Adriamycin-induced oxidative mitochondrial cardiotoxicity
The anticancer agent Adriamycin (ADR) has long been recognized to induce a dose-limiting cardiotoxicity. Numerous studies have attempted to characterize and elucidate the mechanism(s) behind its cardiotoxic effect. Despite a wealth of data covering a wide-range of effects mediated by the drug, the d...
Gespeichert in:
| Veröffentlicht in: | Cell biology and toxicology 2007-01, Vol.23 (1), p.15-25 |
|---|---|
| Hauptverfasser: | , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 25 |
|---|---|
| container_issue | 1 |
| container_start_page | 15 |
| container_title | Cell biology and toxicology |
| container_volume | 23 |
| creator | Berthiaume, J M Wallace, K B |
| description | The anticancer agent Adriamycin (ADR) has long been recognized to induce a dose-limiting cardiotoxicity. Numerous studies have attempted to characterize and elucidate the mechanism(s) behind its cardiotoxic effect. Despite a wealth of data covering a wide-range of effects mediated by the drug, the definitive mechanism remains a matter of debate. However, there is consensus that this toxicity is related to the induction of reactive oxygen species (ROS). Induction of ROS in the heart by ADR occurs via redox cycling of the drug at complex I of the electron transport chain. Many studies support the theory that mitochondria are a primary target of ADR-induced oxidative stress, both acutely and long-term. This review focuses on the effects of ADR redox cycling on the mitochondrion, which support the hypothesis that these organelles are indeed a major factor in ADR cardiotoxicity. This review has been constructed with particular emphasis on studies utilizing cardiac models with clinically relevant doses or concentrations of ADR in the hope of advancing our understanding of the mechanisms of ADR toxicity. This compilation of current data may reveal valuable insights for the development of therapeutic strategies better tailored to minimizing the dose-limiting effect of ADR. |
| doi_str_mv | 10.1007/s10565-006-0140-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_19606995</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>19606995</sourcerecordid><originalsourceid>FETCH-LOGICAL-c357t-5e16721a841870642de175e7f257eb21081ae589309d0f787d8c965a868ab83c3</originalsourceid><addsrcrecordid>eNpdkEtLAzEUhYMotlZ_gBspLtxFbzKT17IUX1Bwo-uQJhlM6UxqMiPOvzelBcHVXdzvHA4fQtcE7gmAeMgEGGcYgGMgNeDxBE0JExXmktJTNAVRU0xBkQm6yHkDBSSCnaMJEQAKlJgitXApmHa0ocOhc4P1bh5_gjN9-PbzNvTRfsZuz2zn1iQXYl_eNvTjJTprzDb7q-OdoY-nx_flC169Pb8uFytsKyZ6zDzhghIjayIF8Jo6XzZ40VAm_JoSkMR4JlUFykEjpHDSKs6M5NKsZWWrGbo79O5S_Bp87nUbsvXbrel8HLImigNXihXw9h-4iUPqyjYtal5XIJksEDlANsWck2_0LoXWpFET0Hup-iBVF1d6L1WPJXNzLB7WrXd_iaPF6heKdXFC</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>746430858</pqid></control><display><type>article</type><title>Adriamycin-induced oxidative mitochondrial cardiotoxicity</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Berthiaume, J M ; Wallace, K B</creator><creatorcontrib>Berthiaume, J M ; Wallace, K B</creatorcontrib><description>The anticancer agent Adriamycin (ADR) has long been recognized to induce a dose-limiting cardiotoxicity. Numerous studies have attempted to characterize and elucidate the mechanism(s) behind its cardiotoxic effect. Despite a wealth of data covering a wide-range of effects mediated by the drug, the definitive mechanism remains a matter of debate. However, there is consensus that this toxicity is related to the induction of reactive oxygen species (ROS). Induction of ROS in the heart by ADR occurs via redox cycling of the drug at complex I of the electron transport chain. Many studies support the theory that mitochondria are a primary target of ADR-induced oxidative stress, both acutely and long-term. This review focuses on the effects of ADR redox cycling on the mitochondrion, which support the hypothesis that these organelles are indeed a major factor in ADR cardiotoxicity. This review has been constructed with particular emphasis on studies utilizing cardiac models with clinically relevant doses or concentrations of ADR in the hope of advancing our understanding of the mechanisms of ADR toxicity. This compilation of current data may reveal valuable insights for the development of therapeutic strategies better tailored to minimizing the dose-limiting effect of ADR.