Cyclooxygenase 1-dependent production of F2-isoprostane and changes in redox status during warm renal ischemia-reperfusion
The detrimental role of oxidative stress has been widely described in tissue damage caused by ischemia-reperfusion. A nonenzymatic, reactive oxygen species-related pathway has been suggested to produce 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)), an epimer of prostaglandin F(2alpha) (PGF(2alph...
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| Veröffentlicht in: | Free radical biology & medicine 2004-04, Vol.36 (8), p.1034-1042 |
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| creator | Favreau, Frederic Petit-Paris, Isabelle Hauet, Thierry Dutheil, Delphine Papet, Yves Mauco, Gerard Tallineau, Claude |
| description | The detrimental role of oxidative stress has been widely described in tissue damage caused by ischemia-reperfusion. A nonenzymatic, reactive oxygen species-related pathway has been suggested to produce 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)), an epimer of prostaglandin F(2alpha) (PGF(2alpha)), which has been proposed as an indicator of oxidative stress. Using an in vivo ischemia-reperfusion model in rat kidneys, we investigated intrarenal accumulation of 8-iso-PGF(2alpha) and PGF(2alpha). Both prostanoids accumulated in the ischemic kidney and disappeared upon reperfusion. In addition, a nonselective (acetylsalicylic acid) or selective cyclooxygenase (COX) 1 inhibitor (SC-560) completely abrogated the 8-iso-PGF(2alpha) and PGF(2alpha) formation in kidneys subjected to ischemia. COX2 inhibition had no effect on the production of these prostanoids. Therefore the two metabolites of arachidonic acid seemed to be produced via an enzymatic COX1-dependent pathway. Neither COX overexpression nor COX activation was detected. We also investigated renal glutathione, which is considered to be the major thiol-disulfide redox buffer of the tissue. Total and oxidized glutathione was decreased during the ischemic period, whereas no further decrease was seen for up to 60 min of reperfusion. These data demonstrate that a dramatic decrease in antioxidant defense was initiated during warm renal ischemia, whereas the 8-iso-PGF(2alpha) was related only to arachidonate conversion by COX1. |
| doi_str_mv | 10.1016/j.freeradbiomed.2004.01.010 |
| format | Article |
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A nonenzymatic, reactive oxygen species-related pathway has been suggested to produce 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)), an epimer of prostaglandin F(2alpha) (PGF(2alpha)), which has been proposed as an indicator of oxidative stress. Using an in vivo ischemia-reperfusion model in rat kidneys, we investigated intrarenal accumulation of 8-iso-PGF(2alpha) and PGF(2alpha). Both prostanoids accumulated in the ischemic kidney and disappeared upon reperfusion. In addition, a nonselective (acetylsalicylic acid) or selective cyclooxygenase (COX) 1 inhibitor (SC-560) completely abrogated the 8-iso-PGF(2alpha) and PGF(2alpha) formation in kidneys subjected to ischemia. COX2 inhibition had no effect on the production of these prostanoids. Therefore the two metabolites of arachidonic acid seemed to be produced via an enzymatic COX1-dependent pathway. Neither COX overexpression nor COX activation was detected. We also investigated renal glutathione, which is considered to be the major thiol-disulfide redox buffer of the tissue. Total and oxidized glutathione was decreased during the ischemic period, whereas no further decrease was seen for up to 60 min of reperfusion. These data demonstrate that a dramatic decrease in antioxidant defense was initiated during warm renal ischemia, whereas the 8-iso-PGF(2alpha) was related only to arachidonate conversion by COX1.</description><identifier>ISSN: 0891-5849</identifier><identifier>DOI: 10.1016/j.freeradbiomed.2004.01.010</identifier><identifier>PMID: 15059644</identifier><language>eng</language><publisher>United States: Elsevier</publisher><subject>Animals ; Arachidonic Acid - metabolism ; Cyclooxygenase 1 ; Dinoprost - analogs & derivatives ; Dinoprost - metabolism ; Enzyme Inhibitors - pharmacology ; F2-Isoprostanes - chemistry ; Free Radicals ; Gas Chromatography-Mass Spectrometry ; Glutathione - metabolism ; Ischemia ; Isoenzymes - metabolism ; Kidney - metabolism ; Kidney - pathology ; Kinetics ; Life Sciences ; Male ; Membrane Proteins ; Oxidation-Reduction ; Oxidative Stress ; Prostaglandin-Endoperoxide Synthases - metabolism ; Pyrazoles - pharmacology ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species ; Reperfusion Injury ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - metabolism ; Time Factors</subject><ispartof>Free radical