| pubmed-article:15629191 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15629191 | lifeskim:mentions | umls-concept:C0000970 | lld:lifeskim |
| pubmed-article:15629191 | lifeskim:mentions | umls-concept:C1511572 | lld:lifeskim |
| pubmed-article:15629191 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:15629191 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
| pubmed-article:15629191 | lifeskim:mentions | umls-concept:C0599918 | lld:lifeskim |
| pubmed-article:15629191 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:15629191 | pubmed:dateCreated | 2005-1-4 | lld:pubmed |
| pubmed-article:15629191 | pubmed:abstractText | Acetaminophen (APAP) nephrotoxicity has been observed both in humans and research animals. Our recent investigations have focused on the possible involvement of glutathione-derived APAP metabolites in APAP nephrotoxicity and have demonstrated that administration of acetaminophen-cysteine (APAP-CYS) potentiated APAP-induced renal injury with no effects on APAP-induced liver injury. Additionally, APAP-CYS treatment alone resulted in a dose-responsive renal GSH depletion. This APAP-CYS-induced renal GSH depletion could interfere with intrarenal detoxification of APAP or its toxic metabolite N-acetyl-p-benzoquinoneimine (NAPQI) and may be the mechanism responsible for the potentiation of APAP nephrotoxicity. Renal-specific GSH depletion has been demonstrated in mice and rats following administration of amino acid gamma-glutamyl acceptor substrates for gamma-glutamyl transpeptidase (gamma-GT). The present study sought to determine if APAP-CYS-induced renal glutathione depletion is the result of disruption of the gamma-glutamyl cycle through interaction with gamma-GT. The results confirmed that APAP-CYS-induced renal GSH depletion was antagonized by the gamma-glutamyl transpeptidase (gamma-GT) inhibitor acivicin. In vitro analysis demonstrated that APAP-CYS is a gamma-glutamyl acceptor for both murine and bovine renal gamma-GT. Analysis of urine from mice pretreated with acivicin and then treated with APAP, APAP-CYS, or acetaminophen-glutathione identified a gamma-glutamyl-cysteinyl-acetaminophen metabolite. These findings are consistent with the hypothesis that APAP-CYS contributes to APAP nephrotoxicity by depletion of renal GSH stores through interaction with the gamma-glutamyl cycle. | lld:pubmed |
| pubmed-article:15629191 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15629191 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15629191 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15629191 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15629191 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15629191 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15629191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15629191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15629191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15629191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15629191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15629191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15629191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15629191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15629191 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15629191 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15629191 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:15629191 | pubmed:issn | 0041-008X | lld:pubmed |
| pubmed-article:15629191 | pubmed:author | pubmed-author:BrunoMary KMK | lld:pubmed |
| pubmed-article:15629191 | pubmed:author | pubmed-author:CohenSteven... | lld:pubmed |
| pubmed-article:15629191 | pubmed:author | pubmed-author:RobertsJeanet... | lld:pubmed |
| pubmed-article:15629191 | pubmed:author | pubmed-author:HortonRobert... | lld:pubmed |
| pubmed-article:15629191 | pubmed:author | pubmed-author:SternStephan... | lld:pubmed |
| pubmed-article:15629191 | pubmed:author | pubmed-author:HillDennis... | lld:pubmed |
| pubmed-article:15629191 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15629191 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:15629191 | pubmed:volume | 202 | lld:pubmed |
| pubmed-article:15629191 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15629191 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15629191 | pubmed:pagination | 160-71 | lld:pubmed |
| pubmed-article:15629191 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:15629191 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15629191 | pubmed:articleTitle | Contribution of acetaminophen-cysteine to acetaminophen nephrotoxicity II. Possible involvement of the gamma-glutamyl cycle. | lld:pubmed |
| pubmed-article:15629191 | pubmed:affiliation | Toxicology Program, Department of Pharmaceutical Sciences, University of Connecticut, Storrs, CT 06268, USA. | lld:pubmed |
| pubmed-article:15629191 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15629191 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:15629191 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15629191 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
