Oxidative stress and heart failure

Various abnormalities have been implicated in the transition of hypertrophy to heart failure but the exact mechanism is still unknown. Thus heart failure subsequent to hypertrophy remains a major clinical problem. Recently, oxidative stress has been suggested to play a critical role in the pathogene...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Molecular and cellular biochemistry 1995-06, Vol.147 (1/2), p.77-81
Hauptverfasser: Singh, N, Dhalla, A.K, Seneviratne, C, Singal, P.K
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 81
container_issue 1/2
container_start_page 77
container_title Molecular and cellular biochemistry
container_volume 147
creator Singh, N
Dhalla, A.K
Seneviratne, C
Singal, P.K
description Various abnormalities have been implicated in the transition of hypertrophy to heart failure but the exact mechanism is still unknown. Thus heart failure subsequent to hypertrophy remains a major clinical problem. Recently, oxidative stress has been suggested to play a critical role in the pathogenesis of heart failure. Here we describe antioxidant changes as well as their significance during hypertrophy and heart failure stages. Heart hypertrophy in rats and guinea pigs, in response to pressure overload, is associated with an increase in 'antioxidant reserve' and a decrease in oxidative stress. Hypertrophied rat hearts show increased tolerance for different oxidative stress conditions such as those imposed by free radicals, hypoxia-reoxygenation and ischemia-reperfusion. On the other hand, heart failure under acute as well as chronic conditions is associated with reduced antioxidant reserve and increased oxidative stress. The latter may have a causal role as suggested by the protection seen with antioxidant treatment in acute as well as in chronic heart failure. It is becoming increasingly apparent that, anytime the available antioxidant reserve in the cell becomes inadequate, myocardial dysfunction is imminent.
doi_str_mv 10.1007/BF00944786
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_77771297</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>77771297</sourcerecordid><originalsourceid>FETCH-LOGICAL-c306t-9a9ff9dae1106f18e499ffc4c9023b6445dd5a8c51c7338549546cd90dc2f4583</originalsourceid><addsrcrecordid>eNpFkE1LAzEQhoMotVYv3sXFgwdhdWaTbJKjFqtCoQftOaT50JVttya7ov_elS46l4F5H16Gh5BThGsEEDd3MwDFmJDlHhkjFzRnCtU-GQMFyCUKcUiOUnoH6HHEERkJphjnckwuFl-VM2316bPURp9SZjYue_MmtlkwVd1Ff0wOgqmTPxn2hCxn9y_Tx3y-eHia3s5zS6Fsc2VUCMoZjwhlQOmZ6g-WWQUFXZWMcee4kZajFZRKzhRnpXUKnC0C45JOyOWudxubj86nVq-rZH1dm41vuqRFP1go0YNXO9DGJqXog97Gam3it0bQv0L0v5AePhtau9Xauz90MNDn57s8mEab11glvXwuACkgB9F_TX8AGyFhzA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>77771297</pqid></control><display><type>article</type><title>Oxidative stress and heart failure</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Singh, N ; Dhalla, A.K ; Seneviratne, C ; Singal, P.K</creator><creatorcontrib>Singh, N ; Dhalla, A.K ; Seneviratne, C ; Singal, P.K</creatorcontrib><description>Various abnormalities have been implicated in the transition of hypertrophy to heart failure but the exact mechanism is still unknown. Thus heart failure subsequent to hypertrophy remains a major clinical problem. Recently, oxidative stress has been suggested to play a critical role in the pathogenesis of heart failure. Here we describe antioxidant changes as well as their significance during hypertrophy and heart failure stages. Heart hypertrophy in rats and guinea pigs, in response to pressure overload, is associated with an increase in 'antioxidant reserve' and a decrease in oxidative stress. Hypertrophied rat hearts show increased tolerance for different oxidative stress conditions such as those imposed by free radicals, hypoxia-reoxygenation and ischemia-reperfusion. On the other hand, heart failure under acute as well as chronic conditions is associated with reduced antioxidant reserve and increased oxidative stress. The latter may have a causal role as suggested by the protection seen with antioxidant treatment in acute as well as in chronic heart failure. It is becoming increasingly apparent that, anytime the available antioxidant reserve in the cell becomes inadequate, myocardial dysfunction is imminent.