</description><identifier>ISSN: 0742-2091</identifier><identifier>EISSN: 1573-6822</identifier><identifier>DOI: 10.1007/s10565-006-0140-y</identifier><identifier>PMID: 17009097</identifier><language>eng</language><publisher>Netherlands: Springer Nature B.V</publisher><subject>Animals ; Antibiotics, Antineoplastic - pharmacokinetics ; Antibiotics, Antineoplastic - toxicity ; Chemotherapy ; Doxorubicin - pharmacokinetics ; Doxorubicin - toxicity ; Electron Transport Complex I - drug effects ; Electron Transport Complex I - metabolism ; Heart ; Humans ; In Vitro Techniques ; Mitochondria ; Mitochondria, Heart - drug effects ; Mitochondria, Heart - metabolism ; Models, Cardiovascular ; Oxidation-Reduction ; Oxidative stress ; Pharmacology ; Reactive Oxygen Species - metabolism ; Toxicity</subject><ispartof>Cell biology and toxicology, 2007-01, Vol.23 (1), p.15-25</ispartof><rights>Springer Science + Business Media, Inc. 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c357t-5e16721a841870642de175e7f257eb21081ae589309d0f787d8c965a868ab83c3</citedby><cites>FETCH-LOGICAL-c357t-5e16721a841870642de175e7f257eb21081ae589309d0f787d8c965a868ab83c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17009097$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Berthiaume, J M</creatorcontrib><creatorcontrib>Wallace, K B</creatorcontrib><title>Adriamycin-induced oxidative mitochondrial cardiotoxicity</title><title>Cell biology and toxicology</title><addtitle>Cell Biol Toxicol</addtitle><description>The anticancer agent Adriamycin (ADR) has long been recognized to induce a dose-limiting cardiotoxicity. Numerous studies have attempted to characterize and elucidate the mechanism(s) behind its cardiotoxic effect. Despite a wealth of data covering a wide-range of effects mediated by the drug, the definitive mechanism remains a matter of debate. However, there is consensus that this toxicity is related to the induction of reactive oxygen species (ROS). Induction of ROS in the heart by ADR occurs via redox cycling of the drug at complex I of the electron transport chain. Many studies support the theory that mitochondria are a primary target of ADR-induced oxidative stress, both acutely and long-term. This review focuses on the effects of ADR redox cycling on the mitochondrion, which support the hypothesis that these organelles are indeed a major factor in ADR cardiotoxicity. This review has been constructed with particular emphasis on studies utilizing cardiac models with clinically relevant doses or concentrations of ADR in the hope of advancing our understanding of the mechanisms of ADR toxicity. This compilation of current data may reveal valuable insights for the development of therapeutic strategies better tailored to minimizing the dose-limiting effect of ADR.</description><subject>Animals</subject><subject>Antibiotics, Antineoplastic - pharmacokinetics</subject><subject>Antibiotics, Antineoplastic - toxicity</subject><subject>Chemotherapy</subject><subject>Doxorubicin - pharmacokinetics</subject><subject>Doxorubicin - toxicity</subject><subject>Electron Transport Complex I - drug effects</subject><subject>Electron Transport Complex I - metabolism</subject><subject>Heart</subject><subject>Humans</subject><subject>In Vitro Techniques</subject><subject>Mitochondria</subject><subject>Mitochondria, Heart - drug effects</subject><subject>Mitochondria, Heart - metabolism</subject><subject>Models, Cardiovascular</subject><subject>Oxidation-Reduction</subject><subject>Oxidative stress</subject><subject>Pharmacology</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Toxicity</subject><issn>0742-2091</issn><issn>1573-6822</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkEtLAzEUhYMotlZ_gBspLtxFbzKT17IUX1Bwo-uQJhlM6UxqMiPOvzelBcHVXdzvHA4fQtcE7gmAeMgEGGcYgGMgNeDxBE0JExXmktJTNAVRU0xBkQm6yHkDBSSCnaMJEQAKlJgitXApmHa0ocOhc4P1bh5_gjN9-PbzNvTRfsZuz2zn1iQXYl_eNvTjJTprzDb7q-OdoY-nx_flC169Pb8uFytsKyZ6zDzhghIjayIF8Jo6XzZ40VAm_JoSkMR4JlUFykEjpHDSKs6M5NKsZWWrGbo79O5S_Bp87nUbsvXbrel8HLImigNXihXw9h-4iUPqyjYtal5XIJksEDlANsWck2_0LoXWpFET0Hup-iBVF1d6L1WPJXNzLB7WrXd_iaPF6heKdXFC</recordid><startdate>200701</startdate><enddate>200701</enddate><creator>Berthiaume, J M</creator><creator>Wallace, K B</creator><general>Springer Nature B.V</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>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7TM</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>200701</creationdate><title>Adriamycin-induced oxidative mitochondrial