Hydroxy-and hydroperoxy-6,8,11,14-eicosatetraenoic acids induce sister chromatid exchanges in cultured mammalian cells
Oxygen radical-induced genetic damage may be mediated by products of lipid peroxidation, in particular, arachidonic acid. Several isomeric hydroxy- and hydroperoxy-6,8,11,14-eicosatetraenoic acids (HETEs and HPETEs), intermediates of arachidonic acid metabolism, were evaluated for their ability to c...
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Veröffentlicht in: | The American journal of the medical sciences 1990, Vol.299 (1), p.50-53 |
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description | Oxygen radical-induced genetic damage may be mediated by products of lipid peroxidation, in particular, arachidonic acid. Several isomeric hydroxy- and hydroperoxy-6,8,11,14-eicosatetraenoic acids (HETEs and HPETEs), intermediates of arachidonic acid metabolism, were evaluated for their ability to cause sister chromatid exchanges (SCEs) in Chinese hamster ovary (CHO) cells. Both HETEs and HPETEs induced SCEs in a dose-dependent fashion at concentrations of 5, 10, and 20 microM. At each concentration, HETEs were more effective in producing SCEs than the corresponding HPETEs. Each of the isomeric forms used were equally effective in producing genetic damage. Antioxidants (superoxide dismutase, catalase and mannitol) were protective suggesting an intermediate role for the hydroxyl radical. Iron chelation by desferrioxamine suppressed SCE induction by 45% and an additional 33% inhibition was observed upon the addition of the calcium chelator EGTA. |
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B</creator><creatorcontrib>WEITBERG, A. B</creatorcontrib><description>Oxygen radical-induced genetic damage may be mediated by products of lipid peroxidation, in particular, arachidonic acid. Several isomeric hydroxy- and hydroperoxy-6,8,11,14-eicosatetraenoic acids (HETEs and HPETEs), intermediates of arachidonic acid metabolism, were evaluated for their ability to cause sister chromatid exchanges (SCEs) in Chinese hamster ovary (CHO) cells. Both HETEs and HPETEs induced SCEs in a dose-dependent fashion at concentrations of 5, 10, and 20 microM. At each concentration, HETEs were more effective in producing SCEs than the corresponding HPETEs. Each of the isomeric forms used were equally effective in producing genetic damage. Antioxidants (superoxide dismutase, catalase and mannitol) were protective suggesting an intermediate role for the hydroxyl radical. Iron chelation by desferrioxamine suppressed SCE induction by 45% and an additional 33% inhibition was observed upon the addition of the calcium chelator EGTA.</description><identifier>ISSN: 0002-9629</identifier><identifier>EISSN: 1538-2990</identifier><identifier>PMID: 2105055</identifier><identifier>CODEN: AJMSA9</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott</publisher><subject>Animals ; Biological and medical sciences ; Catalase - pharmacology ; Cell Line ; Cricetinae ; Deferoxamine - pharmacology ; Egtazic Acid - pharmacology ; Free Radicals ; Fundamental and applied biological sciences. Psychology ; Hydroxyeicosatetraenoic Acids - pharmacology ; Leukotrienes - pharmacology ; Lipid Peroxidation ; Lipid Peroxides - pharmacology ; Mannitol - pharmacology ; Molecular and cellular biology ; Molecular genetics ; Sister Chromatid Exchange - drug effects ; Superoxide Dismutase - pharmacology</subject><ispartof>The American journal of the medical sciences, 1990, Vol.299 (1), p.50-53</ispartof><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4010</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4346844$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2105055$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WEITBERG, A. B</creatorcontrib><title>Hydroxy-and hydroperoxy-6,8,11,14-eicosatetraenoic acids induce sister chromatid exchanges in cultured mammalian cells</title><title>The American journal of the medical sciences</title><addtitle>Am J Med Sci</addtitle><description>Oxygen radical-induced genetic damage may be mediated by products of lipid peroxidation, in particular, arachidonic acid. Several isomeric hydroxy- and hydroperoxy-6,8,11,14-eicosatetraenoic acids (HETEs and HPETEs), intermediates of arachidonic acid metabolism, were evaluated for their ability to cause sister chromatid exchanges (SCEs) in Chinese hamster ovary (CHO) cells. Both HETEs and HPETEs induced SCEs in a dose-dependent fashion at concentrations of 5, 10, and 20 microM. At each concentration, HETEs were more effective in producing SCEs than the corresponding HPETEs. Each of the isomeric forms used were equally effective in producing genetic damage. Antioxidants (superoxide dismutase, catalase and mannitol) were protective suggesting an intermediate role for the hydroxyl radical. Iron chelation by desferrioxamine suppressed SCE induction by 45% and an additional 33% inhibition was observed upon the addition of the calcium chelator EGTA.