Oxygen Radical Injury and Loss of High-Energy Compounds in Anoxic and Reperfused Rat Heart: Prevention By Exogenous Fructose-1, 6-Bisphosphate
Isolated Langendorff-perfused rat hearts after 10 minutes preperfusion, were subjected to a substrate-free anoxic perfusion (20 minutes) followed by 20 minutes reperfusion with a glucose-containing oxygen-balanced medium. Under the same perfusion conditions, the effect of exogenous 5mM fructose-1, 6...
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| Veröffentlicht in: | Free radical research 1990, Vol.10 (3), p.167-176 |
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| creator | Tavazzi, Barbara Cerroni, Loredana Pierro, Donato Di Lazzarino, Giuseppe Nuutinen, Matti Starnes, Joseph W. Giardina, Bruno |
| description | Isolated Langendorff-perfused rat hearts after 10 minutes preperfusion, were subjected to a substrate-free anoxic perfusion (20 minutes) followed by 20 minutes reperfusion with a glucose-containing oxygen-balanced medium. Under the same perfusion conditions, the effect of exogenous 5mM fructose-1, 6-bisphosphate has been investigated. The xanthine dehydrogenase to xanthine oxidase ratio, concentrations of high-energy phosphates and the TBA-reactive material (TBARS) were determined at the end of each perfusion period in both control and fructose-1, 6-bisphosphate-treated hearts. Results indicate that anoxia induces the irreversible transformation of xanthine dehydrogenase into oxidase as a consequence of the sharp decrease of the myocardial energy metabolism. This finding is supported by the protective effect exerted by exogenous fructose-1, 6-bisphosphate which is able to maintain the correct xanthine dehydrogenase/oxidase ratio by preventing the depletion of phosphorylated compounds during anoxia. Moreover, in control hearts, the release oflactate dehydrogenase during reperfusion, is paralleled by a 50% increase in the concentration of tissue TBARS. On the contrary, in fructose-1, 6-bisphosphate-treated hearts this concentration does not significantly change after reoxygenation, while a slight but significant increase of lactate dehydrogenase activity in the perfusates is observed.
On the whole these data indicate a direct contribution of oxygen-derived free radicals to the worsening of post-anoxic hearts. A hypothesis on the mechanism of action of fructose-1, 6-bisphosphate in anoxic and reperfused rat heart and its possible application in the clinical therapy of myocardial infarction are presented. |
| doi_str_mv | 10.3109/10715769009149885 |
| format | Article |
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On the whole these data indicate a direct contribution of oxygen-derived free radicals to the worsening of post-anoxic hearts. A hypothesis on the mechanism of action of fructose-1, 6-bisphosphate in anoxic and reperfused rat heart and its possible application in the clinical therapy of myocardial infarction are presented.</description><identifier>ISSN: 1071-5762</identifier><identifier>ISSN: 8755-0199</identifier><identifier>EISSN: 1029-2470</identifier><identifier>DOI: 10.3109/10715769009149885</identifier><identifier>PMID: 2397920</identifier><language>eng</language><publisher>Chur: Informa UK Ltd</publisher><subject>6-bisphosphate ; Animals ; Anoxia ; Biological and medical sciences ; Cell metabolism, cell oxidation ; Cell physiology ; Energy Metabolism ; Free Radicals ; fructose-1 ; Fructosediphosphates - pharmacology ; Fundamental and applied biological sciences. Psychology ; Hexosediphosphates - pharmacology ; Hypoxia - enzymology ; Hypoxia - metabolism ; In Vitro Techniques ; Lipid Peroxidation ; Male ; Molecular and cellular biology ; Oxygen - toxicity ; rat heart ; Rats ; Rats, Inbred Strains ; reperfusion ; Reperfusion Injury - enzymology ; Reperfusion Injury - etiology ; Reperfusion Injury - prevention & control ; Xanthine Dehydrogenase - metabolism ; Xanthine Oxidase - metabolism</subject><ispartof>Free radical research, 1990, Vol.10 (3), p.167-176</ispartof><rights>1990 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted 1990</rights><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c431t-952e0ec849ca6ebb8f5389ab5d3af67b520317763738bedd309f7b8105a545c13</citedby><cites>FETCH-LOGICAL-c431t-952e0ec849ca6ebb8f5389ab5d3af67b520317763738bedd309f7b8105a545c13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.tandfonline.com/doi/pdf/10.3109/10715769009149885$$EPDF$$P50$$Ginformaworld$$H</linktopdf><linktohtml>$$Uhttps://www.tandfonline.com/doi/full/10.3109/10715769009149885$$EHTML$$P50$$Ginformaworld$$H</linktohtml><link.rule.ids>314,776,780,4009,27902,27903,27904,59623,60412,61197,61378</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19806164$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2397920$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tavazzi, Barbara</creatorcontrib><creatorcontrib>Cerroni, Loredana</creatorcontrib><creatorcontrib>Pierro, Donato Di</creatorcontrib><creatorcontrib>Lazzarino, Giuseppe</creatorcontrib><creatorcontrib>Nuutinen, Matti</creatorcontrib><creatorcontrib>Starnes, Joseph W.