The Influence of Radiation and Chemotherapy-Related DNA Strand Breaks on Carcinogenesis: An Evaluation
Purpose: DNA strand breaks are believed to induce carcinogenesis. This study was conducted to analyze induction and repair of irradiation- and chemotherapy-related strand breaks in vitro. Methods: Friend Leukemia cells were exposed to irradiation and various chemotherapeutic agents at different dose...
Gespeichert in:
| Veröffentlicht in: | Clinical chemistry and laboratory medicine 1999-04, Vol.37 (4), p.403-408 |
|---|---|
| Hauptverfasser: | , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 408 |
|---|---|
| container_issue | 4 |
| container_start_page | 403 |
| container_title | Clinical chemistry and laboratory medicine |
| container_volume | 37 |
| creator | Froelich, Jens J. Schneller, Folker R. G. Zahn, Rudolf K. |
| description | Purpose: DNA strand breaks are believed to induce carcinogenesis. This study was conducted to analyze induction and repair of irradiation- and chemotherapy-related strand breaks in vitro. Methods: Friend Leukemia cells were exposed to irradiation and various chemotherapeutic agents at different doses and concentrations. Occurence of strand breaks was determined fluorometrically, measuring the rate of DNA unwinding immediatly after exposure and 24 hours later. Results: The amount of double-stranded DNA decreased significantly for irradiation, doxorubicin, dactinomycin and etoposide (p ≤ 0.05, t-test). After 24 hours free of exposure, the persistent damage was detectable for all of these agents but not for irradiated cells, with DNA strand breaks being decreased for etoposide, unchanged for doxorubicin and increased for methotrexate as well as for dactinomycin. Conclusions: Severe DNA damage is induced by various chemotherapeutic agents and by irradiation. While repair of chemotherapy-related strand breaks may remain incomplete or prolonged for some chemotherapeutic agents, repair of radiation induced strand breaks is faster and more complete. Therefore chemotherapy-related carcinogenesis may partially be explained by prolonged persistence of DNA strand breaks. |
| doi_str_mv | 10.1515/CCLM.1999.066 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_19890222</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>19890222</sourcerecordid><originalsourceid>FETCH-LOGICAL-c387t-c45aa5da44674eb6d8555df7a56526beaefab70e81edb476d497b98d64c33b833</originalsourceid><addsrcrecordid>eNpNkE1v1DAURa2qiJbCslvkRcUugx1_ht2QFlppaNUylbqzXuwXJjSTDHaC6L8n0xlRVu9K9-g-6RByytmMK64-luXi24wXRTFjWh-QYy6FyaQQ_PA5y0zrnB-RNyn9ZIwrJc1rcsSZ0AXn7JjUyxXSq65uR-w80r6mdxAaGJq-o9AFWq5w3Q8rjLB5yu6whQEDPb-e0-9D3PafI8JjohNdQvRN1__ADlOTPtF5Ry9-Qzs-b70lr2poE77b3xNy_-ViWV5mi5uvV-V8kXlhzZB5qQBUACm1kVjpYJVSoTagtMp1hYA1VIah5RgqaXSQhakKG7T0QlRWiBPyYbe7if2vEdPg1k3y2LbQYT8mxwtbsDzPJzDbgT72KUWs3SY2a4hPjjO3Feu2Yt1WrJvETvz7_fBYrTH8R-9MTsDZHoDkoa0nO75JL5yVVmr78rdJA_75V0N8dNoIo9ztUjpxy87t5QN3ufgLH7-PFw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>19890222</pqid></control><display><type>article</type><title>The Influence of Radiation and Chemotherapy-Related DNA Strand Breaks on Carcinogenesis: An Evaluation</title><source>MEDLINE</source><source>De Gruyter journals</source><creator>Froelich, Jens J. ; Schneller, Folker R. G. ; Zahn, Rudolf K.</creator><creatorcontrib>Froelich, Jens J. ; Schneller, Folker R. G. ; Zahn, Rudolf K.