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Catalase - pharmacology</subject><subject>Cell Line</subject><subject>Cricetinae</subject><subject>Deferoxamine - pharmacology</subject><subject>Egtazic Acid - pharmacology</subject><subject>Free Radicals</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hydroxyeicosatetraenoic Acids - pharmacology</subject><subject>Leukotrienes - pharmacology</subject><subject>Lipid Peroxidation</subject><subject>Lipid Peroxides - pharmacology</subject><subject>Mannitol - pharmacology</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>Sister Chromatid Exchange - drug effects</subject><subject>Superoxide Dismutase - pharmacology</subject><issn>0002-9629</issn><issn>1538-2990</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kE1LAzEQhoMotVZ_gpCDeGogn7vJUYpaoeCl92WaZG1kv0x2pf337uriaWbe92F4Zy7QkimhCTeGXqIlpZQTk3FzjW5S-qSUcc3EAi04o4oqtUTf27OL7elMoHH4OPWd_52ztV4ztmaS-GDbBL3vI_imDRaDDS7h0LjBepxC6n3E9hjbGvrgsD_ZIzQffiKwHap-iN7hGuoaqgCj5Ksq3aKrEqrk7-a6QvuX5_1mS3bvr2-bpx3pNFdEK6OczLQU4w3K5BysBJZLrkqVAWdMCsEZL3XJRsXZEg6ZtFw7JpQS-UGs0OPf2i62X4NPfVGHNAWAxrdDKnKjtKF5NoL3Mzgcau-KLoYa4rmY_zT6D7MPyUJVRmhsSP-YFFNKKX4Au9lxgA</recordid><startdate>1990</startdate><enddate>1990</enddate><creator>WEITBERG, A. 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Psychology</topic><topic>Hydroxyeicosatetraenoic Acids - pharmacology</topic><topic>Leukotrienes - pharmacology</topic><topic>Lipid Peroxidation</topic><topic>Lipid Peroxides - pharmacology</topic><topic>Mannitol - pharmacology</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>Sister Chromatid Exchange - drug effects</topic><topic>Superoxide Dismutase - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>WEITBERG, A. 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B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hydroxy-and hydroperoxy-6,8,11,14-eicosatetraenoic acids induce sister chromatid exchanges in cultured mammalian cells</atitle><jtitle>The American journal of the medical sciences</jtitle><addtitle>Am J Med Sci</addtitle><date>1990</date><risdate>1990</risdate><volume>299</volume><issue>1</issue><spage>50</spage><epage>53</epage><pages>50-53</pages><issn>0002-9629</issn><eissn>1538-2990</eissn><coden>AJMSA9</coden><abstract>Oxygen radical-induced genetic damage may be mediated by products of lipid peroxidation, in particular, arachidonic acid. Several isomeric hydroxy- and hydroperoxy-6,8,11,14-eicosatetraenoic acids (HETEs and HPETEs), intermediates of arachidonic acid metabolism, were evaluated for their ability to cause sister chromatid exchanges (SCEs) in Chinese hamster ovary (CHO) cells. Both HETEs and HPETEs induced SCEs in a dose-dependent fashion at concentrations of 5, 10, and 20 microM. At each concentration, HETEs were more effective in producing SCEs than the corresponding HPETEs. Each of the isomeric forms used were equally effective in producing genetic damage. Antioxidants (superoxide dismutase, catalase and mannitol) were protective suggesting an intermediate role for the hydroxyl radical. Iron chelation by desferrioxamine suppressed SCE induction by 45% and an additional 33% inhibition was observed upon the addition of the calcium chelator EGTA.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott</pub><pmid>2105055</pmid><tpages>4</tpages></addata></record> |
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subjects | Animals Biological and medical sciences Catalase - pharmacology Cell Line Cricetinae Deferoxamine - pharmacology Egtazic Acid - pharmacology Free Radicals Fundamental and applied biological sciences. Psychology Hydroxyeicosatetraenoic Acids - pharmacology Leukotrienes - pharmacology Lipid Peroxidation Lipid Peroxides - pharmacology Mannitol - pharmacology Molecular and cellular biology Molecular genetics Sister Chromatid Exchange - drug effects Superoxide Dismutase - pharmacology |
title | Hydroxy-and hydroperoxy-6,8,11,14-eicosatetraenoic acids induce sister chromatid exchanges in cultured mammalian cells |
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