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10.1196/annals.1433.029 http://scihub22266oqcxt.onion/10.1196/annals.1433.029 18448828!ä!18448828 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       Ann+N+Y+Acad+Sci 2008 ; 1126 (ä): 265-7 Nephropedia Template TP {{tp|p=18448828|t=2008. Pathophysiological role of the glyoxalase system in renal hypoxic injury |pdf=|usr=}}{{18448828}} gab.com Text Pathophysiological role of the glyoxalase system in renal hypoxic injury JO: Ann N Y Acad Sci http://www.kidney.de/pget.php?&tw=1&pmid=18448828 #FOAvip Methylglyoxal (MG), a reactive dicarbonyl compound mainly produced by metabolic pathways, such as glycolysis, binds to proteins or nucleic acids and forms advanced glycation end products. MG is efficiently metabolized by the glyoxalase system where MG is converted by glyoxalase I (GLO I) to S-D-lactoylglutathione. Although the glyoxalase system has been shown to play a pathological role in various diseases, including diabetic complications, its detailed pathophysiological function remains to be elucidated. We are interested in renal hypoxic diseases, but very little information is available regarding the association between the glyoxalase system and renal hypoxic diseases. Therefore, we investigated the biological role of GLO I in renal hypoxic diseases by using the rat ischemia/reperfusion (I/R) injury model. I/R induced the reduction of renal GLO I activity associated with morphological changes and renal dysfunction. Interestingly, the rats that overexpress human GLO I (GLO I Tg rats) showed amelioration of these manifestations in renal I/R (e.g., improvement of the tubulointerstitial injury and renal function). Accumulation of renal MG adducts, carboxyethyllysine, induced by I/R also decreased in GLO I Tg rats compared to wild-type rats. These results demonstrate that GLO I has renoprotective effects in I/R injury via reduction of protein modification by MG. Twit Text FOAVip Pathophysiological role of the glyoxalase system in renal hypoxic injury ????Ann N Y Acad Sci http://www.kidney.de/pget.php?&tw=1&pmid=18448828 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=18448828 #FOAvip English Wikipedia <ref>{{Cite pmid|18448828}}</ref> Pathophysiological role of the glyoxalase system in renal hypoxic injury #MMPMID18448828 Kumagai T; Nangaku M; Inagi R Ann N Y Acad Sci 2008[Apr]; 1126 (ä): 265-7 PMID18448828show ga Methylglyoxal (MG), a reactive dicarbonyl compound mainly produced by metabolic pathways, such as glycolysis, binds to proteins or nucleic acids and forms advanced glycation end products. MG is efficiently metabolized by the glyoxalase system where MG is converted by glyoxalase I (GLO I) to S-D-lactoylglutathione. Although the glyoxalase system has been shown to play a pathological role in various diseases, including diabetic complications, its detailed pathophysiological function remains to be elucidated. We are interested in renal hypoxic diseases, but very little information is available regarding the association between the glyoxalase system and renal hypoxic diseases. Therefore, we investigated the biological role of GLO I in renal hypoxic diseases by using the rat ischemia/reperfusion (I/R) injury model. I/R induced the reduction of renal GLO I activity associated with morphological changes and renal dysfunction. Interestingly, the rats that overexpress human GLO I (GLO I Tg rats) showed amelioration of these manifestations in renal I/R (e.g., improvement of the tubulointerstitial injury and renal function). Accumulation of renal MG adducts, carboxyethyllysine, induced by I/R also decreased in GLO I Tg rats compared to wild-type rats. These results demonstrate that GLO I has renoprotective effects in I/R injury via reduction of protein modification by MG. |Acute Kidney Injury/enzymology/*physiopathology/prevention & control[MESH] |Glycation End Products, Advanced/metabolism[MESH] |Humans[MESH] |Hypoxia/enzymology/*physiopathology[MESH] |Kidney Diseases/enzymology/physiopathology/prevention & control[MESH] |Lactoylglutathione Lyase/*metabolism[MESH]Pathophysiological role of the glyoxalase system in renal hypoxic inju(epmc).pdf DeepDyve Pubget Overpricing