</creatorcontrib><creatorcontrib>Giardina, Bruno</creatorcontrib><title>Oxygen Radical Injury and Loss of High-Energy Compounds in Anoxic and Reperfused Rat Heart: Prevention By Exogenous Fructose-1, 6-Bisphosphate</title><title>Free radical research</title><addtitle>Free Radic Res Commun</addtitle><description>Isolated Langendorff-perfused rat hearts after 10 minutes preperfusion, were subjected to a substrate-free anoxic perfusion (20 minutes) followed by 20 minutes reperfusion with a glucose-containing oxygen-balanced medium. Under the same perfusion conditions, the effect of exogenous 5mM fructose-1, 6-bisphosphate has been investigated. The xanthine dehydrogenase to xanthine oxidase ratio, concentrations of high-energy phosphates and the TBA-reactive material (TBARS) were determined at the end of each perfusion period in both control and fructose-1, 6-bisphosphate-treated hearts. Results indicate that anoxia induces the irreversible transformation of xanthine dehydrogenase into oxidase as a consequence of the sharp decrease of the myocardial energy metabolism. This finding is supported by the protective effect exerted by exogenous fructose-1, 6-bisphosphate which is able to maintain the correct xanthine dehydrogenase/oxidase ratio by preventing the depletion of phosphorylated compounds during anoxia. Moreover, in control hearts, the release oflactate dehydrogenase during reperfusion, is paralleled by a 50% increase in the concentration of tissue TBARS. On the contrary, in fructose-1, 6-bisphosphate-treated hearts this concentration does not significantly change after reoxygenation, while a slight but significant increase of lactate dehydrogenase activity in the perfusates is observed.
On the whole these data indicate a direct contribution of oxygen-derived free radicals to the worsening of post-anoxic hearts. A hypothesis on the mechanism of action of fructose-1, 6-bisphosphate in anoxic and reperfused rat heart and its possible application in the clinical therapy of myocardial infarction are presented.</description><subject>6-bisphosphate</subject><subject>Animals</subject><subject>Anoxia</subject><subject>Biological and medical sciences</subject><subject>Cell metabolism, cell oxidation</subject><subject>Cell physiology</subject><subject>Energy Metabolism</subject><subject>Free Radicals</subject><subject>fructose-1</subject><subject>Fructosediphosphates - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hexosediphosphates - pharmacology</subject><subject>Hypoxia - enzymology</subject><subject>Hypoxia - metabolism</subject><subject>In Vitro Techniques</subject><subject>Lipid Peroxidation</subject><subject>Male</subject><subject>Molecular and cellular biology</subject><subject>Oxygen - toxicity</subject><subject>rat heart</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>reperfusion</subject><subject>Reperfusion Injury - enzymology</subject><subject>Reperfusion Injury - etiology</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Xanthine Dehydrogenase - metabolism</subject><subject>Xanthine Oxidase - metabolism</subject><issn>1071-5762</issn><issn>8755-0199</issn><issn>1029-2470</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFu1DAQhiMEKqXwAByQfOFGwI7jOAYu7WrLVlqpqIJzNHHGu15l7chOYPMSPDMuu4AQUg-WR5r_G3u-LHvJ6FvOqHrHqGRCVopSxUpV1-JRds5oofKilPTxfS1ZngLF0-xZjDtKGS-FPMvOCq6kKuh59uP2MG_QkTvorIae3LjdFGYCriNrHyPxhqzsZpsvHYbNTBZ-P_jJdZFYRy6dP1j9K3uHAwYzRUwljGSFEMb35HPAb-hG6x25msny4NNLforkOkx69BFz9oZU-ZWNw9anAyM-z54Y6CO-ON0X2dfr5ZfFKl_ffrpZXK5zXXI25koUSFHXpdJQYdvWRvBaQSs6DqaSrSgoZ1JWXPK6xa7jVBnZ1owKEKXQjF9k7DhXh7RlQNMMwe4hzA2jzb3a5j-1iXl1ZIap3WP3hzi5TP3Xpz7EpNIEcNrGv4NVTStWlSn38Zizzviwh-8-9F0zwtz78BviD33jwz_4FqEftxoCNjs_BZe0PbDET_Empsk</recordid><startdate>1990</startdate><enddate>1990</enddate><creator>Tavazzi, Barbara</creator><creator>Cerroni, Loredana</creator><creator>Pierro, Donato Di</creator><creator>Lazzarino, Giuseppe</creator><creator>Nuutinen, Matti</creator><creator>Starnes, Joseph W.</creator><creator>Giardina, Bruno</creator><general>Informa UK Ltd</general><general>Taylor & Francis</general><general>Harwood</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>1990</creationdate><title>Oxygen Radical Injury and Loss of High-Energy Compounds in Anoxic and Reperfused Rat Heart: Prevention By Exogenous Fructose-1, 6-Bisphosphate</title><author>Tavazzi, Barbara ; Cerroni, Loredana ; Pierro, Donato Di ; Lazzarino, Giuseppe ; Nuutinen, Matti ; Starnes, Joseph W. ; Giardina, Bruno</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c431t-952e0ec849ca6ebb8f5389ab5d3af67b520317763738bedd309f7b8105a545c13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>6-bisphosphate</topic><topic>Animals</topic><topic>Anoxia</topic><topic>Biological and medical sciences</topic><topic>Cell