, Gpx4, Sepp1, Selo, Selk, Selu, Selh, Selm, Sepw1, and Sep15 . The −Se chicks also had decreased ( P P P P
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selenoproteins protect against avian Nutritional Muscular Dystrophy by metabolizing peroxides and regulating redox apoptotic signaling
Free Radical Biology and Medicine, 2015Co-Authors: Jia-qiang Huang, Xin Gen Lei, Chen Xiao, Fazheng Ren, Yunyun JiangAbstract:Nutritional Muscular Dystrophy (NMD) of chicks is induced by dietary selenium (Se)/vitamin E (Vit. E) deficiencies and may be associated with oxidative cell damage. To reveal the underlying mechanisms related to the presumed oxidative cell damage, we fed four groups of 1-day-old broiler chicks (n = 40/group) with a basal diet (BD; 10 μg Se/kg; no Vit. E added, -Se -Vit. E) or the BD plus all-rac-α-tocopheryl acetate at 50mg/kg (-Se +Vit. E), Se (as sodium selenite) at 0.3mg/kg (+Se -Vit. E), or both of these nutrients (+Se +Vit. E) for 6 weeks. High incidences of NMD (93%) and mortality (36%) of the chicks were induced by the BD, starting at week 3. Dietary Se deficiency alone also induced muscle fiber rupture and coagulation necrosis in the pectoral muscle of chicks at week 3 and thereafter, with increased (P < 0.05) malondialdehyde, decreased (P < 0.05) total antioxidant capacity, and diminished (P < 0.05) glutathione peroxidase activities in the muscle. To link these oxidative damages of the muscle cells to the Se-deficiency-induced NMD, we first determined gene expression of the potential 26 selenoproteins in the muscle of the chicks at week 2 before the onset of symptoms. Compared with the +Se chicks, the -Se chicks had lower (P < 0.05) muscle mRNA levels of Gpx1, Gpx3, Gpx4, Sepp1, Selo, Selk, Selu, Selh, Selm, Sepw1, and Sep15. The -Se chicks also had decreased (P < 0.05) production of 6 selenoproteins (long-form selenoprotein P (SelP-L), GPx1, GPx4, Sep15, SelW, and SelN), but increased levels (P < 0.05) of the short-form selenoprotein P in muscle at weeks 2 and 4. Dietary Se deficiency elevated (P < 0.05) muscle p53, cleaved caspase 3, cleaved caspase 9, cyclooxygenase 2 (COX2), focal adhesion kinase (FAK), phosphatidylinositol 3-kinase (PI3K), phospho-Akt, nuclear factor-κB (NF-κB), p38 mitogen-activated protein kinase (p38 MAPK), phospho-p38 MAPK, phospho-JNK, and phospho-ERK and decreased (P < 0.05) muscle procaspase 3, procaspase 9, and NF-κB inhibitor α. In conclusion, the downregulation of SelP-L, GPx1, GPx4, Sep15, SelW, and SelN by dietary Se deficiency might account for induced oxidative stress and the subsequent peroxidative damage of chick muscle cells via the activation of the p53/caspase 9/caspase 3, COX2/FAK/PI3K/Akt/NF-κB, and p38 MAPK/JNK/ERK signaling pathways. Metabolism of peroxides and redox regulation are likely to be the mechanisms whereby these selenoproteins prevented the onset of NMD in chicks.