Free radical production and labile iron pool decrease triggered by subtoxic concentration of aclarubicin in human leukemia cell lines
Aclarubicin (ACLA), which belongs to the antracycline class of antineoplasic agents, has been demonstrated as a differentiating agent for a broad range of human solid tumors and leukemia. By using dihydroethidium as a fluorescent probe, we show the ability of subtoxic (i.e. differentiating) concentr...
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Veröffentlicht in: | Leukemia research 2002-10, Vol.26 (10), p.927-931 |
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description | Aclarubicin (ACLA), which belongs to the antracycline class of antineoplasic agents, has been demonstrated as a differentiating agent for a broad range of human solid tumors and leukemia. By using dihydroethidium as a fluorescent probe, we show the ability of subtoxic (i.e. differentiating) concentration of ACLA to generate reactive oxygen species in both K562 and HL-60 leukemia cell lines. Besides, we have used a calcein-based spectrofluorimetric assay to determine the influence of ACLA treatment on the cellular labile iron pool (LIP). In both cell lines, the LIP level was markedly decreased in the presence of ACLA. Nevertheless, whereas ACLA-induced differentiation was obviously ROS-dependent, the LIP decrease was rather ROS-independent. |
doi_str_mv | 10.1016/S0145-2126(02)00030-9 |
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By using dihydroethidium as a fluorescent probe, we show the ability of subtoxic (i.e. differentiating) concentration of ACLA to generate reactive oxygen species in both K562 and HL-60 leukemia cell lines. Besides, we have used a calcein-based spectrofluorimetric assay to determine the influence of ACLA treatment on the cellular labile iron pool (LIP). In both cell lines, the LIP level was markedly decreased in the presence of ACLA. Nevertheless, whereas ACLA-induced differentiation was obviously ROS-dependent, the LIP decrease was rather ROS-independent.</description><identifier>ISSN: 0145-2126</identifier><identifier>EISSN: 1873-5835</identifier><identifier>EISSN: 0145-2126</identifier><identifier>DOI: 10.1016/S0145-2126(02)00030-9</identifier><identifier>PMID: 12163054</identifier><identifier>CODEN: LEREDD</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Aclarubicin ; Aclarubicin - pharmacology ; Antibiotics, Antineoplastic ; Antibiotics, Antineoplastic - pharmacology ; Antineoplastic agents ; Biochemistry, Molecular Biology ; Biological and medical sciences ; Cell Differentiation ; Cell Differentiation - drug effects ; Differentiation ; Fluorescent Dyes ; Free Radicals ; Free Radicals - metabolism ; General aspects ; HL-60 ; HL-60 Cells ; HL-60 Cells - drug effects ; Humans ; Iron ; Iron - metabolism ; K562 ; K562 Cells ; K562 Cells - drug effects ; Labile iron pool ; Leukemia ; Leukemia - metabolism ; Leukemia - pathology ; Life Sciences ; Medical sciences ; Oxidative stress ; Pharmacology. Drug treatments ; Reactive Oxygen Species ; Reactive Oxygen Species - metabolism</subject><ispartof>Leukemia research, 2002-10, Vol.26 (10), p.927-931</ispartof><rights>2002 Elsevier Science Ltd</rights><rights>2002 INIST-CNRS</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c472t-54cb1a4953117f86e38d9b218db9d3dd1f7cfd172719dbfd384b91cf1837eb033</citedby><cites>FETCH-LOGICAL-c472t-54cb1a4953117f86e38d9b218db9d3dd1f7cfd172719dbfd384b91cf1837eb033</cites><orcidid>0000-0003-2441-1966 ; 0000-0003-1959-7807</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0145212602000309$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13841912$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12163054$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00422915$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Richard, Doriane</creatorcontrib><creatorcontrib>Morjani, Hamid</creatorcontrib><creatorcontrib>Chénais, Benoı̂t</creatorcontrib><title>Free