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Kuoping Huang - One of the best experts on this subject based on the ideXlab platform.
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glutathiolation of proteins by glutathione disulfide s oxide derived from s nitrosoglutathione modifications of rat brain neurogranin rc3 and neuromodulin gap 43
Journal of Biological Chemistry, 2001Co-Authors: Junfa Li, Freesia L Huang, Kuoping HuangAbstract:Abstract S-Nitrosoglutathione (GSNO) undergoes spontaneous degradation that generates several nitrogen-containing compounds and oxidized glutathione derivatives. We identified glutathione sulfonic acid, glutathione disulfideS-oxide (GS(O)SG), glutathione disulfideS-dioxide, and GSSG as the major decomposition products of GSNO. Each of these compounds and GSNO were tested for their efficacies to modify rat brain neurogranin/RC3 (Ng) and neuromodulin/GAP-43 (Nm). Among them, GS(O)SG was found to be the most potent in causing glutathiolation of both proteins; four glutathiones were incorporated into the four Cys residues of Ng, and two were incorporated into the two Cys residues of Nm. Ng and Nm are two in vivo substrates of protein kinase C; their phosphorylations by protein kinase C attenuate the binding affinities of both proteins for calmodulin. When compared with their respective unmodified forms, the glutathiolated Ng was a poorer substrate and glutathiolated Nm a better substrate for protein kinase C. Glutathiolation of these two proteins caused no change in their binding affinities for calmodulin. Treatment of [35S]cysteine-labeled rat brain slices with xanthine/xanthine oxidase or a combination of xanthine/xanthine oxidase with sodium nitroprusside resulted in an increase in cellular level of GS(O)SG. These treatments, as well as those by other oxidants, all resulted in an increase in thiolation of proteins; among them, thiolation of Ng was positively identified by immunoprecipitation. These results show that GS(O)SG is one of the most potent glutathiolating agents generated upon oxidative stress.
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glutathiolation of proteins by glutathione disulfides oxide derived from s nitrosoglutathione modifications of rat brain neurogranin rc3 and neuromodulin gap 43
Journal of Biological Chemistry, 2001Co-Authors: Freesia L Huang, Kuoping HuangAbstract:Abstract S-Nitrosoglutathione (GSNO) undergoes spontaneous degradation that generates several nitrogen-containing compounds and oxidized glutathione derivatives. We identified glutathione sulfonic acid, glutathione disulfideS-oxide (GS(O)SG), glutathione disulfideS-dioxide, and GSSG as the major decomposition products of GSNO. Each of these compounds and GSNO were tested for their efficacies to modify rat brain neurogranin/RC3 (Ng) and neuromodulin/GAP-43 (Nm). Among them, GS(O)SG was found to be the most potent in causing glutathiolation of both proteins; four glutathiones were incorporated into the four Cys residues of Ng, and two were incorporated into the two Cys residues of Nm. Ng and Nm are two in vivo substrates of protein kinase C; their phosphorylations by protein kinase C attenuate the binding affinities of both proteins for calmodulin. When compared with their respective unmodified forms, the glutathiolated Ng was a poorer substrate and glutathiolated Nm a better substrate for protein kinase C. Glutathiolation of these two proteins caused no change in their binding affinities for calmodulin. Treatment of [35S]cysteine-labeled rat brain slices with xanthine/xanthine oxidase or a combination of xanthine/xanthine oxidase with sodium nitroprusside resulted in an increase in cellular level of GS(O)SG. These treatments, as well as those by other oxidants, all resulted in an increase in thiolation of proteins; among them, thiolation of Ng was positively identified by immunoprecipitation. These results show that GS(O)SG is one of the most potent glutathiolating agents generated upon oxidative stress.
Lihai Shang - One of the best experts on this subject based on the ideXlab platform.