biology & medicine, 2004-04, Vol.36 (8), p.1034-1042</ispartof><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c266t-9dfe534b5570caf37fc5693f3706b34a95b23188d19a88af62cd9aff1f62a3463</citedby><cites>FETCH-LOGICAL-c266t-9dfe534b5570caf37fc5693f3706b34a95b23188d19a88af62cd9aff1f62a3463</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15059644$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.inrae.fr/hal-02678018$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Favreau, Frederic</creatorcontrib><creatorcontrib>Petit-Paris, Isabelle</creatorcontrib><creatorcontrib>Hauet, Thierry</creatorcontrib><creatorcontrib>Dutheil, Delphine</creatorcontrib><creatorcontrib>Papet, Yves</creatorcontrib><creatorcontrib>Mauco, Gerard</creatorcontrib><creatorcontrib>Tallineau, Claude</creatorcontrib><title>Cyclooxygenase 1-dependent production of F2-isoprostane and changes in redox status during warm renal ischemia-reperfusion</title><title>Free radical biology & medicine</title><addtitle>Free Radic Biol Med</addtitle><description>The detrimental role of oxidative stress has been widely described in tissue damage caused by ischemia-reperfusion. A nonenzymatic, reactive oxygen species-related pathway has been suggested to produce 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)), an epimer of prostaglandin F(2alpha) (PGF(2alpha)), which has been proposed as an indicator of oxidative stress. Using an in vivo ischemia-reperfusion model in rat kidneys, we investigated intrarenal accumulation of 8-iso-PGF(2alpha) and PGF(2alpha). Both prostanoids accumulated in the ischemic kidney and disappeared upon reperfusion. In addition, a nonselective (acetylsalicylic acid) or selective cyclooxygenase (COX) 1 inhibitor (SC-560) completely abrogated the 8-iso-PGF(2alpha) and PGF(2alpha) formation in kidneys subjected to ischemia. COX2 inhibition had no effect on the production of these prostanoids. Therefore the two metabolites of arachidonic acid seemed to be produced via an enzymatic COX1-dependent pathway. Neither COX overexpression nor COX activation was detected. We also investigated renal glutathione, which is considered to be the major thiol-disulfide redox buffer of the tissue. Total and oxidized glutathione was decreased during the ischemic period, whereas no further decrease was seen for up to 60 min of reperfusion. These data demonstrate that a dramatic decrease in antioxidant defense was initiated during warm renal ischemia, whereas the 8-iso-PGF(2alpha) was related only to arachidonate conversion by COX1.</description><subject>Animals</subject><subject>Arachidonic Acid - metabolism</subject><subject>Cyclooxygenase 1</subject><subject>Dinoprost - analogs & derivatives</subject><subject>Dinoprost - metabolism</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>F2-Isoprostanes - chemistry</subject><subject>Free Radicals</subject><subject>Gas Chromatography-Mass Spectrometry</subject><subject>Glutathione - metabolism</subject><subject>Ischemia</subject><subject>Isoenzymes - metabolism</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kinetics</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Membrane Proteins</subject><subject>Oxidation-Reduction</subject><subject>Oxidative Stress</subject><subject>Prostaglandin-Endoperoxide Synthases - metabolism</subject><subject>Pyrazoles - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive Oxygen Species</subject><subject>Reperfusion Injury</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - metabolism</subject><subject>Time Factors</subject><issn>0891-5849</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUU1rGzEQ1aGhSdP-hSIIFHpYR1qttFp6CiZfYMglPYtZfdgyu5Ij7bZxfn1kbAKBgRnmvXnSzEPoipIFJVRcbxcuWZvA9D6O1ixqQpoFoSXIF3RBZEcrLpvuHH3LeUsKyJn8is4pJ7wTTXOB3pZ7PcT4ul_bANliWhm7s8HYMOFdimbWk48BR4fv6srnWHp5gmAxBIP1BsLaZuwDTtbEV1ygac7YzMmHNf4PaSxAgAH7rDd29FClop7cnIvod3TmYMj2xylfor93t8_Lh2r1dP-4vFlVuhZiqjrjLGdNz3lLNDjWOs1Fx0pBRM8a6HhfMyqloR1ICU7U2nTgHC0VsEawS_T7qLuBQe2SHyHtVQSvHm5W6tAjtWglofIfLdxfR27Z82W2eVJj-bodhrJynLNqaStb2bBC_HMk6nKQnKz7UKZEHaxRW_XJGnWwRhFagpTpn6dn5v6AfcyefGHvpUWTXg</recordid><startdate>20040415</startdate><enddate>20040415</enddate><creator>Favreau, Frederic</creator><creator>Petit-Paris, Isabelle</creator><creator>Hauet, Thierry</creator><creator>Dutheil, Delphine</creator><creator>Papet, Yves</creator><creator>Mauco, Gerard</creator><creator>Tallineau, Claude</creator><general>Elsevier</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope></search><sort><creationdate>20040415</creationdate><title>Cyclooxygenase 1-dependent production of F2-isoprostane and changes in redox status during warm renal ischemia-reperfusion</title><author>Favreau, Frederic ; Petit-Paris, Isabelle ; Hauet, Thierry ; Dutheil, Delphine ; Papet, Yves ; Mauco, Gerard ; Tallineau, Claude</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c266t-9dfe534b5570caf37fc5693f3706b34a95b23188d19a88af62cd9aff1f62a3463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Arachidonic Acid - metabolism</topic><topic>Cyclooxygenase 1</topic><topic>Dinoprost - analogs & derivatives</topic><topic>Dinoprost - metabolism</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>F2-Isoprostanes - chemistry</topic><topic>Free Radicals</topic><topic>Gas Chromatography-Mass Spectrometry</topic><topic>Glutathione - metabolism</topic><topic>Ischemia</topic><topic>Isoenzymes - metabolism</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kinetics</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Membrane Proteins</topic><topic>Oxidation-Reduction</topic><topic>Oxidative Stress</topic><topic>Prostaglandin-Endoperoxide Synthases - metabolism</topic><topic>Pyrazoles - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive Oxygen Species</topic><topic>Reperfusion Injury</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - metabolism</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Favreau, Frederic</creatorcontrib><creatorcontrib>Petit-Paris, Isabelle</creatorcontrib><creatorcontrib>Hauet, Thierry</creatorcontrib><creatorcontrib>Dutheil, Delphine</creatorcontrib><creatorcontrib>Papet, Yves</creatorcontrib><creatorcontrib>Mauco, Gerard</creatorcontrib><creatorcontrib>Tallineau, Claude</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Free radical biology & medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Favreau, Frederic</au><au>Petit-Paris, Isabelle</au><au>Hauet, Thierry</au><au>Dutheil, Delphine</au><au>Papet, Yves</au><au>Mauco, Gerard</au><au>Tallineau, Claude</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclooxygenase 1-dependent production of F2-isoprostane and changes in redox status during warm renal ischemia-reperfusion</atitle><jtitle>Free radical biology & medicine</jtitle><addtitle>Free Radic Biol Med</addtitle><date>2004-04-15</date><risdate>2004</risdate><volume>36</volume><issue>8</issue><spage>1034</spage><epage>1042</epage><pages>1034-1042</pages><issn>0891-5849</issn><abstract>The detrimental role of oxidative stress has been widely described in tissue damage caused by ischemia-reperfusion. A nonenzymatic, reactive oxygen species-related pathway has been suggested to produce 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)), an epimer of prostaglandin F(2alpha) (PGF(2alpha)), which has been proposed as an indicator of oxidative stress. Using an in vivo ischemia-reperfusion model in rat kidneys, we investigated intrarenal accumulation of 8-iso-PGF(2alpha) and PGF(2alpha). Both prostanoids accumulated in the ischemic kidney and disappeared upon reperfusion. In addition, a nonselective (acetylsalicylic acid) or selective cyclooxygenase (COX) 1 inhibitor (SC-560) completely abrogated the 8-iso-PGF(2alpha) and PGF(2alpha) formation in kidneys subjected to ischemia. COX2 inhibition had no effect on the production of these prostanoids. Therefore the two metabolites of arachidonic acid seemed to be produced via an enzymatic COX1-dependent pathway. Neither COX overexpression nor COX activation was detected. We also investigated renal glutathione, which is considered to be the major thiol-disulfide redox buffer of the tissue. Total and oxidized glutathione was decreased during the ischemic period, whereas no further decrease was seen for up to 60 min of reperfusion. These data demonstrate that a dramatic decrease in antioxidant defense was initiated during warm renal ischemia, whereas the 8-iso-PGF(2alpha) was related only to arachidonate conversion by COX1.</abstract><cop>United States</cop><pub>Elsevier</pub><pmid>15059644</pmid><doi>10.1016/j.freeradbiomed.2004.01.010</doi><tpages>9</tpages></addata></record> |
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| subjects | Animals Arachidonic Acid - metabolism Cyclooxygenase 1 Dinoprost - analogs & derivatives Dinoprost - metabolism Enzyme Inhibitors - pharmacology F2-Isoprostanes - chemistry Free Radicals Gas Chromatography-Mass Spectrometry Glutathione - metabolism Ischemia Isoenzymes - metabolism Kidney - metabolism Kidney - pathology Kinetics Life Sciences Male Membrane Proteins Oxidation-Reduction Oxidative Stress Prostaglandin-Endoperoxide Synthases - metabolism Pyrazoles - pharmacology Rats Rats, Sprague-Dawley Reactive Oxygen Species Reperfusion Injury Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - metabolism Time Factors |
| title | Cyclooxygenase 1-dependent production of F2-isoprostane and changes in redox status during warm renal ischemia-reperfusion |
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