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Postischemic recovery of contractile function is impaired in SOD2+/- but not SOD1+/- mouse hearts
Reactive oxygen species (ROS) contribute to myocardial stunning. Superoxide dismutase (SOD) is a major defense mechanism against ROS. The purpose of this study was to evaluate the contributions of cytosolic (SOD1) and mitochondrial (SOD2) isoforms to protect against myocardial stunning. Isolated hea...
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| Published in: | Circulation (New York, N.Y.) N.Y.), 2002-02, Vol.105 (8), p.981-986 |
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| container_issue | 8 |
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| container_title | Circulation (New York, N.Y.) |
| container_volume | 105 |
| creator | ASIMAKIS, Gregory K LICK, Scott PATTERSON, Cam |
| description | Reactive oxygen species (ROS) contribute to myocardial stunning. Superoxide dismutase (SOD) is a major defense mechanism against ROS. The purpose of this study was to evaluate the contributions of cytosolic (SOD1) and mitochondrial (SOD2) isoforms to protect against myocardial stunning.
Isolated hearts from wild-type, heterozygous (+/-) SOD1 and SOD2 knockout mice received 30 minutes of ischemia followed by 60 minutes of reperfusion. After 60 minutes of reperfusion, the heart rate multiplied by the developed pressure (HRxDP) in the wild-type and SOD1(+/-) hearts recovered to 92 +/- 9 and 85 +/- 7 of preischemic baseline values, respectively (P=NS). In contrast, the HRxDP was significantly lower (63 +/- 7%) in the SOD2(+/-) hearts compared with the wild-type hearts. Western blot analysis and enzymatic activity of tissue lysates confirmed reduction of activities of specific SOD isoforms without compensatory increase in the other isoform in the knockout animals studied.
Postischemic functional recovery is more sensitive to a partial deficiency of SOD2 than a partial deficiency of SOD1. Therefore, modulation of the mitochondrial SOD isoform is a critical determinant in the tolerance of the heart to oxidative stress. |
| doi_str_mv | 10.1161/hc0802.104502 |
| format | article |
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Isolated hearts from wild-type, heterozygous (+/-) SOD1 and SOD2 knockout mice received 30 minutes of ischemia followed by 60 minutes of reperfusion. After 60 minutes of reperfusion, the heart rate multiplied by the developed pressure (HRxDP) in the wild-type and SOD1(+/-) hearts recovered to 92 +/- 9 and 85 +/- 7 of preischemic baseline values, respectively (P=NS). In contrast, the HRxDP was significantly lower (63 +/- 7%) in the SOD2(+/-) hearts compared with the wild-type hearts. Western blot analysis and enzymatic activity of tissue lysates confirmed reduction of activities of specific SOD isoforms without compensatory increase in the other isoform in the knockout animals studied.
Postischemic functional recovery is more sensitive to a partial deficiency of SOD2 than a partial deficiency of SOD1. Therefore, modulation of the mitochondrial SOD isoform is a critical determinant in the tolerance of the heart to oxidative stress.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/hc0802.104502</identifier><identifier>PMID: 11864929</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Biological and medical sciences ; Blood Pressure ; Cardiology. Vascular system ; Coronary Circulation ; Coronary heart disease ; Diastole ; Enzyme Activation - genetics ; Female ; Heart ; Heterozygote ; In Vitro Techniques ; Isoenzymes - genetics ; Isoenzymes - metabolism ; L-Lactate Dehydrogenase - metabolism ; Lipid Peroxides - metabolism ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria - enzymology ; Myocardial Contraction ; Myocardial Ischemia - physiopathology ; Myocardial Reperfusion ; Myocardium - enzymology ; Oxidative Stress ; Recovery of Function - genetics ; Superoxide Dismutase - genetics ; Superoxide Dismutase - metabolism ; Superoxide Dismutase-1</subject><ispartof>Circulation (New York, N.Y.), 2002-02, Vol.105 (8), p.981-986</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Feb 26, 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c426t-c8b0e0c688329d6a0560acba0281fdd6d41ed74207ceeb3989ba52eee6c2940c3</citedby><cites>FETCH-LOGICAL-c426t-c8b0e0c688329d6a0560acba0281fdd6d41ed74207ceeb3989ba52eee6c2940c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13510138$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11864929$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ASIMAKIS, Gregory K</creatorcontrib><creatorcontrib>LICK, Scott</creatorcontrib><creatorcontrib>PATTERSON, Cam</creatorcontrib><title>Postischemic recovery of contractile function is impaired in SOD2+/- but not SOD1+/- mouse hearts</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Reactive oxygen species (ROS) contribute to myocardial stunning. Superoxide dismutase (SOD) is a major defense mechanism against ROS. The purpose of this study was to evaluate the contributions of cytosolic (SOD1) and mitochondrial (SOD2) isoforms to protect against myocardial stunning.
