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Prayad Pokethitiyook - One of the best experts on this subject based on the ideXlab platform.
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biochemical and histopathological effects of glyphosate herbicide on nile tilapia oreochromis niloticus
Environmental Toxicology, 2003Co-Authors: Wannee Jiraungkoorskul, E S Upatham, Maleeya Kruatrachue, Somphong Sahaphong, Suksiri Vichasrigrams, Prayad PokethitiyookAbstract:In Oreochromis niloticus that had been exposed for 3 months to sublethal concentrations (5 and 15 ppm) of the commercial glyphosate herbicide (C3H8NO5P) Roundup, the organs exhibited varying degrees of histopathological change. In the gills filament cell proliferation, lamellar cell hyperplasia, lamellar fusion, epithelial lifting, and aneurysm were observed. In the liver there were vacuolation of hepatocytes and nuclear Pyknosis. Kidney lesions consisted of dilation of Bowman's space and accumulation of hyaline droplets in the tubular epithelial cells. The structural damages could be correlated to the significant increase (p ≤ 0.05) in aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase activities in the second and third months of exposure. The results indicated that long-term exposure to glyphosate at sublethal concentrations had adverse effects on the histopathological and biochemical alterations of the fish. © 2003 Wiley Periodicals, Inc. Environ Toxicol 18: 260–267, 2003.
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biochemical and histopathological effects of glyphosate herbicide on nile tilapia oreochromis niloticus
Environmental Toxicology, 2003Co-Authors: Wannee Jiraungkoorskul, E S Upatham, Maleeya Kruatrachue, Somphong Sahaphong, Suksiri Vichasrigrams, Prayad PokethitiyookAbstract:In Oreochromis niloticus that had been exposed for 3 months to sublethal concentrations (5 and 15 ppm) of the commercial glyphosate herbicide (C(3)H(8)NO(5)P) Roundup, the organs exhibited varying degrees of histopathological change. In the gills filament cell proliferation, lamellar cell hyperplasia, lamellar fusion, epithelial lifting, and aneurysm were observed. In the liver there were vacuolation of hepatocytes and nuclear Pyknosis. Kidney lesions consisted of dilation of Bowman's space and accumulation of hyaline droplets in the tubular epithelial cells. The structural damages could be correlated to the significant increase (p term exposure to glyphosate at sublethal concentrations had adverse effects on the histopathological and biochemical alterations of the fish.
Wannee Jiraungkoorskul - One of the best experts on this subject based on the ideXlab platform.
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biochemical and histopathological effects of glyphosate herbicide on nile tilapia oreochromis niloticus
Environmental Toxicology, 2003Co-Authors: Wannee Jiraungkoorskul, E S Upatham, Maleeya Kruatrachue, Somphong Sahaphong, Suksiri Vichasrigrams, Prayad PokethitiyookAbstract:In Oreochromis niloticus that had been exposed for 3 months to sublethal concentrations (5 and 15 ppm) of the commercial glyphosate herbicide (C3H8NO5P) Roundup, the organs exhibited varying degrees of histopathological change. In the gills filament cell proliferation, lamellar cell hyperplasia, lamellar fusion, epithelial lifting, and aneurysm were observed. In the liver there were vacuolation of hepatocytes and nuclear Pyknosis. Kidney lesions consisted of dilation of Bowman's space and accumulation of hyaline droplets in the tubular epithelial cells. The structural damages could be correlated to the significant increase (p ≤ 0.05) in aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase activities in the second and third months of exposure. The results indicated that long-term exposure to glyphosate at sublethal concentrations had adverse effects on the histopathological and biochemical alterations of the fish. © 2003 Wiley Periodicals, Inc. Environ Toxicol 18: 260–267, 2003.
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biochemical and histopathological effects of glyphosate herbicide on nile tilapia oreochromis niloticus
Environmental Toxicology, 2003Co-Authors: Wannee Jiraungkoorskul, E S Upatham, Maleeya Kruatrachue, Somphong Sahaphong, Suksiri Vichasrigrams, Prayad PokethitiyookAbstract:In Oreochromis niloticus that had been exposed for 3 months to sublethal concentrations (5 and 15 ppm) of the commercial glyphosate herbicide (C(3)H(8)NO(5)P) Roundup, the organs exhibited varying degrees of histopathological change. In the gills filament cell proliferation, lamellar cell hyperplasia, lamellar fusion, epithelial lifting, and aneurysm were observed. In the liver there were vacuolation of hepatocytes and nuclear Pyknosis. Kidney lesions consisted of dilation of Bowman's space and accumulation of hyaline droplets in the tubular epithelial cells. The structural damages could be correlated to the significant increase (p term exposure to glyphosate at sublethal concentrations had adverse effects on the histopathological and biochemical alterations of the fish.
