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10.1016/j.freeradbiomed.2014.01.001 http://scihub22266oqcxt.onion/10.1016/j.freeradbiomed.2014.01.001 C3960325!3960325!24412858     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Free+Radic+Biol+Med 2014 ; 69 (ä): 403-16 Nephropedia Template TP {{tp|p=24412858|t=2014. Chronic Ethanol Ingestion Induces Oxidative Kidney Injury through Taurine-inhibitable Inflammation |pdf=|usr=}}{{24412858}} gab.com Text Chronic Ethanol Ingestion Induces Oxidative Kidney Injury through Taurine-inhibitable Inflammation JO: Free Radic Biol Med http://www.kidney.de/pget.php?&tw=1&pmid=24412858 #FOAvip Chronic ethanol ingestion mildly damages liver through oxidative stress and lipid oxidation, which is ameliorated by dietary supplementation with the anti-inflammatory ?-amino acid taurine. Kidney, like liver, expresses cytochrome P450 2E1 that catabolizes ethanol with free radical formation, and so also may be damaged by ethanol catabolism. Sudden loss of kidney function, and not liver disease itself, foreshadows mortality in patients with alcoholic hepatitis [J. Altamirano, Clin Gastroenterol Hepatol. 2012, 10:65]. We found ethanol ingestion in the Lieber-deCarli rat model increased kidney lipid oxidation, 4-hydroxynonenal protein adduction, and oxidatively truncated phospholipids that attract and activate leukocytes. Chronic ethanol ingestion increased myeloperoxidase-expressing cells in kidney and induced an inflammatory cell infiltrate. Apoptotic Terminal deoxynucleotidyl transferase Nick End Labeling (TUNEL)-positive cells and active caspase-3 increased in kidney after ethanol ingestion, with reduced filtration with increased circulating Blood Urea Nitrogen and creatinine. These events were accompanied by release of albumin, myeloperoxidase, and the Acute Kidney Injury biomarkers Kidney Injury Molecule-1 (KIM-1), Neutrophil Gelatinase-associated Lipocalin (NGAL), and Cystatin c to urine. Taurine sequesters HOCl from myeloperoxidase of activated leukocytes, and taurine supplementation reduced renal lipid oxidation, reduced leukocyte infiltration, and reduced the increase in myeloperoxidase-positive cells during ethanol feeding. Taurine supplementation also normalized circulating BUN and creatinine levels, and suppressed enhanced myeloperoxidase, albumin, KIM-1 and cystatin c in urine. Thus, chronic ethanol ingestion oxidatively damages kidney lipids and proteins, damages renal function, and induces Acute Kidney Injury through an inflammatory cell infiltrate. The anti-inflammatory nutraceutical taurine effectively interrupts this ethanol-induced inflammatory cycle in kidney. Twit Text FOAVip Chronic Ethanol Ingestion Induces Oxidative Kidney Injury through Taurine-inhibitable Inflammation ????Free Radic Biol Med http://www.kidney.de/pget.php?&tw=1&pmid=24412858 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24412858 #FOAvip English Wikipedia <ref>{{Cite pmid|24412858}}</ref> Chronic Ethanol Ingestion Induces Oxidative Kidney Injury through Taurine-inhibitable Inflammation #MMPMID24412858 Latchoumycandane C; Nagy LE; McIntyre TM Free Radic Biol Med 2014[Apr]; 69 (ä): 403-16 PMID24412858show ga Chronic ethanol ingestion mildly damages liver through oxidative stress and lipid oxidation, which is ameliorated by dietary supplementation with the anti-inflammatory ?-amino acid taurine. Kidney, like liver, expresses cytochrome P450 2E1 that catabolizes ethanol with free radical formation, and so also may be damaged by ethanol catabolism. Sudden loss of kidney function, and not liver disease itself, foreshadows mortality in patients with alcoholic hepatitis [J. Altamirano, Clin Gastroenterol Hepatol. 2012, 10:65]. We found ethanol ingestion in the Lieber-deCarli rat model increased kidney lipid oxidation, 4-hydroxynonenal protein adduction, and oxidatively truncated phospholipids that attract and activate leukocytes. Chronic ethanol ingestion increased myeloperoxidase-expressing cells in kidney and induced an inflammatory cell infiltrate. Apoptotic Terminal deoxynucleotidyl transferase Nick End Labeling (TUNEL)-positive cells and active caspase-3 increased in kidney after ethanol ingestion, with reduced filtration with increased circulating Blood Urea Nitrogen and creatinine. These events were accompanied by release of albumin, myeloperoxidase, and the Acute Kidney Injury biomarkers Kidney Injury Molecule-1 (KIM-1), Neutrophil Gelatinase-associated Lipocalin (NGAL), and Cystatin c to urine. Taurine sequesters HOCl from myeloperoxidase of activated leukocytes, and taurine supplementation reduced renal lipid oxidation, reduced leukocyte infiltration, and reduced the increase in myeloperoxidase-positive cells during ethanol feeding. Taurine supplementation also normalized circulating BUN and creatinine levels, and suppressed enhanced myeloperoxidase, albumin, KIM-1 and cystatin c in urine. Thus, chronic ethanol ingestion oxidatively damages kidney lipids and proteins, damages renal function, and induces Acute Kidney Injury through an inflammatory cell infiltrate. The anti-inflammatory nutraceutical taurine effectively interrupts this ethanol-induced inflammatory cycle in kidney. äChronic Ethanol Ingestion Induces Oxidative Kidney Injury through Taur(epmc).pdf DeepDyve Pubget Overpricing