Isolated hearts from wild-type, heterozygous (+/-) SOD1 and SOD2 knockout mice received 30 minutes of ischemia followed by 60 minutes of reperfusion. After 60 minutes of reperfusion, the heart rate multiplied by the developed pressure (HRxDP) in the wild-type and SOD1(+/-) hearts recovered to 92 +/- 9 and 85 +/- 7 of preischemic baseline values, respectively (P=NS). In contrast, the HRxDP was significantly lower (63 +/- 7%) in the SOD2(+/-) hearts compared with the wild-type hearts. Western blot analysis and enzymatic activity of tissue lysates confirmed reduction of activities of specific SOD isoforms without compensatory increase in the other isoform in the knockout animals studied.
Postischemic functional recovery is more sensitive to a partial deficiency of SOD2 than a partial deficiency of SOD1. Therefore, modulation of the mitochondrial SOD isoform is a critical determinant in the tolerance of the heart to oxidative stress.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Cardiology. Vascular system</subject><subject>Coronary Circulation</subject><subject>Coronary heart disease</subject><subject>Diastole</subject><subject>Enzyme Activation - genetics</subject><subject>Female</subject><subject>Heart</subject><subject>Heterozygote</subject><subject>In Vitro Techniques</subject><subject>Isoenzymes - genetics</subject><subject>Isoenzymes - metabolism</subject><subject>L-Lactate Dehydrogenase - metabolism</subject><subject>Lipid Peroxides - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mitochondria - enzymology</subject><subject>Myocardial Contraction</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Myocardial Reperfusion</subject><subject>Myocardium - enzymology</subject><subject>Oxidative Stress</subject><subject>Recovery of Function - genetics</subject><subject>Superoxide Dismutase - genetics</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Superoxide Dismutase-1</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNpd0F1L5DAUBuAgio66l3u7BGG9kY4nH02TS3H9AmGEda9Lmp4ykbYZk1bw32-GGRC8ynnh4XDyEvKTwZIxxa7XDjTwJQNZAj8gC1ZyWchSmEOyAABTVILzE3Ka0luOSlTlMTlhTCtpuFkQ-xLS5JNb4-AdjejCB8ZPGjrqwjhF6ybfI-3mMQ9hpD5RP2ysj9hSP9K_qz_86rqgzTzRMUzbzLZ5CHNCukYbp3ROjjrbJ_yxf8_Iv_u719vH4nn18HR781w4ydVUON0AglNaC25aZaFUYF1jgWvWta1qJcO2khwqh9gIo01jS46IynEjwYkzcrnbu4nhfcY01UP-F_a9HTGfU1dMal5VZYYX3-BbmOOYb6s540pXSpuMih1yMaQUsas30Q82ftYM6m3x9a74eld89r_2S-dmwPZL75vO4Pce2ORs30U7Op--nCgZMKHFf8jmiUE</recordid><startdate>20020226</startdate><enddate>20020226</enddate><creator>ASIMAKIS, Gregory K</creator><creator>LICK, Scott</creator><creator>PATTERSON, Cam</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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><scope>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20020226</creationdate><title>Postischemic recovery of contractile function is impaired in SOD2+/- but not SOD1+/- mouse hearts</title><author>ASIMAKIS, Gregory K ; LICK, Scott ; PATTERSON, Cam</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c426t-c8b0e0c688329d6a0560acba0281fdd6d41ed74207ceeb3989ba52eee6c2940c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Cardiology. Vascular system</topic><topic>Coronary Circulation</topic><topic>Coronary heart disease</topic><topic>Diastole</topic><topic>Enzyme Activation - genetics</topic><topic>Female</topic><topic>Heart</topic><topic>Heterozygote</topic><topic>In Vitro Techniques</topic><topic>Isoenzymes - genetics</topic><topic>Isoenzymes - metabolism</topic><topic>L-Lactate Dehydrogenase - metabolism</topic><topic>Lipid Peroxides - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mitochondria - enzymology</topic><topic>Myocardial Contraction</topic><topic>Myocardial Ischemia - physiopathology</topic><topic>Myocardial Reperfusion</topic><topic>Myocardium - enzymology</topic><topic>Oxidative Stress</topic><topic>Recovery of Function - genetics</topic><topic>Superoxide Dismutase - genetics</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Superoxide Dismutase-1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ASIMAKIS, Gregory K</creatorcontrib><creatorcontrib>LICK, Scott</creatorcontrib><creatorcontrib>PATTERSON, Cam</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><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ASIMAKIS, Gregory K</au><au>LICK, Scott</au><au>PATTERSON, Cam</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Postischemic recovery of contractile function is impaired in SOD2+/- but not SOD1+/- mouse hearts</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2002-02-26</date><risdate>2002</risdate><volume>105</volume><issue>8</issue><spage>981</spage><epage>986</epage><pages>981-986</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Reactive oxygen species (ROS) contribute to myocardial stunning. Superoxide dismutase (SOD) is a major defense mechanism against ROS. The purpose of this study was to evaluate the contributions of cytosolic (SOD1) and mitochondrial (SOD2) isoforms to protect against myocardial stunning.
Isolated hearts from wild-type, heterozygous (+/-) SOD1 and SOD2 knockout mice received 30 minutes of ischemia followed by 60 minutes of reperfusion. After 60 minutes of reperfusion, the heart rate multiplied by the developed pressure (HRxDP) in the wild-type and SOD1(+/-) hearts recovered to 92 +/- 9 and 85 +/- 7 of preischemic baseline values, respectively (P=NS). In contrast, the HRxDP was significantly lower (63 +/- 7%) in the SOD2(+/-) hearts compared with the wild-type hearts. Western blot analysis and enzymatic activity of tissue lysates confirmed reduction of activities of specific SOD isoforms without compensatory increase in the other isoform in the knockout animals studied.
Postischemic functional recovery is more sensitive to a partial deficiency of SOD2 than a partial deficiency of SOD1. Therefore, modulation of the mitochondrial SOD isoform is a critical determinant in the tolerance of the heart to oxidative stress.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>11864929</pmid><doi>10.1161/hc0802.104502</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Blood Pressure Cardiology. Vascular system Coronary Circulation Coronary heart disease Diastole Enzyme Activation - genetics Female Heart Heterozygote In Vitro Techniques Isoenzymes - genetics Isoenzymes - metabolism L-Lactate Dehydrogenase - metabolism Lipid Peroxides - metabolism Male Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Mitochondria - enzymology Myocardial Contraction Myocardial Ischemia - physiopathology Myocardial Reperfusion Myocardium - enzymology Oxidative Stress Recovery of Function - genetics Superoxide Dismutase - genetics Superoxide Dismutase - metabolism Superoxide Dismutase-1 |
| title | Postischemic recovery of contractile function is impaired in SOD2+/- but not SOD1+/- mouse hearts |
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