</creatorcontrib><description>Purpose: DNA strand breaks are believed to induce carcinogenesis. This study was conducted to analyze induction and repair of irradiation- and chemotherapy-related strand breaks in vitro. Methods: Friend Leukemia cells were exposed to irradiation and various chemotherapeutic agents at different doses and concentrations. Occurence of strand breaks was determined fluorometrically, measuring the rate of DNA unwinding immediatly after exposure and 24 hours later. Results: The amount of double-stranded DNA decreased significantly for irradiation, doxorubicin, dactinomycin and etoposide (p ≤ 0.05, t-test). After 24 hours free of exposure, the persistent damage was detectable for all of these agents but not for irradiated cells, with DNA strand breaks being decreased for etoposide, unchanged for doxorubicin and increased for methotrexate as well as for dactinomycin. Conclusions: Severe DNA damage is induced by various chemotherapeutic agents and by irradiation. While repair of chemotherapy-related strand breaks may remain incomplete or prolonged for some chemotherapeutic agents, repair of radiation induced strand breaks is faster and more complete. Therefore chemotherapy-related carcinogenesis may partially be explained by prolonged persistence of DNA strand breaks.</description><identifier>ISSN: 1434-6621</identifier><identifier>EISSN: 1437-4331</identifier><identifier>DOI: 10.1515/CCLM.1999.066</identifier><identifier>PMID: 10369110</identifier><language>eng</language><publisher>Berlin: Walter de Gruyter</publisher><subject>Animals ; Antibiotics, Antineoplastic - pharmacology ; Antimetabolites, Antineoplastic - pharmacology ; Antineoplastic Agents - adverse effects ; Antineoplastic Agents, Phytogenic - pharmacology ; Biological and medical sciences ; Carcinogenesis, carcinogens and anticarcinogens ; Cisplatin - pharmacology ; Dactinomycin - pharmacology ; DNA Damage ; DNA, Neoplasm - drug effects ; DNA, Neoplasm - radiation effects ; Dose-Response Relationship, Drug ; Dose-Response Relationship, Radiation ; Doxorubicin - pharmacology ; Etoposide - pharmacology ; Leukemia, Experimental - drug therapy ; Leukemia, Experimental - genetics ; Leukemia, Experimental - radiotherapy ; Medical sciences ; Methotrexate - pharmacology ; Mice ; Physical agents ; Tumor Cells, Cultured ; Tumors ; Vincristine - pharmacology</subject><ispartof>Clinical chemistry and laboratory medicine, 1999-04, Vol.37 (4), p.403-408</ispartof><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-c45aa5da44674eb6d8555df7a56526beaefab70e81edb476d497b98d64c33b833</citedby><cites>FETCH-LOGICAL-c387t-c45aa5da44674eb6d8555df7a56526beaefab70e81edb476d497b98d64c33b833</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27915,27916</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1848468$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10369110$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Froelich, Jens J.</creatorcontrib><creatorcontrib>Schneller, Folker R. G.</creatorcontrib><creatorcontrib>Zahn, Rudolf K.</creatorcontrib><title>The Influence of Radiation and Chemotherapy-Related DNA Strand Breaks on Carcinogenesis: An Evaluation</title><title>Clinical chemistry and laboratory medicine</title><addtitle>Clinical Chemistry and Laboratory Medicine</addtitle><description>Purpose: DNA strand breaks are believed to induce carcinogenesis. This study was conducted to analyze induction and repair of irradiation- and chemotherapy-related strand breaks in vitro. Methods: Friend Leukemia cells were exposed to irradiation and various chemotherapeutic agents at different doses and concentrations. Occurence of strand breaks was determined fluorometrically, measuring the rate of DNA unwinding immediatly after exposure and 24 hours later. Results: The amount of double-stranded DNA decreased significantly for irradiation, doxorubicin, dactinomycin and etoposide (p ≤ 0.05, t-test). After 24 hours free of exposure, the persistent damage was detectable for all of these agents but not for irradiated cells, with DNA strand breaks being decreased for etoposide, unchanged for doxorubicin and increased for methotrexate as well as for dactinomycin. Conclusions: Severe DNA damage is induced by various chemotherapeutic agents and by irradiation. While repair of chemotherapy-related strand breaks may remain incomplete or prolonged for some chemotherapeutic agents, repair of radiation induced strand breaks is faster and more complete. Therefore chemotherapy-related carcinogenesis may partially be explained by prolonged persistence of DNA strand breaks.