Effects of Perfluorooctylbromide and vitamin E on Ischemia Induced Retinal Oxidative Tissue Damage
The aim of this study was to investigate the extent to which ischemia and reperfusion lead to oxidative damage of the retinal tissue and investigate how ischemic and reperfused retinal tissues react to the application of perfluorooctylbromide (PFOB) and, if this reaction can be influenced by protect...
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| Veröffentlicht in: | Experimental eye research 1998-01, Vol.66 (1), p.19-24 |
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| creator | AUGUSTIN, A.J. SPITZNAS, M. KOCH, F. GRUS, F. LUTZ, J. |
| description | The aim of this study was to investigate the extent to which ischemia and reperfusion lead to oxidative damage of the retinal tissue and investigate how ischemic and reperfused retinal tissues react to the application of perfluorooctylbromide (PFOB) and, if this reaction can be influenced by protective drugs such as vitamin E (Vit.E). The experiments were performed with 60 male Wistar rats, divided into 12 groups using an established model of reversible ischemia and reperfusion of the globe. Grouping of animals was carried out according to different ischemia and reperfusion periods and different therapeutic regimens (PFOB, Vit.E). Treatment with PFOB and/or Vit.E was performed after 60 min of ischemia with 60 min of reperfusion. At the end of the experiments thiobarbituric acid reactive substances (TBARS) were determined in the retinal tissues and served as parameters of oxidative tissue damage. Ischemia of up to 60 min led to a significant increase in TBARS values. Ninety and 120 min of ischemia led to no further significant elevation compared to the 60 min or 90 min group. Following 60 min of ischemia, a reperfusion period of 15 min led to an increase in TBARS values that was significant (P |
| doi_str_mv | 10.1006/exer.1997.0399 |
| format | Article |
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The experiments were performed with 60 male Wistar rats, divided into 12 groups using an established model of reversible ischemia and reperfusion of the globe. Grouping of animals was carried out according to different ischemia and reperfusion periods and different therapeutic regimens (PFOB, Vit.E). Treatment with PFOB and/or Vit.E was performed after 60 min of ischemia with 60 min of reperfusion. At the end of the experiments thiobarbituric acid reactive substances (TBARS) were determined in the retinal tissues and served as parameters of oxidative tissue damage. Ischemia of up to 60 min led to a significant increase in TBARS values. Ninety and 120 min of ischemia led to no further significant elevation compared to the 60 min or 90 min group. Following 60 min of ischemia, a reperfusion period of 15 min led to an increase in TBARS values that was significant (P<0.05) after 30 and 60 min. Addition of PFOB resulted in a further significant (P<0.05) increase in TBARS values as compared to the respective group without treatment. Vit. E alone did not change the values significantly compared to the respective group without treatment. However, the application of Vit.E in addition to PFOB led to a significant reduction in TBARS values. Ischemia resulted in severe oxidative retinal tissue damage, which increased during reperfusion. The reperfusion damage might be due to the known depletion of protecting substances such as vitamin E. Enhancement of oxygen supply by PFOB during reperfusion without any tissue protection leads to more severe damage. Thus, additional protection of the tissue by powerful antioxidants is necessary when providing oxygen for better tissue recovery.</description><identifier>ISSN: 0014-4835</identifier><identifier>EISSN: 1096-0007</identifier><identifier>DOI: 10.1006/exer.1997.0399</identifier><identifier>PMID: 9533827</identifier><identifier>CODEN: EXERA6</identifier><language>eng</language><publisher>London: Elsevier Ltd</publisher><subject>Animals ; Biological and medical sciences ; Fluorocarbons - metabolism ; Fluorocarbons - pharmacology ; ischemia ; Ischemia - metabolism ; Ischemia - prevention & control ; Male ; Medical sciences ; Ophthalmology ; oxidative tissue damage ; Perfluorooctylbromide ; Peroxides - metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury - metabolism ; Reperfusion Injury - prevention & control ; retina ; Retina - drug effects ; Retinal Diseases - chemically induced ; Retinal Diseases - prevention & control ; Retinopathies ; Thiobarbiturates - analysis ; Time Factors ; vitamin E ; Vitamin E - pharmacology</subject><ispartof>Experimental eye research, 1998-01, Vol.66 (1), p.19-24</ispartof><rights>1998 Academic Press</rights><rights>1998 INIST-CNRS</rights><rights>Copyright 1998 Academic Press Limited.