radical production and labile iron pool decrease triggered by subtoxic concentration of aclarubicin in human leukemia cell lines</title><title>Leukemia research</title><addtitle>Leuk Res</addtitle><description>Aclarubicin (ACLA), which belongs to the antracycline class of antineoplasic agents, has been demonstrated as a differentiating agent for a broad range of human solid tumors and leukemia. By using dihydroethidium as a fluorescent probe, we show the ability of subtoxic (i.e. differentiating) concentration of ACLA to generate reactive oxygen species in both K562 and HL-60 leukemia cell lines. Besides, we have used a calcein-based spectrofluorimetric assay to determine the influence of ACLA treatment on the cellular labile iron pool (LIP). In both cell lines, the LIP level was markedly decreased in the presence of ACLA. Nevertheless, whereas ACLA-induced differentiation was obviously ROS-dependent, the LIP decrease was rather ROS-independent.</description><subject>Aclarubicin</subject><subject>Aclarubicin - pharmacology</subject><subject>Antibiotics, Antineoplastic</subject><subject>Antibiotics, Antineoplastic - pharmacology</subject><subject>Antineoplastic agents</subject><subject>Biochemistry, Molecular Biology</subject><subject>Biological and medical sciences</subject><subject>Cell Differentiation</subject><subject>Cell Differentiation - drug effects</subject><subject>Differentiation</subject><subject>Fluorescent Dyes</subject><subject>Free Radicals</subject><subject>Free Radicals - metabolism</subject><subject>General aspects</subject><subject>HL-60</subject><subject>HL-60 Cells</subject><subject>HL-60 Cells - drug effects</subject><subject>Humans</subject><subject>Iron</subject><subject>Iron - metabolism</subject><subject>K562</subject><subject>K562 Cells</subject><subject>K562 Cells - drug effects</subject><subject>Labile iron pool</subject><subject>Leukemia</subject><subject>Leukemia - metabolism</subject><subject>Leukemia - pathology</subject><subject>Life Sciences</subject><subject>Medical sciences</subject><subject>Oxidative stress</subject><subject>Pharmacology. Drug treatments</subject><subject>Reactive Oxygen Species</subject><subject>Reactive Oxygen Species - metabolism</subject><issn>0145-2126</issn><issn>1873-5835</issn><issn>0145-2126</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtrFTEUgINY7LX6E5RsFLsYzUnmlVUpxVrhQhfqOuRxpo1mJtdkptgf0P_d3AftUgiEHL7zyPkIeQfsMzBov_xgUDcVB95-YvyUMSZYJV-QFfSdqJpeNC_J6gk5Jq9z_l2gRoJ8RY6BQytYU6_Iw2VCpEk7b3WgmxTdYmcfJ6onR4M2PiD1qbw3MQbq0CbUGemc_M0NJnTU3NO8mDn-85baOFmc5qR3FeJAtQ06LcZbP9FybpdRTzTg8gdHr6nFEGjwE-Y35GjQIePbw31Cfl1-_XlxVa2vv32_OF9Xtu74XDW1NaBr2QiAbuhbFL2ThkPvjHTCORg6OzjoeAfSmcGJvjYS7AC96NAwIU7I6b7urQ5qk_yo072K2qur87XaxhirOZfQ3EFhP-7ZspS_C-ZZjT5vR9YTxiWr0qOAoi1gswdtijknHJ4qA1NbV2rnSm1FKMbVzpWSJe_9ocFiRnTPWQc5BfhwAHQudoakJ-vzM1e-BxJ44c72HJbV3XlMKluPRYXzCe2sXPT_GeUR5XmxuA</recordid><startdate>20021001</startdate><enddate>20021001</enddate><creator>Richard, Doriane</creator><creator>Morjani, Hamid</creator><creator>Chénais, Benoı̂t</creator><general>Elsevier Ltd</general><general>Elsevier Science</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><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><orcidid>https://orcid.org/0000-0003-2441-1966</orcidid><orcidid>https://orcid.org/0000-0003-1959-7807</orcidid></search><sort><creationdate>20021001</creationdate><title>Free radical production and labile iron pool decrease triggered by subtoxic concentration of aclarubicin in human leukemia cell lines</title><author>Richard, Doriane ; Morjani, Hamid ; Chénais, Benoı̂t</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c472t-54cb1a4953117f86e38d9b218db9d3dd1f7cfd172719dbfd384b91cf1837eb033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Aclarubicin</topic><topic>Aclarubicin - pharmacology</topic><topic>Antibiotics, Antineoplastic</topic><topic>Antibiotics, Antineoplastic - pharmacology</topic><topic>Antineoplastic agents</topic><topic>Biochemistry, Molecular Biology</topic><topic>Biological and medical sciences</topic><topic>Cell Differentiation</topic><topic>Cell Differentiation - drug effects</topic><topic>Differentiation</topic><topic>Fluorescent Dyes</topic><topic>Free Radicals</topic><topic>Free Radicals - metabolism</topic><topic>General aspects</topic><topic>HL-60</topic><topic>HL-60 Cells</topic><topic>HL-60 Cells - drug effects</topic><topic>Humans</topic><topic>Iron</topic><topic>Iron - metabolism</topic><topic>K562</topic><topic>K562 Cells</topic><topic>K562 Cells - drug effects</topic><topic>Labile iron pool</topic><topic>Leukemia</topic><topic>Leukemia - metabolism</topic><topic>Leukemia - pathology</topic><topic>Life Sciences</topic><topic>Medical sciences</topic><topic>Oxidative stress</topic><topic>Pharmacology. Drug treatments</topic><topic>Reactive Oxygen Species</topic><topic>Reactive Oxygen Species - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Richard, Doriane</creatorcontrib><creatorcontrib>Morjani, Hamid</creatorcontrib><creatorcontrib>Chénais, Benoı̂t</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>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><jtitle>Leukemia research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Richard, Doriane</au><au>Morjani, Hamid</au><au>Chénais, Benoı̂t</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Free radical production and labile iron pool decrease triggered by subtoxic concentration of aclarubicin in human leukemia cell lines</atitle><jtitle>Leukemia research</jtitle><addtitle>Leuk Res</addtitle><date>2002-10-01</date><risdate>2002</risdate><volume>26</volume><issue>10</issue><spage>927</spage><epage>931</epage><pages>927-931</pages><issn>0145-2126</issn><eissn>1873-5835</eissn><eissn>0145-2126</eissn><coden>LEREDD</coden><abstract>Aclarubicin (ACLA), which belongs to the antracycline class of antineoplasic agents, has been demonstrated as a differentiating agent for a broad range of human solid tumors and leukemia. By using dihydroethidium as a fluorescent probe, we show the ability of subtoxic (i.e. differentiating) concentration of ACLA to generate reactive oxygen species in both K562 and HL-60 leukemia cell lines. Besides, we have used a calcein-based spectrofluorimetric assay to determine the influence of ACLA treatment on the cellular labile iron pool (LIP). In both cell lines, the LIP level was markedly decreased in the presence of ACLA. Nevertheless, whereas ACLA-induced differentiation was obviously ROS-dependent, the LIP decrease was rather ROS-independent.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>12163054</pmid><doi>10.1016/S0145-2126(02)00030-9</doi><tpages>5</tpages><orcidid>https://orcid.org/0000-0003-2441-1966</orcidid><orcidid>https://orcid.org/0000-0003-1959-7807</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Aclarubicin Aclarubicin - pharmacology Antibiotics, Antineoplastic Antibiotics, Antineoplastic - pharmacology Antineoplastic agents Biochemistry, Molecular Biology Biological and medical sciences Cell Differentiation Cell Differentiation - drug effects Differentiation Fluorescent Dyes Free Radicals Free Radicals - metabolism General aspects HL-60 HL-60 Cells HL-60 Cells - drug effects Humans Iron Iron - metabolism K562 K562 Cells K562 Cells - drug effects Labile iron pool Leukemia Leukemia - metabolism Leukemia - pathology Life Sciences Medical sciences Oxidative stress Pharmacology. Drug treatments Reactive Oxygen Species Reactive Oxygen Species - metabolism |
title | Free radical production and labile iron pool decrease triggered by subtoxic concentration of aclarubicin in human leukemia cell lines |
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