metabolism, cell oxidation</topic><topic>Cell physiology</topic><topic>Energy Metabolism</topic><topic>Free Radicals</topic><topic>fructose-1</topic><topic>Fructosediphosphates - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hexosediphosphates - pharmacology</topic><topic>Hypoxia - enzymology</topic><topic>Hypoxia - metabolism</topic><topic>In Vitro Techniques</topic><topic>Lipid Peroxidation</topic><topic>Male</topic><topic>Molecular and cellular biology</topic><topic>Oxygen - toxicity</topic><topic>rat heart</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>reperfusion</topic><topic>Reperfusion Injury - enzymology</topic><topic>Reperfusion Injury - etiology</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Xanthine Dehydrogenase - metabolism</topic><topic>Xanthine Oxidase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tavazzi, Barbara</creatorcontrib><creatorcontrib>Cerroni, Loredana</creatorcontrib><creatorcontrib>Pierro, Donato Di</creatorcontrib><creatorcontrib>Lazzarino, Giuseppe</creatorcontrib><creatorcontrib>Nuutinen, Matti</creatorcontrib><creatorcontrib>Starnes, Joseph W.</creatorcontrib><creatorcontrib>Giardina, Bruno</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Free radical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tavazzi, Barbara</au><au>Cerroni, Loredana</au><au>Pierro, Donato Di</au><au>Lazzarino, Giuseppe</au><au>Nuutinen, Matti</au><au>Starnes, Joseph W.</au><au>Giardina, Bruno</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxygen Radical Injury and Loss of High-Energy Compounds in Anoxic and Reperfused Rat Heart: Prevention By Exogenous Fructose-1, 6-Bisphosphate</atitle><jtitle>Free radical research</jtitle><addtitle>Free Radic Res Commun</addtitle><date>1990</date><risdate>1990</risdate><volume>10</volume><issue>3</issue><spage>167</spage><epage>176</epage><pages>167-176</pages><issn>1071-5762</issn><issn>8755-0199</issn><eissn>1029-2470</eissn><abstract>Isolated Langendorff-perfused rat hearts after 10 minutes preperfusion, were subjected to a substrate-free anoxic perfusion (20 minutes) followed by 20 minutes reperfusion with a glucose-containing oxygen-balanced medium. Under the same perfusion conditions, the effect of exogenous 5mM fructose-1, 6-bisphosphate has been investigated. The xanthine dehydrogenase to xanthine oxidase ratio, concentrations of high-energy phosphates and the TBA-reactive material (TBARS) were determined at the end of each perfusion period in both control and fructose-1, 6-bisphosphate-treated hearts. Results indicate that anoxia induces the irreversible transformation of xanthine dehydrogenase into oxidase as a consequence of the sharp decrease of the myocardial energy metabolism. This finding is supported by the protective effect exerted by exogenous fructose-1, 6-bisphosphate which is able to maintain the correct xanthine dehydrogenase/oxidase ratio by preventing the depletion of phosphorylated compounds during anoxia. Moreover, in control hearts, the release oflactate dehydrogenase during reperfusion, is paralleled by a 50% increase in the concentration of tissue TBARS. On the contrary, in fructose-1, 6-bisphosphate-treated hearts this concentration does not significantly change after reoxygenation, while a slight but significant increase of lactate dehydrogenase activity in the perfusates is observed.
On the whole these data indicate a direct contribution of oxygen-derived free radicals to the worsening of post-anoxic hearts. A hypothesis on the mechanism of action of fructose-1, 6-bisphosphate in anoxic and reperfused rat heart and its possible application in the clinical therapy of myocardial infarction are presented.</abstract><cop>Chur</cop><cop>Reading</cop><cop>Paris</cop><pub>Informa UK Ltd</pub><pmid>2397920</pmid><doi>10.3109/10715769009149885</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1071-5762 |
| ispartof | Free radical research, 1990, Vol.10 (3), p.167-176 |
| issn | 1071-5762 8755-0199 1029-2470 |
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| source | MEDLINE; Taylor & Francis Journals Complete |
| subjects | 6-bisphosphate Animals Anoxia Biological and medical sciences Cell metabolism, cell oxidation Cell physiology Energy Metabolism Free Radicals fructose-1 Fructosediphosphates - pharmacology Fundamental and applied biological sciences. Psychology Hexosediphosphates - pharmacology Hypoxia - enzymology Hypoxia - metabolism In Vitro Techniques Lipid Peroxidation Male Molecular and cellular biology Oxygen - toxicity rat heart Rats Rats, Inbred Strains reperfusion Reperfusion Injury - enzymology Reperfusion Injury - etiology Reperfusion Injury - prevention & control Xanthine Dehydrogenase - metabolism Xanthine Oxidase - metabolism |
| title | Oxygen Radical Injury and Loss of High-Energy Compounds in Anoxic and Reperfused Rat Heart: Prevention By Exogenous Fructose-1, 6-Bisphosphate |
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