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mercury distribution and speciation in water and fish from abandoned hg mines in wanshan guizhou province china
Science of The Total Environment, 2009Co-Authors: Guangle Qiu, Xinbin Feng, Shaofeng Wang, Lihai ShangAbstract:Concentrations of total mercury (Hg-T), methylmercury (MeHg), and its speciation in water samples as well as fish collected from abandoned Hg mines in Wanshan, Guizhou province, China, were measured to show regional dispersion of Hg contaminations that are not well known. High Hg-T and MeHgT (total methylmercury) concentrations obtained in waters from mining areas, ranged from 15 to 9300 ng/l and 0.31 to 25 ng/l, respectively. MeHgT were not correlated with Hg-T, whereas, peak values in both cases were in accord with high concentrations of particulate fraction, which appeared to be enhanced during high-flow regime with ratios reaching to 99%. Elevated Hg concentrations in the particulate form indicated that particles released from Hg mining tailings (calcines) might be an important pathway of Hg to the aquatic system. The concentrations of total Hg in fish muscle were elevated ranging from 0.061 to 0.68 mg/kg, but MeHg were generally low ranging from 0.024 to 0.098 mg/kg with a mean ratio of 28%. The concentrations and distribution patterns of Hg in aquatic systems suggested derivation from historic Hg mining sites in the Wanshan area. (C) 2009 Elsevier B.V. All rights reserved.
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mercury and methylmercury in riparian soil sediments mine waste calcines and moss from abandoned hg mines in east guizhou province southwestern china
Applied Geochemistry, 2005Co-Authors: Xinbin Feng, Shaofeng Wang, Lihai ShangAbstract:Abstract Concentrations of total Hg and methylmercury (MMHg) in riparian soil, mine-waste calcine, sediment, and moss samples collected from abandoned Hg mines in Wanshan district, Guizhou province, China, were measured to show regional dispersion of Hg-contamination. High total Hg and MMHg concentrations obtained in riparian soils from mined areas, ranged from 5.1 to 790 mg kg −1 and 0.13 to 15 ng g −1 , respectively. However, total Hg and MMHg concentrations in the soils collected from control sites were significantly lower varying from 0.1 to 1.2 mg kg −1 and 0.10 to 1.6 ng g −1 , respectively. Total Hg and MMHg concentrations in sediments varied from 90 to 930 mg kg −1 and 3.0 to 20 ng g −1 , respectively. Total Hg concentrations in mine-waste calcines were highly elevated ranging from 5.7 to 4400 mg kg −1 , but MMHg concentrations were generally low ranging from 0.17 to 1.1 ng g −1 . Similar to the high Hg concentrations in soil and sediments, moss samples collected from rocks ranged from 1.0 to 95 mg kg −1 in total Hg and from 0.21 to 20 ng g −1 in MMHg. Elevated Hg concentrations in mosses suggest that atmospheric deposition might be an important pathway of Hg to the local terrestrial system. Moreover, the spatial distribution patterns of Hg contamination in the local environment suggest derivation from historic Hg mining sites in the Wanshan area.
Freesia L Huang - One of the best experts on this subject based on the ideXlab platform.
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glutathiolation of proteins by glutathione disulfide s oxide derived from s nitrosoglutathione modifications of rat brain neurogranin rc3 and neuromodulin gap 43
Journal of Biological Chemistry, 2001Co-Authors: Junfa Li, Freesia L Huang, Kuoping HuangAbstract:Abstract S-Nitrosoglutathione (GSNO) undergoes spontaneous degradation that generates several nitrogen-containing compounds and oxidized glutathione derivatives. We identified glutathione sulfonic acid, glutathione disulfideS-oxide (GS(O)SG), glutathione disulfideS-dioxide, and GSSG as the major decomposition products of GSNO. Each of these compounds and GSNO were tested for their efficacies to modify rat brain neurogranin/RC3 (Ng) and neuromodulin/GAP-43 (Nm). Among them, GS(O)SG was found to be the most potent in causing glutathiolation of both proteins; four glutathiones were incorporated into the four Cys residues of Ng, and two were incorporated into the two Cys residues of Nm. Ng and Nm are two in vivo substrates of protein kinase C; their phosphorylations by protein kinase C attenuate the binding affinities of both proteins for calmodulin. When compared with their respective unmodified forms, the glutathiolated Ng was a poorer substrate and glutathiolated Nm a better substrate for protein kinase C. Glutathiolation of these two proteins caused no change in their binding affinities for calmodulin. Treatment of [35S]cysteine-labeled rat brain slices with xanthine/xanthine oxidase or a combination of xanthine/xanthine oxidase with sodium nitroprusside resulted in an increase in cellular level of GS(O)SG. These treatments, as well as those by other oxidants, all resulted in an increase in thiolation of proteins; among them, thiolation of Ng was positively identified by immunoprecipitation. These results show that GS(O)SG is one of the most potent glutathiolating agents generated upon oxidative stress.