cardiotoxicity</title><author>Berthiaume, J M ; Wallace, K B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c357t-5e16721a841870642de175e7f257eb21081ae589309d0f787d8c965a868ab83c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Antibiotics, Antineoplastic - pharmacokinetics</topic><topic>Antibiotics, Antineoplastic - toxicity</topic><topic>Chemotherapy</topic><topic>Doxorubicin - pharmacokinetics</topic><topic>Doxorubicin - toxicity</topic><topic>Electron Transport Complex I - drug effects</topic><topic>Electron Transport Complex I - metabolism</topic><topic>Heart</topic><topic>Humans</topic><topic>In Vitro Techniques</topic><topic>Mitochondria</topic><topic>Mitochondria, Heart - drug effects</topic><topic>Mitochondria, Heart - metabolism</topic><topic>Models, Cardiovascular</topic><topic>Oxidation-Reduction</topic><topic>Oxidative stress</topic><topic>Pharmacology</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Berthiaume, J M</creatorcontrib><creatorcontrib>Wallace, K B</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Environmental Science Collection</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Cell biology and toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Berthiaume, J M</au><au>Wallace, K B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adriamycin-induced oxidative mitochondrial cardiotoxicity</atitle><jtitle>Cell biology and toxicology</jtitle><addtitle>Cell Biol Toxicol</addtitle><date>2007-01</date><risdate>2007</risdate><volume>23</volume><issue>1</issue><spage>15</spage><epage>25</epage><pages>15-25</pages><issn>0742-2091</issn><eissn>1573-6822</eissn><abstract>The anticancer agent Adriamycin (ADR) has long been recognized to induce a dose-limiting cardiotoxicity. Numerous studies have attempted to characterize and elucidate the mechanism(s) behind its cardiotoxic effect. Despite a wealth of data covering a wide-range of effects mediated by the drug, the definitive mechanism remains a matter of debate. However, there is consensus that this toxicity is related to the induction of reactive oxygen species (ROS). Induction of ROS in the heart by ADR occurs via redox cycling of the drug at complex I of the electron transport chain. Many studies support the theory that mitochondria are a primary target of ADR-induced oxidative stress, both acutely and long-term. This review focuses on the effects of ADR redox cycling on the mitochondrion, which support the hypothesis that these organelles are indeed a major factor in ADR cardiotoxicity. This review has been constructed with particular emphasis on studies utilizing cardiac models with clinically relevant doses or concentrations of ADR in the hope of advancing our understanding of the mechanisms of ADR toxicity. This compilation of current data may reveal valuable insights for the development of therapeutic strategies better tailored to minimizing the dose-limiting effect of ADR.</abstract><cop>Netherlands</cop><pub>Springer Nature B.V</pub><pmid>17009097</pmid><doi>10.1007/s10565-006-0140-y</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0742-2091 |
| ispartof | Cell biology and toxicology, 2007-01, Vol.23 (1), p.15-25 |
| issn | 0742-2091 1573-6822 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_19606995 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Animals Antibiotics, Antineoplastic - pharmacokinetics Antibiotics, Antineoplastic - toxicity Chemotherapy Doxorubicin - pharmacokinetics Doxorubicin - toxicity Electron Transport Complex I - drug effects Electron Transport Complex I - metabolism Heart Humans In Vitro Techniques Mitochondria Mitochondria, Heart - drug effects Mitochondria, Heart - metabolism Models, Cardiovascular Oxidation-Reduction Oxidative stress Pharmacology Reactive Oxygen Species - metabolism Toxicity |
| title | Adriamycin-induced oxidative mitochondrial cardiotoxicity |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-01T02%3A27%3A30IST&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=Adriamycin-induced%20oxidative%20mitochondrial%20cardiotoxicity&rft.jtitle=Cell%20biology%20and%20toxicology&rft.au=Berthiaume,%20J%20M&rft.date=2007-01&rft.volume=23&rft.issue=1&rft.spage=15&rft.epage=25&rft.pages=15-25&rft.issn=0742-2091&rft.eissn=1573-6822&rft_id=info:doi/10.1007/s10565-006-0140-y&rft_dat=%3Cproquest_cross%3E19606995%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=746430858&rft_id=info:pmid/17009097&rfr_iscdi=true |