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10.1016/j.arcmed.2004.01.001 http://scihub22266oqcxt.onion/10.1016/j.arcmed.2004.01.001 15163458!ä!15163458 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 280.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Arch+Med+Res 2004 ; 35 (3): 185-93 Nephropedia Template TP {{tp|p=15163458|t=2004. Transition metal-induced apoptosis in lymphocytes via hydroxyl radical generation, mitochondria dysfunction, and caspase-3 activation: an in vitro model for neurodegeneration |pdf=|usr=}}{{15163458}} gab.com Text Transition metal-induced apoptosis in lymphocytes via hydroxyl radical generation, mitochondria dysfunction, and caspase-3 activation: an in vitro model for neurodegeneration JO: Arch Med Res http://www.kidney.de/pget.php?&tw=1&pmid=15163458 #FOAvip BACKGROUND: Redox transition metals have been implicated as crucial players in pathogenesis of neurodegenerative diseases. Intracellular signaling mechanism(s) responsible for oxidative stress and death in single-cell model exposed to metals has not yet been fully elucidated. The objective of the study was to determine the mechanism by which metals induced apoptosis in human peripheral blood lymphocytes (PBL). METHODS: PBL were exposed to 50, 100, 250, 500, and 1,000 microM (Fe2+), (Mn2+), (Cu2+), and (Zn2+)-(SO4). Apoptotic/necrotic morphology was assessed with acridine orange/ethidium bromide staining. Further evaluations comprised production of H2O2, generation of hydroxyl radical (.OH), disruption of mitochondrial transmembrane potential (DeltaPsim), caspase-3 activation, and activation of NF-kappaB and p53 transcriptional factors. RESULTS: Morphologic analysis showed that 500 microM provoked maximal percentage of apoptosis (22-30% AO/EB) and minimal necrosis (3-7%), whereas low concentrations were innocuous but 1,000 microM induced mainly necrosis (>40% AO/EB). Metals generated both H2O2 and (.OH) by Fenton reaction. Hydroxyl scavengers protected PBL from metal-induced apoptosis. All metals induced mitochondrial depolarization (17-62% nonfluorescent cells) and activated caspase-3 concomitantly with apoptotic morphology (25-32% AO/EB) at 24 h, and neither NF-kappaB nor p53 transcription factor showed activation. CONCLUSIONS: This study provides evidence that redox-active (Fe2+), (Mn2+), (Cu2+), and (Zn2+) ion-induced apoptosis in PBL by (H2O2)/(.OH) generation, resulting in mitochondria depolarization, caspase-3 activation, and nuclear fragmentation independent of NF-kappaB and p53 transcription factors activation. Our data highlight the potential use of lymphocytes as a model to screen antioxidant strategies designed to remove H2O2/.OH associated with metal-catalyzed reactions in neurodegenerative disorders. Twit Text FOAVip Transition metal-induced apoptosis in lymphocytes via hydroxyl radical generation, mitochondria dysfunction, and caspase-3 activation: an in vitro model for neurodegeneration ????Arch Med Res http://www.kidney.de/pget.php?&tw=1&pmid=15163458 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=15163458 #FOAvip English Wikipedia <ref>{{Cite pmid|15163458}}</ref> Transition metal-induced apoptosis in lymphocytes via hydroxyl radical generation, mitochondria dysfunction, and caspase-3 activation: an in vitro model for neurodegeneration #MMPMID15163458 Jimenez Del Rio M; Velez-Pardo C Arch Med Res 2004[May]; 35 (3): 185-93 PMID15163458show ga BACKGROUND: Redox transition metals have been implicated as crucial players in pathogenesis of neurodegenerative diseases. Intracellular signaling mechanism(s) responsible for oxidative stress and death in single-cell model exposed to metals has not yet been fully elucidated. The objective of the study was to determine the mechanism by which metals induced apoptosis in human peripheral blood lymphocytes (PBL). METHODS: PBL were exposed to 50, 100, 250, 500, and 1,000 microM (Fe2+), (Mn2+), (Cu2+), and (Zn2+)-(SO4). Apoptotic/necrotic morphology was assessed with acridine orange/ethidium bromide staining. Further evaluations comprised production of H2O2, generation of hydroxyl radical (.OH), disruption of mitochondrial transmembrane potential (DeltaPsim), caspase-3 activation, and activation of NF-kappaB and p53 transcriptional factors. RESULTS: Morphologic analysis showed that 500 microM provoked maximal percentage of apoptosis (22-30% AO/EB) and minimal necrosis (3-7%), whereas low concentrations were innocuous but 1,000 microM induced mainly necrosis (>40% AO/EB). Metals generated both H2O2 and (.OH) by Fenton reaction. Hydroxyl scavengers protected PBL from metal-induced apoptosis. All metals induced mitochondrial depolarization (17-62% nonfluorescent cells) and activated caspase-3 concomitantly with apoptotic morphology (25-32% AO/EB) at 24 h, and neither NF-kappaB nor p53 transcription factor showed activation. CONCLUSIONS: This study provides evidence that redox-active (Fe2+), (Mn2+), (Cu2+), and (Zn2+) ion-induced apoptosis in PBL by (H2O2)/(.OH) generation, resulting in mitochondria depolarization, caspase-3 activation, and nuclear fragmentation independent of NF-kappaB and p53 transcription factors activation. Our data highlight the potential use of lymphocytes as a model to screen antioxidant strategies designed to remove H2O2/.OH associated with metal-catalyzed reactions in neurodegenerative disorders. |*Apoptosis[MESH] |*Hydroxyl Radical[MESH] |Adult[MESH] |Antioxidants/pharmacology[MESH] |Caspase 3[MESH] |Caspases/metabolism[MESH] |Cell Nucleus/metabolism[MESH] |Copper/metabolism[MESH] |Enzyme Activation[MESH] |Free Radicals[MESH] |Humans[MESH] |Hydrogen Peroxide/pharmacology[MESH] |Immunohistochemistry[MESH] |Intracellular Membranes/metabolism[MESH] |Ions[MESH] |Iron/metabolism[MESH] |Lymphocytes/metabolism/*pathology[MESH] |Magnesium/metabolism[MESH] |Male[MESH] |Membrane Potentials[MESH] |Mitochondria/metabolism[MESH] |Models, Biological[MESH] |NF-kappa B/metabolism[MESH] |Necrosis[MESH] |Neurodegenerative Diseases/pathology[MESH] |Oxidation-Reduction[MESH] |Oxidative Stress[MESH] |Reactive Oxygen Species[MESH] |Signal Transduction[MESH] |Transcription Factors/metabolism[MESH] |Tumor Suppressor Protein p53/metabolism[MESH]Transition metal-induced apoptosis in lymphocytes via hydroxyl radical(epmc).pdf DeepDyve Pubget Overpricing