</description><subject>Animals</subject><subject>Antibiotics, Antineoplastic - pharmacology</subject><subject>Antimetabolites, Antineoplastic - pharmacology</subject><subject>Antineoplastic Agents - adverse effects</subject><subject>Antineoplastic Agents, Phytogenic - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>Cisplatin - pharmacology</subject><subject>Dactinomycin - pharmacology</subject><subject>DNA Damage</subject><subject>DNA, Neoplasm - drug effects</subject><subject>DNA, Neoplasm - radiation effects</subject><subject>Dose-Response Relationship, Drug</subject><subject>Dose-Response Relationship, Radiation</subject><subject>Doxorubicin - pharmacology</subject><subject>Etoposide - pharmacology</subject><subject>Leukemia, Experimental - drug therapy</subject><subject>Leukemia, Experimental - genetics</subject><subject>Leukemia, Experimental - radiotherapy</subject><subject>Medical sciences</subject><subject>Methotrexate - pharmacology</subject><subject>Mice</subject><subject>Physical agents</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><subject>Vincristine - pharmacology</subject><issn>1434-6621</issn><issn>1437-4331</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkE1v1DAURa2qiJbCslvkRcUugx1_ht2QFlppaNUylbqzXuwXJjSTDHaC6L8n0xlRVu9K9-g-6RByytmMK64-luXi24wXRTFjWh-QYy6FyaQQ_PA5y0zrnB-RNyn9ZIwrJc1rcsSZ0AXn7JjUyxXSq65uR-w80r6mdxAaGJq-o9AFWq5w3Q8rjLB5yu6whQEDPb-e0-9D3PafI8JjohNdQvRN1__ADlOTPtF5Ry9-Qzs-b70lr2poE77b3xNy_-ViWV5mi5uvV-V8kXlhzZB5qQBUACm1kVjpYJVSoTagtMp1hYA1VIah5RgqaXSQhakKG7T0QlRWiBPyYbe7if2vEdPg1k3y2LbQYT8mxwtbsDzPJzDbgT72KUWs3SY2a4hPjjO3Feu2Yt1WrJvETvz7_fBYrTH8R-9MTsDZHoDkoa0nO75JL5yVVmr78rdJA_75V0N8dNoIo9ztUjpxy87t5QN3ufgLH7-PFw</recordid><startdate>19990401</startdate><enddate>19990401</enddate><creator>Froelich, Jens J.</creator><creator>Schneller, Folker R. G.</creator><creator>Zahn, Rudolf K.</creator><general>Walter de Gruyter</general><scope>BSCLL</scope><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>7TM</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>19990401</creationdate><title>The Influence of Radiation and Chemotherapy-Related DNA Strand Breaks on Carcinogenesis: An Evaluation</title><author>Froelich, Jens J. ; Schneller, Folker R. G. ; Zahn, Rudolf K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-c45aa5da44674eb6d8555df7a56526beaefab70e81edb476d497b98d64c33b833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Antibiotics, Antineoplastic - pharmacology</topic><topic>Antimetabolites, Antineoplastic - pharmacology</topic><topic>Antineoplastic Agents - adverse effects</topic><topic>Antineoplastic Agents, Phytogenic - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Carcinogenesis, carcinogens and anticarcinogens</topic><topic>Cisplatin - pharmacology</topic><topic>Dactinomycin - pharmacology</topic><topic>DNA Damage</topic><topic>DNA, Neoplasm - drug effects</topic><topic>DNA, Neoplasm - radiation effects</topic><topic>Dose-Response Relationship, Drug</topic><topic>Dose-Response Relationship, Radiation</topic><topic>Doxorubicin - pharmacology</topic><topic>Etoposide - pharmacology</topic><topic>Leukemia, Experimental - drug therapy</topic><topic>Leukemia, Experimental - genetics</topic><topic>Leukemia, Experimental - radiotherapy</topic><topic>Medical sciences</topic><topic>Methotrexate - pharmacology</topic><topic>Mice</topic><topic>Physical agents</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><topic>Vincristine - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Froelich, Jens J.</creatorcontrib><creatorcontrib>Schneller, Folker R. G.</creatorcontrib><creatorcontrib>Zahn, Rudolf K.