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glutathiolation of proteins by glutathione disulfides oxide derived from s nitrosoglutathione modifications of rat brain neurogranin rc3 and neuromodulin gap 43
Journal of Biological Chemistry, 2001Co-Authors: Freesia L Huang, Kuoping HuangAbstract:Abstract S-Nitrosoglutathione (GSNO) undergoes spontaneous degradation that generates several nitrogen-containing compounds and oxidized glutathione derivatives. We identified glutathione sulfonic acid, glutathione disulfideS-oxide (GS(O)SG), glutathione disulfideS-dioxide, and GSSG as the major decomposition products of GSNO. Each of these compounds and GSNO were tested for their efficacies to modify rat brain neurogranin/RC3 (Ng) and neuromodulin/GAP-43 (Nm). Among them, GS(O)SG was found to be the most potent in causing glutathiolation of both proteins; four glutathiones were incorporated into the four Cys residues of Ng, and two were incorporated into the two Cys residues of Nm. Ng and Nm are two in vivo substrates of protein kinase C; their phosphorylations by protein kinase C attenuate the binding affinities of both proteins for calmodulin. When compared with their respective unmodified forms, the glutathiolated Ng was a poorer substrate and glutathiolated Nm a better substrate for protein kinase C. Glutathiolation of these two proteins caused no change in their binding affinities for calmodulin. Treatment of [35S]cysteine-labeled rat brain slices with xanthine/xanthine oxidase or a combination of xanthine/xanthine oxidase with sodium nitroprusside resulted in an increase in cellular level of GS(O)SG. These treatments, as well as those by other oxidants, all resulted in an increase in thiolation of proteins; among them, thiolation of Ng was positively identified by immunoprecipitation. These results show that GS(O)SG is one of the most potent glutathiolating agents generated upon oxidative stress.
Borba, Fernanda Katharine De Souza Lins - One of the best experts on this subject based on the ideXlab platform.
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Estudo da atividade dos sulfatos de condroitina e glucosamina na formação de vasos sanguíneos em modelos in vitro e in vivo
Programa de Pós-Graduação em Biociência Animal, 2012Co-Authors: Borba, Fernanda Katharine De Souza LinsAbstract:Sulfato de glucosamina (SG) e Sulfato de condroitina (SC) são constituintes funcionais dos tecidos de vertebrados. O SG é um aminoaçúcar e o SC integra o grupo das glicosaminoglicanas (GAG). Estudos apontam propriedades antiinflamatórias do SC e SG, e demonstram ainda que essas substâncias promovem a cicatrização e a proliferação de fibroblastos, os quais expressam moléculas que atuam na formação de vasos sanguíneos (angiogênese). Os objetivos deste estudo foram avaliar a ação do SC e SG em modelos in vitro sobre a viabilidade (citotoxicidade pelo MTT), proliferação (incorporação por BrdU) e diferenciação (tubulogênese em suporte matrigel) na linhagem de células endoteliais de veia umbilical humana (HUVEC). Também se investigou a angiogênese in vivo: (1) em membranas anexas de embriões de Gallus domesticus (número de vasos corioalantóides - ensaio da CAM, e vitelínicos – ensaio da YSM; e análise por geometria fractal); (2) e no tecido subcutâneo de camundongos adultos por meio de quantificação da hemoglobina em implantes de Gelfoam. No ensaio com HUVEC, SC e SG (1-3000 g/mL) exerceram efeito citotóxico parcial (~50% de viabilidade), e somente nas respectivas maiores concentrações (3000 e 1000 g/mL). Verificou-se que o SC (3 g/mL), mas não o SG, estimulou a proliferação e a tubulogênese de HUVEC em 40% (p < 0,05) e em 64% (p < 0,05) respectivamente, em relação ao controle (meio RPMI-1640). Estes efeitos não diferiram estatisticamente dos 28% e 53%, respectivamente, promovidos pelo bem conhecido fator de crescimento angiogênico FGF-2 (50 