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10.1093/toxsci/kfu141 http://scihub22266oqcxt.onion/10.1093/toxsci/kfu141 C4271045!4271045 !25015657     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25015657 &cmd=llinks): Failed to open stream: HTTP request failed! 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MDR1 transporter protects against paraquat-induced toxicity in human and mouse proximal tubule cells |pdf=|usr=}}{{25015657 }} gab.com Text MDR1 transporter protects against paraquat-induced toxicity in human and mouse proximal tubule cells JO: Toxicol Sci http://www.kidney.de/pget.php?&tw=1&pmid=25015657 #FOAvip Paraquat is a herbicide that is highly toxic to the lungs and kidneys following acute exposures. Prior studies have demonstrated that the organic cation transporter 2 and multidrug and toxin extrusion protein 1 contribute to the urinary secretion of paraquat in the kidneys. The purpose of this study was to determine whether the multidrug resistance protein 1 (MDR1/Mdr1, ABCB1, or P-glycoprotein) also participates in the removal of paraquat from the kidneys and protects against renal injury. Paraquat transport and toxicity were quantified in human renal proximal tubule epithelial cells (RPTEC) that endogenously express MDR1, HEK293 cells overexpressing MDR1, and Mdr1a/1b knockout mice. In RPTEC cells, reduction of MDR1 activity using the antagonist PSC833 or siRNA transfection increased the cellular accumulation of paraquat by 50%. Reduced efflux of paraquat corresponded with enhanced cytotoxicity in PSC833-treated cells. Likewise, stable overexpression of the human MDR1 gene in HEK293 cells reduced intracellular levels of paraquat by 50%. In vivo studies assessed the renal accumulation and subsequent nephrotoxicity of paraquat (10 or 30 mg/kg ip) in wild-type and Mdr1a/1b knockout mice. At 4 h after paraquat treatment, renal concentrations of paraquat in the kidneys of Mdr1a/1b knockout mice were 750% higher than wild-type mice. By 72 h, paraquat-treated Mdr1a/1b knockout mice had more extensive tubular degeneration and significantly greater mRNA expression of kidney injury-responsive genes, including kidney injury molecule-1, lipocalin-2, and NAD(P)H quinone oxidoreductase 1, compared with wild-type mice. In conclusion, MDR1/Mdr1 participates in the elimination of paraquat from the kidneys and protects against subsequent toxicity. Twit Text FOAVip MDR1 transporter protects against paraquat-induced toxicity in human and mouse proximal tubule cells ????Toxicol Sci http://www.kidney.de/pget.php?&tw=1&pmid=25015657 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25015657 #FOAvip English Wikipedia <ref>{{Cite pmid|25015657 }}</ref> MDR1 transporter protects against paraquat-induced toxicity in human and mouse proximal tubule cells #MMPMID25015657 Wen X ; Gibson CJ ; Yang I ; Buckley B ; Goedken MJ ; Richardson JR ; Aleksunes LM Toxicol Sci 2014[Oct]; 141 (2 ): 475-83 PMID25015657 show ga Paraquat is a herbicide that is highly toxic to the lungs and kidneys following acute exposures. Prior studies have demonstrated that the organic cation transporter 2 and multidrug and toxin extrusion protein 1 contribute to the urinary secretion of paraquat in the kidneys. The purpose of this study was to determine whether the multidrug resistance protein 1 (MDR1/Mdr1, ABCB1, or P-glycoprotein) also participates in the removal of paraquat from the kidneys and protects against renal injury. Paraquat transport and toxicity were quantified in human renal proximal tubule epithelial cells (RPTEC) that endogenously express MDR1, HEK293 cells overexpressing MDR1, and Mdr1a/1b knockout mice. In RPTEC cells, reduction of MDR1 activity using the antagonist PSC833 or siRNA transfection increased the cellular accumulation of paraquat by 50%. Reduced efflux of paraquat corresponded with enhanced cytotoxicity in PSC833-treated cells. Likewise, stable overexpression of the human MDR1 gene in HEK293 cells reduced intracellular levels of paraquat by 50%. In vivo studies assessed the renal accumulation and subsequent nephrotoxicity of paraquat (10 or 30 mg/kg ip) in wild-type and Mdr1a/1b knockout mice. At 4 h after paraquat treatment, renal concentrations of paraquat in the kidneys of Mdr1a/1b knockout mice were 750% higher than wild-type mice. By 72 h, paraquat-treated Mdr1a/1b knockout mice had more extensive tubular degeneration and significantly greater mRNA expression of kidney injury-responsive genes, including kidney injury molecule-1, lipocalin-2, and NAD(P)H quinone oxidoreductase 1, compared with wild-type mice. In conclusion, MDR1/Mdr1 participates in the elimination of paraquat from the kidneys and protects against subsequent toxicity. |*Herbicides/metabolism [MESH] |*Paraquat/metabolism [MESH] |*Renal Elimination/drug effects [MESH] |ATP Binding Cassette Transporter, Subfamily B/antagonists & inhibitors/deficiency/genetics/*metabolism [MESH] |ATP-Binding Cassette Sub-Family B Member 4 [MESH] |Animals [MESH] |Cyclosporins/pharmacology [MESH] |Disease Models, Animal [MESH] |Gene Expression Regulation/drug effects [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Kidney Diseases/chemically induced/genetics/metabolism/pathology/*prevention & control [MESH] |Kidney Tubules, Proximal/drug effects/*metabolism/pathology [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |RNA Interference [MESH] |RNA, Messenger/metabolism [MESH] |Time Factors [MESH]MDR1 transporter protects against paraquat-induced toxicity in human a(epmc).pdf DeepDyve Pubget Overpricing