Ralf Gerhard - One of the best experts on this subject based on the ideXlab platform.
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Quantitative Phosphoproteome Analysis of Clostridioides difficile Toxin B Treated Human Epithelial Cells
'Frontiers Media SA', 2018Co-Authors: Johannes Junemann, Ralf Gerhard, Ingo Just, Andreas PichAbstract:The large clostridial glucosylating toxin B (TcdB) is a major virulence factor of the nosocomial pathogen Clostridioides difficile. TcdB inhibits small GTPases by glucosylation leading to impaired downstream signaling. TcdB also possesses a glucosyltransferase independent effect described as Pyknosis. To elucidate the impact of TcdB and its glucosylation-inactive mutant TcdBNXN on the kinome of human cells, SILAC labeled HEp-2 cells were treated with 2 nM TcdB for 8 h. Phosphopeptides were enriched using SCX chromatography, IMAC and TiO2 followed shotgun mass spectrometry analysis. Overall 4,197 phosphopeptides were identified; more than 1,200 phosphosites responded to treatment with TcdB or TcdBNXN. The data suggested that predominantly stress-activated MAPK-dependent signaling pathways were triggered by toxin B treatment
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Data_Sheet_2_Quantitative Phosphoproteome Analysis of Clostridioides difficile Toxin B Treated Human Epithelial Cells.xlsx
2018Co-Authors: Johannes Junemann, Ralf Gerhard, Ingo Just, Andreas PichAbstract:The large clostridial glucosylating toxin B (TcdB) is a major virulence factor of the nosocomial pathogen Clostridioides difficile. TcdB inhibits small GTPases by glucosylation leading to impaired downstream signaling. TcdB also possesses a glucosyltransferase independent effect described as Pyknosis. To elucidate the impact of TcdB and its glucosylation-inactive mutant TcdBNXN on the kinome of human cells, SILAC labeled HEp-2 cells were treated with 2 nM TcdB for 8 h. Phosphopeptides were enriched using SCX chromatography, IMAC and TiO2 followed shotgun mass spectrometry analysis. Overall 4,197 phosphopeptides were identified; more than 1,200 phosphosites responded to treatment with TcdB or TcdBNXN. The data suggested that predominantly stress-activated MAPK-dependent signaling pathways were triggered by toxin B treatment.
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pyknotic cell death induced by clostridium difficile tcdb chromatin condensation and nuclear blister are induced independently of the glucosyltransferase activity
Cellular Microbiology, 2014Co-Authors: Katharina Wohlan, Sebastian Goy, Alexandra Olling, Sangar Srivaratharajan, Helma Tatge, Harald Genth, Ralf GerhardAbstract:Summary TcdA and TcdB are the main pathogenicity factors of Clostridium difficile-associated diseases. Both toxins inhibit Rho GTPases, and consequently, apoptosis is induced in the affected cells. We found that TcdB at higher concentrations exhibits cytotoxic effects that are independent on Rho glucosylation. TcdB and the glucosyltransferase-deficient mutant TcdB D286/288N induced pyknotic cell death which was associated with chromatin condensation and reduced H3 phosphorylation. Affected cells showed ballooning of the nuclear envelope and loss of the integrity of the plasma membrane. Furthermore, pyknotic cells were positively stained with dihydroethidium indicating production of reactive oxygen species. In line with this, Pyknosis was reduced by apocynin, an inhibitor of the NADPH oxidase. Bafilomycin A1 prevented cytotoxic effects showing that the newly observed Pyknosis depends on intracellular action of TcdB rather than on a receptor-mediated effect. Blister formation and chromatin condensation was specifically induced by the glucosyltransferase domain of TcdB from strain VPI10473 since neither TcdBF from cdi1470 nor the chimera of TcdB harbouring the glucosyltransferase domain of TcdBF was able to induce these effects. In summary, TcdB induces two different and independent phenotypes: (i) cell rounding due to glucosylation of Rho GTPases and (ii) shrinkage of cells and nuclear blister induced by the high concentrations of TcdB independent of Rho glucosylation.