ng/mL). No ensaio de vasculo-angiogênese na YSM de embriões de 2-4 dias de idade o SG (0,001-0,1mg/disco) principalmente, e o SC (0,030-0,1mg/disco) aumentaram o número de vasos em relação ao grupo controle (p < 0,05). Os efeitos da administração de SC e SG (0,1 mg/disco) não diferiram do observado no grupo tratado com 50 ng/mL de FGF-2. No ensaio de angiogênese na CAM de embriões de 6-8 dias de idade, ambos, SC e SG também elevaram o número de vasos em relação ao controle na concentração elevada de 2,0 mg/disco. Este efeito também não diferiu do observado no grupo exposto a 50 ng/mL de FGF- 2. O efeito pró-angiogênico do SC (2 mg/disco) na angiogênese embrionária foi confirmado na angiogênese avançada de camundongos adultos. Apenas o grupo que recebeu SC (2 mg/implante) mostrou um aumento significativo de vasos sanguíneos, expresso como conteúdo de hemoglobina (0,52 ± 0,08g/dL), comparado ao controle (veículo; PBS; 0,20 ± 0,07 g/dL). Este efeito pró-angiogênico não diferiu do obtido com FGF2 (0,53 ± 0.1g/dL). Os resultados in vitro e in vivo demonstram as propriedades pró-angiogênicas do SC e SG, contudo o SC (GAG) foi o mais efetivo nos ensaios. Como um constituinte de proteoglicanas, o SC sugere exercer seus efeitos pela interação com o FGF e outros fatores angiogênicos na matriz extracelular, estabilizando-os nos receptores e modulando assim, positivamente, o sinal pró-angiogênico nas células endoteliais. Embora mecanismos celulares subjacentes à atividade de SC e SG demandem mais estudos, evidencia-se um potencial papel terapêutico das duas substâncias em situações clínicas relacionadas à defasagem vascular.Chondroitin Sulfate (CS) and Glucosamine Sulfate (GS) are functional constituents of vertebrate tissues. GS is an amino sugar and CS is part of the glucosaminoglycans group (GAGs). Studies have suggested CS and GS to have anti-inflammatory properties, however it has also been shown that these compounds promote scarring and proliferation of fibroblasts, which express molecules important for blood vessel growth (angiogenesis). This study was aimed at evaluating the effects of CS and GS on in vitro models regarding cell viability (cytotoxicity - MTT), proliferation (BrdU incorporation) and differentiation (tubulogenesis in Matrigel support) on human umbilical vein endothelial cells (HUVEC line). In vivo angiogenesis was also evaluated in (1) extraembryonic membranes of Gallus domesticus (number of chorioallantoic vessels - CAM assay and vitelinic YSM assay; and fractal geometry analysis); (2) and subcutaneous tissue of adult mice (Mus muscullus) by hemoglobin quantification (Spectroscopy) in Gelfoam implants. In the HUVEC assay, both CS and GS (1-3000 g/mL) displayed partial cytotoxic effect (~50% viability), but only in the highest tested concentrations (3000 and 1000 g/mL). It was observed that CS (3 g/mL), but not GS, promoted proliferation and tubulogenesis of HUVEC in 40% (P < 0.05) and 64% (P < 0.05), respectively, relative to control (RPMI-1640 medium). These effects did not significantly differ from the respective 28% and 53% promoted by the well known angiogenic growth factor FGF-2 (50 ng/mL). In the in vivo vasculoangiogenesis YSM assay on 2 to 4-day old embryos, GS (0.001-0.1mg/disk) and, to a lesser extent, CS (0.030-0.1mg/disk) increased the amount of vessels relative to control (P < 0.05). The effects of administration of CS and GS (0.1mg/disk) did not differ from what was observed in groups treated with 50 ng/mL FGF2. In the CAM angiogenesis assay on 6 to 8-days old embryos, again both CS and GS increased the amount of vessels relative to control, but only in concentrations as high as 2.0 mg/disk. This effect was no different from what was observed in groups treated with 50 ng/mL FGF2. The pro-angiogenic effects of CS (2 mg/disk) in embryonary angiogenesis were confirmed in the advanced angiogenesis of mice: only the group treated with CS (2 mg/implant) displayed a significant increase in the amount of blood vessels, expressed as hemoglobin content (0.52 ± 0.08g/dL), relative to control (vehicle; PBS; 0.20 ± 0.07 g/dL). This pro-angiogenic effect was no different than that of FGF2 (0.53 ± 0.1g/dL). The in vitro and in vivo results indicate the pro-angiogenic properties of CS and GS. However, CS (GAG) was the more effective compound in the tests performed. As a constituent of proteoglycans, it is suggested that CS exerts its effects by interacting with FGF and other angiogenic factors in the extracellular matrix, stabilizing the receptor, and thus positively modulating the pro-angiogenic signal in endothelial cells. While the cellular mechanisms underlying CS and GS activity demand more specific research, there is an evident potential therapeutic use for both compounds in clinical situations, such as those related to vascular discrepancy.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPE
Fernanda Katharine De Souza Lins Borba - One of the best experts on this subject based on the ideXlab platform.
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Estudo da atividade dos sulfatos de condroitina e glucosamina na formação de vasos sanguíneos em modelos in vitro e in vivo.
Universidade Federal Rural de Pernambuco, 2012Co-Authors: Fernanda Katharine De Souza Lins BorbaAbstract:Sulfato de glucosamina (SG) e Sulfato de condroitina (SC) são constituintes funcionais dos tecidos de vertebrados. O SG é um aminoaçúcar e o SC integra o grupo das glicosaminoglicanas (GAG). Estudos apontam propriedades antiinflamatórias do SC e SG, e demonstram ainda que essas substâncias promovem a cicatrização e a proliferação de fibroblastos, os quais expressam moléculas que atuam na formação de vasos sanguíneos (angiogênese). Os objetivos deste estudo foram avaliar a ação do SC e SG em modelos in vitro sobre a viabilidade (citotoxicidade pelo MTT), proliferação (incorporação por BrdU) e diferenciação (tubulogênese em suporte matrigel) na linhagem de células endoteliais de veia umbilical humana (HUVEC). Também se investigou a angiogênese in vivo: (1) em membranas anexas de embriões de Gallus domesticus (número de vasos corioalantóides - ensaio da CAM, e vitelínicos ensaio da YSM; e análise por geometria fractal); (2) e no tecido subcutâneo de camundongos adultos por meio de quantificação da hemoglobina em implantes de Gelfoam. No ensaio com HUVEC, SC e SG (1-3000 g/mL) exerceram efeito citotóxico parcial (~50% de viabilidade), e somente nas respectivas maiores concentrações (3000 e 1000 g/mL). Verificou-se que o SC (3 g/mL), mas não o SG, estimulou a proliferação e a tubulogênese de HUVEC em 40% (p < 0,05) e em 64% (p < 0,05) respectivamente, em relação ao controle (meio RPMI-1640). Estes efeitos não diferiram estatisticamente dos 28% e 53%, respectivamente, promovidos pelo bem conhecido fator de crescimento angiogênico FGF-2 (50 ng/mL). No ensaio de vasculo-angiogênese na YSM de embriões de 2-4 dias de idade o SG (0,001-0,1mg/disco) principalmente, e o SC (0,030-0,1mg/disco) aumentaram o número de vasos em relação ao grupo controle (p < 0,05). Os efeitos da administração de SC e SG (0,1 mg/disco) não diferiram do observado no grupo tratado com 50 ng/mL de FGF-2. No ensaio de angiogênese na CAM de embriões de 6-8 dias de idade, ambos, SC e SG também elevaram o número de vasos em relação ao controle na concentração elevada de 2,0 mg/disco. Este efeito também não diferiu do observado no grupo exposto a 50 ng/mL de FGF- 2. O efeito pró-angiogênico do SC (2 mg/disco) na angiogênese embrionária foi confirmado na angiogênese avançada de camundongos adultos. Apenas o grupo que recebeu SC (2 mg/implante) mostrou um aumento significativo de vasos sanguíneos, expresso como conteúdo de hemoglobina (0,52 0,08g/dL), comparado ao controle (veículo; PBS; 0,20 0,07 