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c368t-baddb881569e01a247255d2631b7f303d5561da23f75ff4464b149b25d1d4263</citedby><cites>FETCH-LOGICAL-c368t-baddb881569e01a247255d2631b7f303d5561da23f75ff4464b149b25d1d4263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/exer.1997.0399$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,4022,27922,27923,27924,45994</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2122801$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9533827$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>AUGUSTIN, A.J.</creatorcontrib><creatorcontrib>SPITZNAS, M.</creatorcontrib><creatorcontrib>KOCH, F.</creatorcontrib><creatorcontrib>GRUS, F.</creatorcontrib><creatorcontrib>LUTZ, J.</creatorcontrib><title>Effects of Perfluorooctylbromide and vitamin E on Ischemia Induced Retinal Oxidative Tissue Damage</title><title>Experimental eye research</title><addtitle>Exp Eye Res</addtitle><description>The aim of this study was to investigate the extent to which ischemia and reperfusion lead to oxidative damage of the retinal tissue and investigate how ischemic and reperfused retinal tissues react to the application of perfluorooctylbromide (PFOB) and, if this reaction can be influenced by protective drugs such as vitamin E (Vit.E). The experiments were performed with 60 male Wistar rats, divided into 12 groups using an established model of reversible ischemia and reperfusion of the globe. Grouping of animals was carried out according to different ischemia and reperfusion periods and different therapeutic regimens (PFOB, Vit.E). Treatment with PFOB and/or Vit.E was performed after 60 min of ischemia with 60 min of reperfusion. At the end of the experiments thiobarbituric acid reactive substances (TBARS) were determined in the retinal tissues and served as parameters of oxidative tissue damage. Ischemia of up to 60 min led to a significant increase in TBARS values. Ninety and 120 min of ischemia led to no further significant elevation compared to the 60 min or 90 min group. Following 60 min of ischemia, a reperfusion period of 15 min led to an increase in TBARS values that was significant (P<0.05) after 30 and 60 min. Addition of PFOB resulted in a further significant (P<0.05) increase in TBARS values as compared to the respective group without treatment. Vit. E alone did not change the values significantly compared to the respective group without treatment. However, the application of Vit.E in addition to PFOB led to a significant reduction in TBARS values. Ischemia resulted in severe oxidative retinal tissue damage, which increased during reperfusion. The reperfusion damage might be due to the known depletion of protecting substances such as vitamin E. Enhancement of oxygen supply by PFOB during reperfusion without any tissue protection leads to more severe damage. Thus, additional protection of the tissue by powerful antioxidants is necessary when providing oxygen for better tissue recovery.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Fluorocarbons - metabolism</subject><subject>Fluorocarbons - pharmacology</subject><subject>ischemia</subject><subject>Ischemia - metabolism</subject><subject>Ischemia - prevention & control</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Ophthalmology</subject><subject>oxidative tissue damage</subject><subject>Perfluorooctylbromide</subject><subject>Peroxides - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - prevention & control</subject><subject>retina</subject><subject>Retina - drug effects</subject><subject>Retinal Diseases - chemically induced</subject><subject>Retinal Diseases - prevention & control</subject><subject>Retinopathies</subject><subject>Thiobarbiturates - analysis</subject><subject>Time Factors</subject><subject>vitamin E</subject><subject>Vitamin E - pharmacology</subject><issn>0014-4835</issn><issn>1096-0007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEtLAzEQgIMotVav3oQcvO6a5z6OUqsWChXpfckmE43soyTbYv-9WVp68zQw883rQ-iekpQSkj3BL_iUlmWeEl6WF2hKSZklhJD8Ek0JoSIRBZfX6CaEn5jlIhcTNCkl5wXLp6heWAt6CLi3-AO8bXa973s9HJra960zgFVn8N4NqnUdXuC-w8ugv6F1Ci87s9Ng8CcMrlMNXv86owa3B7xxIewAv6hWfcEturKqCXB3ijO0eV1s5u_Jav22nD-vEs2zYkhqZUxdFFRmJRCqmMiZlIZlnNa55YQbKTNqFOM2l9YKkYmairJm0lAjIjZD6XGs9n0IHmy19a5V_lBRUo2qqlFVNaqqRlWx4eHYsN3VLZgzfnIT64-nugpaNdarTrtwxhhlrCA0YsURg_jb3sUVQTvoohjno9nK9O6_C_4AJkmFFQ</recordid><startdate>199801</startdate><enddate>199801</enddate><creator>AUGUSTIN, A.J.</creator><creator>SPITZNAS, M.</creator><creator>KOCH, F.</creator><creator>GRUS, F.</creator><creator>LUTZ, J.