</creatorcontrib><collection>Istex</collection><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>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Clinical chemistry and laboratory medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Froelich, Jens J.</au><au>Schneller, Folker R. G.</au><au>Zahn, Rudolf K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Influence of Radiation and Chemotherapy-Related DNA Strand Breaks on Carcinogenesis: An Evaluation</atitle><jtitle>Clinical chemistry and laboratory medicine</jtitle><addtitle>Clinical Chemistry and Laboratory Medicine</addtitle><date>1999-04-01</date><risdate>1999</risdate><volume>37</volume><issue>4</issue><spage>403</spage><epage>408</epage><pages>403-408</pages><issn>1434-6621</issn><eissn>1437-4331</eissn><abstract>Purpose: DNA strand breaks are believed to induce carcinogenesis. This study was conducted to analyze induction and repair of irradiation- and chemotherapy-related strand breaks in vitro. Methods: Friend Leukemia cells were exposed to irradiation and various chemotherapeutic agents at different doses and concentrations. Occurence of strand breaks was determined fluorometrically, measuring the rate of DNA unwinding immediatly after exposure and 24 hours later. Results: The amount of double-stranded DNA decreased significantly for irradiation, doxorubicin, dactinomycin and etoposide (p ≤ 0.05, t-test). After 24 hours free of exposure, the persistent damage was detectable for all of these agents but not for irradiated cells, with DNA strand breaks being decreased for etoposide, unchanged for doxorubicin and increased for methotrexate as well as for dactinomycin. Conclusions: Severe DNA damage is induced by various chemotherapeutic agents and by irradiation. While repair of chemotherapy-related strand breaks may remain incomplete or prolonged for some chemotherapeutic agents, repair of radiation induced strand breaks is faster and more complete. Therefore chemotherapy-related carcinogenesis may partially be explained by prolonged persistence of DNA strand breaks.</abstract><cop>Berlin</cop><cop>New York, NY</cop><pub>Walter de Gruyter</pub><pmid>10369110</pmid><doi>10.1515/CCLM.1999.066</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1434-6621 |
| ispartof | Clinical chemistry and laboratory medicine, 1999-04, Vol.37 (4), p.403-408 |
| issn | 1434-6621 1437-4331 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_19890222 |
| source | MEDLINE; De Gruyter journals |
| subjects | Animals Antibiotics, Antineoplastic - pharmacology Antimetabolites, Antineoplastic - pharmacology Antineoplastic Agents - adverse effects Antineoplastic Agents, Phytogenic - pharmacology Biological and medical sciences Carcinogenesis, carcinogens and anticarcinogens Cisplatin - pharmacology Dactinomycin - pharmacology DNA Damage DNA, Neoplasm - drug effects DNA, Neoplasm - radiation effects Dose-Response Relationship, Drug Dose-Response Relationship, Radiation Doxorubicin - pharmacology Etoposide - pharmacology Leukemia, Experimental - drug therapy Leukemia, Experimental - genetics Leukemia, Experimental - radiotherapy Medical sciences Methotrexate - pharmacology Mice Physical agents Tumor Cells, Cultured Tumors Vincristine - pharmacology |
| title | The Influence of Radiation and Chemotherapy-Related DNA Strand Breaks on Carcinogenesis: An Evaluation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-15T05%3A12%3A06IST&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=The%20Influence%20of%20Radiation%20and%20Chemotherapy-Related%20DNA%20Strand%20Breaks%20on%20Carcinogenesis:%20An%20Evaluation&rft.jtitle=Clinical%20chemistry%20and%20laboratory%20medicine&rft.au=Froelich,%20Jens%20J.&rft.date=1999-04-01&rft.volume=37&rft.issue=4&rft.spage=403&rft.epage=408&rft.pages=403-408&rft.issn=1434-6621&rft.eissn=1437-4331&rft_id=info:doi/10.1515/CCLM.1999.066&rft_dat=%3Cproquest_cross%3E19890222%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=19890222&rft_id=info:pmid/10369110&rfr_iscdi=true |