g/dL). Este efeito pró-angiogênico não diferiu do obtido com FGF2 (0,53 0.1g/dL). Os resultados in vitro e in vivo demonstram as propriedades pró-angiogênicas do SC e SG, contudo o SC (GAG) foi o mais efetivo nos ensaios. Como um constituinte de proteoglicanas, o SC sugere exercer seus efeitos pela interação com o FGF e outros fatores angiogênicos na matriz extracelular, estabilizando-os nos receptores e modulando assim, positivamente, o sinal pró-angiogênico nas células endoteliais. Embora mecanismos celulares subjacentes à atividade de SC e SG demandem mais estudos, evidencia-se um potencial papel terapêutico das duas substâncias em situações clínicas relacionadas à defasagem vascular.Chondroitin Sulfate (CS) and Glucosamine Sulfate (GS) are functional constituents of vertebrate tissues. GS is an amino sugar and CS is part of the glucosaminoglycans group (GAGs). Studies have suggested CS and GS to have anti-inflammatory properties, however it has also been shown that these compounds promote scarring and proliferation of fibroblasts, which express molecules important for blood vessel growth (angiogenesis). This study was aimed at evaluating the effects of CS and GS on in vitro models regarding cell viability (cytotoxicity - MTT), proliferation (BrdU incorporation) and differentiation (tubulogenesis in Matrigel support) on human umbilical vein endothelial cells (HUVEC line). In vivo angiogenesis was also evaluated in (1) extraembryonic membranes of Gallus domesticus (number of chorioallantoic vessels - CAM assay and vitelinic YSM assay; and fractal geometry analysis); (2) and subcutaneous tissue of adult mice (Mus muscullus) by hemoglobin quantification (Spectroscopy) in Gelfoam implants. In the HUVEC assay, both CS and GS (1-3000 g/mL) displayed partial cytotoxic effect (~50% viability), but only in the highest tested concentrations (3000 and 1000 g/mL). It was observed that CS (3 g/mL), but not GS, promoted proliferation and tubulogenesis of HUVEC in 40% (P < 0.05) and 64% (P < 0.05), respectively, relative to control (RPMI-1640 medium). These effects did not significantly differ from the respective 28% and 53% promoted by the well known angiogenic growth factor FGF-2 (50 ng/mL). In the in vivo vasculoangiogenesis YSM assay on 2 to 4-day old embryos, GS (0.001-0.1mg/disk) and, to a lesser extent, CS (0.030-0.1mg/disk) increased the amount of vessels relative to control (P < 0.05). The effects of administration of CS and GS (0.1mg/disk) did not differ from what was observed in groups treated with 50 ng/mL FGF2. In the CAM angiogenesis assay on 6 to 8-days old embryos, again both CS and GS increased the amount of vessels relative to control, but only in concentrations as high as 2.0 mg/disk. This effect was no different from what was observed in groups treated with 50 ng/mL FGF2. The pro-angiogenic effects of CS (2 mg/disk) in embryonary angiogenesis were confirmed in the advanced angiogenesis of mice: only the group treated with CS (2 mg/implant) displayed a significant increase in the amount of blood vessels, expressed as hemoglobin content (0.52 0.08g/dL), relative to control (vehicle; PBS; 0.20 0.07 g/dL). This pro-angiogenic effect was no different than that of FGF2 (0.53 0.1g/dL). The in vitro and in vivo results indicate the pro-angiogenic properties of CS and GS. However, CS (GAG) was the more effective compound in the tests performed. As a constituent of proteoglycans, it is suggested that CS exerts its effects by interacting with FGF and other angiogenic factors in the extracellular matrix, stabilizing the receptor, and thus positively modulating the pro-angiogenic signal in endothelial cells. While the cellular mechanisms underlying CS and GS activity demand more specific research, there is an evident potential therapeutic use for both compounds in clinical situations, such as those related to vascular discrepancy