</creator><general>Elsevier Ltd</general><general>Elsevier</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>199801</creationdate><title>Effects of Perfluorooctylbromide and vitamin E on Ischemia Induced Retinal Oxidative Tissue Damage</title><author>AUGUSTIN, A.J. ; SPITZNAS, M. ; KOCH, F. ; GRUS, F. ; LUTZ, J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c368t-baddb881569e01a247255d2631b7f303d5561da23f75ff4464b149b25d1d4263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Fluorocarbons - metabolism</topic><topic>Fluorocarbons - pharmacology</topic><topic>ischemia</topic><topic>Ischemia - metabolism</topic><topic>Ischemia - prevention & control</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Ophthalmology</topic><topic>oxidative tissue damage</topic><topic>Perfluorooctylbromide</topic><topic>Peroxides - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - prevention & control</topic><topic>retina</topic><topic>Retina - drug effects</topic><topic>Retinal Diseases - chemically induced</topic><topic>Retinal Diseases - prevention & control</topic><topic>Retinopathies</topic><topic>Thiobarbiturates - analysis</topic><topic>Time Factors</topic><topic>vitamin E</topic><topic>Vitamin E - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>AUGUSTIN, A.J.</creatorcontrib><creatorcontrib>SPITZNAS, M.</creatorcontrib><creatorcontrib>KOCH, F.</creatorcontrib><creatorcontrib>GRUS, F.</creatorcontrib><creatorcontrib>LUTZ, J.</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>Experimental eye research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>AUGUSTIN, A.J.</au><au>SPITZNAS, M.</au><au>KOCH, F.</au><au>GRUS, F.</au><au>LUTZ, J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of Perfluorooctylbromide and vitamin E on Ischemia Induced Retinal Oxidative Tissue Damage</atitle><jtitle>Experimental eye research</jtitle><addtitle>Exp Eye Res</addtitle><date>1998-01</date><risdate>1998</risdate><volume>66</volume><issue>1</issue><spage>19</spage><epage>24</epage><pages>19-24</pages><issn>0014-4835</issn><eissn>1096-0007</eissn><coden>EXERA6</coden><abstract>The aim of this study was to investigate the extent to which ischemia and reperfusion lead to oxidative damage of the retinal tissue and investigate how ischemic and reperfused retinal tissues react to the application of perfluorooctylbromide (PFOB) and, if this reaction can be influenced by protective drugs such as vitamin E (Vit.E). The experiments were performed with 60 male Wistar rats, divided into 12 groups using an established model of reversible ischemia and reperfusion of the globe. Grouping of animals was carried out according to different ischemia and reperfusion periods and different therapeutic regimens (PFOB, Vit.E). Treatment with PFOB and/or Vit.E was performed after 60 min of ischemia with 60 min of reperfusion. At the end of the experiments thiobarbituric acid reactive substances (TBARS) were determined in the retinal tissues and served as parameters of oxidative tissue damage. Ischemia of up to 60 min led to a significant increase in TBARS values. Ninety and 120 min of ischemia led to no further significant elevation compared to the 60 min or 90 min group. Following 60 min of ischemia, a reperfusion period of 15 min led to an increase in TBARS values that was significant (P<0.05) after 30 and 60 min. Addition of PFOB resulted in a further significant (P<0.05) increase in TBARS values as compared to the respective group without treatment. Vit. E alone did not change the values significantly compared to the respective group without treatment. However, the application of Vit.E in addition to PFOB led to a significant reduction in TBARS values. Ischemia resulted in severe oxidative retinal tissue damage, which increased during reperfusion. The reperfusion damage might be due to the known depletion of protecting substances such as vitamin E. Enhancement of oxygen supply by PFOB during reperfusion without any tissue protection leads to more severe damage. Thus, additional protection of the tissue by powerful antioxidants is necessary when providing oxygen for better tissue recovery.</abstract><cop>London</cop><pub>Elsevier Ltd</pub><pmid>9533827</pmid><doi>10.1006/exer.1997.0399</doi><tpages>6</tpages></addata></record> |
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| ispartof | Experimental eye research, 1998-01, Vol.66 (1), p.19-24 |
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| subjects | Animals Biological and medical sciences Fluorocarbons - metabolism Fluorocarbons - pharmacology ischemia Ischemia - metabolism Ischemia - prevention & control Male Medical sciences Ophthalmology oxidative tissue damage Perfluorooctylbromide Peroxides - metabolism Rats Rats, Wistar Reperfusion Injury - metabolism Reperfusion Injury - prevention & control retina Retina - drug effects Retinal Diseases - chemically induced Retinal Diseases - prevention & control Retinopathies Thiobarbiturates - analysis Time Factors vitamin E Vitamin E - pharmacology |
| title | Effects of Perfluorooctylbromide and vitamin E on Ischemia Induced Retinal Oxidative Tissue Damage |
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