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/BF00944786</identifier><identifier>PMID: 7494558</identifier><language>eng</language><publisher>Netherlands</publisher><subject>Animals ; antioxidants ; Antioxidants - metabolism ; Cardiomegaly - metabolism ; Cardiomegaly - pathology ; free radicals ; Free Radicals - metabolism ; guinea pigs ; heart diseases ; Heart Failure - metabolism ; Heart Failure - pathology ; Heart Failure - physiopathology ; hypertrophy ; lipid peroxidation ; Microscopy, Electron ; Myocardium - metabolism ; Myocardium - ultrastructure ; oxidation ; Oxidative Stress ; rats ; stress ; Superoxide Dismutase - metabolism</subject><ispartof>Molecular and cellular biochemistry, 1995-06, Vol.147 (1/2), p.77-81</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c306t-9a9ff9dae1106f18e499ffc4c9023b6445dd5a8c51c7338549546cd90dc2f4583</citedby><cites>FETCH-LOGICAL-c306t-9a9ff9dae1106f18e499ffc4c9023b6445dd5a8c51c7338549546cd90dc2f4583</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27928,27929</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7494558$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Singh, N</creatorcontrib><creatorcontrib>Dhalla, A.K</creatorcontrib><creatorcontrib>Seneviratne, C</creatorcontrib><creatorcontrib>Singal, P.K</creatorcontrib><title>Oxidative stress and heart failure</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><description>Various abnormalities have been implicated in the transition of hypertrophy to heart failure but the exact mechanism is still unknown. Thus heart failure subsequent to hypertrophy remains a major clinical problem. Recently, oxidative stress has been suggested to play a critical role in the pathogenesis of heart failure. Here we describe antioxidant changes as well as their significance during hypertrophy and heart failure stages. Heart hypertrophy in rats and guinea pigs, in response to pressure overload, is associated with an increase in 'antioxidant reserve' and a decrease in oxidative stress. Hypertrophied rat hearts show increased tolerance for different oxidative stress conditions such as those imposed by free radicals, hypoxia-reoxygenation and ischemia-reperfusion. On the other hand, heart failure under acute as well as chronic conditions is associated with reduced antioxidant reserve and increased oxidative stress. The latter may have a causal role as suggested by the protection seen with antioxidant treatment in acute as well as in chronic heart failure. It is becoming increasingly apparent that, anytime the available antioxidant reserve in the cell becomes inadequate, myocardial dysfunction is imminent.</description><subject>Animals</subject><subject>antioxidants</subject><subject>Antioxidants - metabolism</subject><subject>Cardiomegaly - metabolism</subject><subject>Cardiomegaly - pathology</subject><subject>free radicals</subject><subject>Free Radicals - metabolism</subject><subject>guinea pigs</subject><subject>heart diseases</subject><subject>Heart Failure - metabolism</subject><subject>Heart Failure - pathology</subject><subject>Heart Failure - physiopathology</subject><subject>hypertrophy</subject><subject>lipid peroxidation</subject><subject>Microscopy, Electron</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - ultrastructure</subject><subject>oxidation</subject><subject>Oxidative Stress</subject><subject>rats</subject><subject>stress</subject><subject>Superoxide Dismutase - metabolism</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1LAzEQhoMotVYv3sXFgwdhdWaTbJKjFqtCoQftOaT50JVttya7ov_elS46l4F5H16Gh5BThGsEEDd3MwDFmJDlHhkjFzRnCtU-GQMFyCUKcUiOUnoH6HHEERkJphjnckwuFl-VM2316bPURp9SZjYue_MmtlkwVd1Ff0wOgqmTPxn2hCxn9y_Tx3y-eHia3s5zS6Fsc2VUCMoZjwhlQOmZ6g-WWQUFXZWMcee4kZajFZRKzhRnpXUKnC0C45JOyOWudxubj86nVq-rZH1dm41vuqRFP1go0YNXO9DGJqXog97Gam3it0bQv0L0v5AePhtau9Xauz90MNDn57s8mEab11glvXwuACkgB9F_TX8AGyFhzA</recordid><startdate>19950607</startdate><enddate>19950607</enddate><creator>Singh, N</creator><creator>Dhalla, A.K</creator><creator>Seneviratne, C</creator><creator>Singal, P.K</creator><scope>FBQ</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>7X8</scope></search><sort><creationdate>19950607</creationdate><title>Oxidative stress and heart failure</title><author>Singh, N ; Dhalla, A.K ; Seneviratne, C ; Singal, P.K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c306t-9a9ff9dae1106f18e499ffc4c9023b6445dd5a8c51c7338549546cd90dc2f4583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Animals</topic><topic>antioxidants</topic><topic>Antioxidants - metabolism</topic><topic>Cardiomegaly - metabolism</topic><topic>Cardiomegaly - pathology</topic><topic>free radicals</topic><topic>Free Radicals - metabolism</topic><topic>guinea pigs</topic><topic>heart diseases</topic><topic>Heart Failure - metabolism</topic><topic>Heart Failure - pathology</topic><topic>Heart Failure - physiopathology</topic><topic>hypertrophy</topic><topic>lipid peroxidation</topic><topic>Microscopy, Electron</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - ultrastructure</topic><topic>oxidation</topic><topic>Oxidative Stress</topic><topic>rats</topic><topic>stress</topic><topic>Superoxide Dismutase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Singh, N</creatorcontrib><creatorcontrib>Dhalla, A.K</creatorcontrib><creatorcontrib>Seneviratne, C</creatorcontrib><creatorcontrib>Singal, P.K</creatorcontrib><collection>AGRIS</collection><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><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Singh, N</au><au>Dhalla, A.K</au><au>Seneviratne, C</au><au>Singal, P.K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxidative stress and heart failure</atitle><jtitle>Molecular and cellular biochemistry</jtitle><addtitle>Mol Cell Biochem</addtitle><date>1995-06-07</date><risdate>1995</risdate><volume>147</volume><issue>1/2</issue><spage>77</spage><epage>81</epage><pages>77-81</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Various abnormalities have been implicated in the transition of hypertrophy to heart failure but the exact mechanism is still unknown. Thus heart failure subsequent to hypertrophy remains a major clinical problem. Recently, oxidative stress has been suggested to play a critical role in the pathogenesis of heart failure. Here we describe antioxidant changes as well as their significance during hypertrophy and heart failure stages. Heart hypertrophy in rats and guinea pigs, in response to pressure overload, is associated with an increase in 'antioxidant reserve' and a decrease in oxidative stress. Hypertrophied rat hearts show increased tolerance for different oxidative stress conditions such as those imposed by free radicals, hypoxia-reoxygenation and ischemia-reperfusion. On the other hand, heart failure under acute as well as chronic conditions is associated with reduced antioxidant reserve and increased oxidative stress. The latter may have a causal role as suggested by the protection seen with antioxidant treatment in acute as well as in chronic heart failure. It is becoming increasingly apparent that, anytime the available antioxidant reserve in the cell becomes inadequate, myocardial dysfunction is imminent.</abstract><cop>Netherlands</cop><pmid>7494558</pmid><doi>10.1007/BF00944786</doi><tpages>5</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0300-8177
ispartof Molecular and cellular biochemistry, 1995-06, Vol.147 (1/2), p.77-81
issn 0300-8177
1573-4919
language eng
recordid cdi_proquest_miscellaneous_77771297
source MEDLINE; SpringerNature Journals
subjects Animals
antioxidants
Antioxidants - metabolism
Cardiomegaly - metabolism
Cardiomegaly - pathology
free radicals
Free Radicals - metabolism
guinea pigs
heart diseases
Heart Failure - metabolism
Heart Failure - pathology
Heart Failure - physiopathology
hypertrophy
lipid peroxidation
Microscopy, Electron
Myocardium - metabolism
Myocardium - ultrastructure
oxidation
Oxidative Stress
rats
stress
Superoxide Dismutase - metabolism
title Oxidative stress and heart failure
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-17T10%3A52%3A38IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Oxidative%20stress%20and%20heart%20failure&rft.jtitle=Molecular%20and%20cellular%20biochemistry&rft.au=Singh,%20N&rft.date=1995-06-07&rft.volume=147&rft.issue=1/2&rft.spage=77&rft.epage=81&rft.pages=77-81&rft.issn=0300-8177&rft.eissn=1573-4919&rft_id=info:doi/10.1007/BF00944786&rft_dat=%3Cproquest_cross%3E77771297%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=77771297&rft_id=info:pmid/7494558&rfr_iscdi=true