V H Perry - One of the best experts on this subject based on the ideXlab platform.
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astrocytosis microglia activation oligodendrocyte degeneration and Pyknosis following acute spinal cord injury
Experimental Neurology, 2004Co-Authors: Walace Gomesleal, D J Corkill, Marco Aurelio M Freire, C W Picancodiniz, V H PerryAbstract:Glial activation and degeneration are important outcomes in the pathophysiology of acute brain and spinal cord injury (SCI). Our main goal was to investigate the pattern of glial activation and degeneration during secondary degeneration in both gray matter (GM) and white matter (WM) following SCI. Adult rats were deeply anesthetized and injected with 20 nmol of N-methyl-d-aspartate (NMDA) into the ventral horn of rat spinal cord (SC) on T7. Animals were perfused after survival times of 1, 3, and 7 days. Ten-micrometer sections were submitted to immunocytochemistry for activated macrophages/microglia, astrocytes, oligodendrocytes, and myelin. Astrocyte activation was more intense in the vacuolated white matter than in gray matter and was first noticed in this former region. Microglial activation was more intense in the gray matter and was clear by 24 h following NMDA injection. Both astrocytosis and microglial activation were more intense in the later survival times. Conspicuous WM vacuolation was present mainly at the 3-day survival time and decreased by 7 days after the primary damage. Quantitative analysis revealed an increase in the number of pyknotic bodies mainly at the 7-day survival time in both ventral and lateral white matter. These pyknotic bodies were frequently found inside white matter vacuoles like for degenerating oligodendrocytes. These results suggest a differential pattern of astrocytosis and microglia activation for white and gray matter following SCI. This phenomenon can be related to the different pathological outcomes for this two SC regions following acute injury.
Suksiri Vichasrigrams - One of the best experts on this subject based on the ideXlab platform.
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biochemical and histopathological effects of glyphosate herbicide on nile tilapia oreochromis niloticus
Environmental Toxicology, 2003Co-Authors: Wannee Jiraungkoorskul, E S Upatham, Maleeya Kruatrachue, Somphong Sahaphong, Suksiri Vichasrigrams, Prayad PokethitiyookAbstract:In Oreochromis niloticus that had been exposed for 3 months to sublethal concentrations (5 and 15 ppm) of the commercial glyphosate herbicide (C3H8NO5P) Roundup, the organs exhibited varying degrees of histopathological change. In the gills filament cell proliferation, lamellar cell hyperplasia, lamellar fusion, epithelial lifting, and aneurysm were observed. In the liver there were vacuolation of hepatocytes and nuclear Pyknosis. Kidney lesions consisted of dilation of Bowman's space and accumulation of hyaline droplets in the tubular epithelial cells. The structural damages could be correlated to the significant increase (p ≤ 0.05) in aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase activities in the second and third months of exposure. The results indicated that long-term exposure to glyphosate at sublethal concentrations had adverse effects on the histopathological and biochemical alterations of the fish. © 2003 Wiley Periodicals, Inc. Environ Toxicol 18: 260–267, 2003.
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biochemical and histopathological effects of glyphosate herbicide on nile tilapia oreochromis niloticus
Environmental Toxicology, 2003Co-Authors: Wannee Jiraungkoorskul, E S Upatham, Maleeya Kruatrachue, Somphong Sahaphong, Suksiri Vichasrigrams, Prayad PokethitiyookAbstract:In Oreochromis niloticus that had been exposed for 3 months to sublethal concentrations (5 and 15 ppm) of the commercial glyphosate herbicide (C(3)H(8)NO(5)P) Roundup, the organs exhibited varying degrees of histopathological change. In the gills filament cell proliferation, lamellar cell hyperplasia, lamellar fusion, epithelial lifting, and aneurysm were observed. In the liver there were vacuolation of hepatocytes and nuclear Pyknosis. Kidney lesions consisted of dilation of Bowman's space and accumulation of hyaline droplets in the tubular epithelial cells. The structural damages could be correlated to the significant increase (p term exposure to glyphosate at sublethal concentrations had adverse effects on the histopathological and biochemical alterations of the fish.
