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10.1111/j.1742-7843.2009.00391.x http://scihub22266oqcxt.onion/10.1111/j.1742-7843.2009.00391.x 19413654!ä!19413654 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Basic+Clin+Pharmacol+Toxicol 2009 ; 104 (5): 345-51 Nephropedia Template TP {{tp|p=19413654|t=2009. Cadmium-induced cytosolic Ca2+ elevation and subsequent apoptosis in renal tubular cells |pdf=|usr=}}{{19413654}} gab.com Text Cadmium-induced cytosolic Ca2+ elevation and subsequent apoptosis in renal tubular cells JO: Basic Clin Pharmacol Toxicol http://www.kidney.de/pget.php?&tw=1&pmid=19413654 #FOAvip Cadmium (Cd2+) is an industrial and environmental metal. The effect of Cd2+ on intracellular free-Ca2+ levels ([Ca2+](i)) and viability in Madin Darby canine kidney cells was explored. Cd2+increased [Ca2+](i) in a concentration-dependent manner with an EC50 of 85 microM. Cd2+-induced Mn2+ entry demonstrated Ca2+ influx. Removal of extracellular Ca2+ decreased the [Ca2+](i) signal by 60%. The [Ca2+](i) signal was inhibited by La3+ but not by L-type Ca2+ channel blockers. In Ca2+-free medium, Cd2+-induced [Ca2+]i signal was abolished by pre-treatment with 1 microM thapsigargin (an endoplasmic reticulum Ca2+pump inhibitor) and 2 microM carbonylcyanide m-chlorophenylhydrazone (CCCP; a mitochondrial uncoupler). Cd2+-induced Ca2+ release was not altered by inhibition of phospholipase C. At concentrations between 10 and 100 microM, Cd2+killed cells in a concentration-dependent manner. The cytotoxic effect of 100 microM Cd2+was reversed by pre-chelating cytosolic Ca2+with BAPTA. Cd2+-induced apoptosis was demonstrated by propidium iodide. Collectively, this study shows that Cd2+ induced a [Ca2+](i) increase in Madin Darby canine kidney cells via evoking Ca2+ entry through non-selective Ca2+ channels, and releasing stored Ca2+ from endoplasmic reticulum and mitochondria in a phospholipase C-independent manner. Twit Text FOAVip Cadmium-induced cytosolic Ca2+ elevation and subsequent apoptosis in renal tubular cells ????Basic Clin Pharmacol Toxicol http://www.kidney.de/pget.php?&tw=1&pmid=19413654 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19413654 #FOAvip English Wikipedia <ref>{{Cite pmid|19413654}}</ref> Cadmium-induced cytosolic Ca2+ elevation and subsequent apoptosis in renal tubular cells #MMPMID19413654 Yeh JH; Huang CC; Yeh MY; Wang JS; Lee JK; Jan CR Basic Clin Pharmacol Toxicol 2009[May]; 104 (5): 345-51 PMID19413654show ga Cadmium (Cd2+) is an industrial and environmental metal. The effect of Cd2+ on intracellular free-Ca2+ levels ([Ca2+](i)) and viability in Madin Darby canine kidney cells was explored. Cd2+increased [Ca2+](i) in a concentration-dependent manner with an EC50 of 85 microM. Cd2+-induced Mn2+ entry demonstrated Ca2+ influx. Removal of extracellular Ca2+ decreased the [Ca2+](i) signal by 60%. The [Ca2+](i) signal was inhibited by La3+ but not by L-type Ca2+ channel blockers. In Ca2+-free medium, Cd2+-induced [Ca2+]i signal was abolished by pre-treatment with 1 microM thapsigargin (an endoplasmic reticulum Ca2+pump inhibitor) and 2 microM carbonylcyanide m-chlorophenylhydrazone (CCCP; a mitochondrial uncoupler). Cd2+-induced Ca2+ release was not altered by inhibition of phospholipase C. At concentrations between 10 and 100 microM, Cd2+killed cells in a concentration-dependent manner. The cytotoxic effect of 100 microM Cd2+was reversed by pre-chelating cytosolic Ca2+with BAPTA. Cd2+-induced apoptosis was demonstrated by propidium iodide. Collectively, this study shows that Cd2+ induced a [Ca2+](i) increase in Madin Darby canine kidney cells via evoking Ca2+ entry through non-selective Ca2+ channels, and releasing stored Ca2+ from endoplasmic reticulum and mitochondria in a phospholipase C-independent manner. |Animals[MESH] |Apoptosis/*drug effects[MESH] |Cadmium Compounds/*toxicity[MESH] |Calcium Channel Blockers/pharmacology[MESH] |Calcium/*metabolism[MESH] |Cell Survival/drug effects[MESH] |Cells, Cultured[MESH] |Cytosol/*drug effects/metabolism[MESH] |Dogs[MESH] |Environmental Pollutants/*toxicity[MESH] |Kidney Tubules/*drug effects/metabolism/pathology[MESH] |Magnesium/metabolism[MESH]Cadmium-induced cytosolic Ca2+ elevation and subsequent apoptosis in r(epmc).pdf DeepDyve Pubget Overpricing