Uptake and Protection against Oxidative Stress by Estrogen Esters in THP-1 Human Macrophage Cell Lines
Estrogen replacement therapy offers protection from coronary artery disease in postmenopausal women. However, there is serious concern that long-term unopposed estrogen use increases the risk of breast and endometrial cancer through estrogen-receptor-driven mechanisms. In this communication, we have...
Gespeichert in:
| Veröffentlicht in: | Gynecologic and obstetric investigation 2001-01, Vol.51 (2), p.81-84 |
|---|---|
| Hauptverfasser: | , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 84 |
|---|---|
| container_issue | 2 |
| container_start_page | 81 |
| container_title | Gynecologic and obstetric investigation |
| container_volume | 51 |
| creator | Abplanalp, W. Ravi Subbiah, M.T. |
| description | Estrogen replacement therapy offers protection from coronary artery disease in postmenopausal women. However, there is serious concern that long-term unopposed estrogen use increases the risk of breast and endometrial cancer through estrogen-receptor-driven mechanisms. In this communication, we have explored an alternate route of estrogen delivery to macrophages using hydrophobic derivatives that associate with lipoproteins. Unlike free estradiol (E 2 ), long-chain fatty acid esters of E 2 associate extensively with low-density lipoprotein (LDL). In THP-1 cells, E 2 esters accumulated to a significantly higher level when compared to E 2 in the presence of LDL. In the presence of oxidized LDL even greater amounts of E 2 esters accumulated in cells. In THP-1 cells, E 2 esters were capable of preventing the azo-bis-induced increase in oxidative stress (hydrogen peroxide formation). These studies suggest that (a) hydrophobic esters of estrogens that associate with LDL can be delivered to macrophages and (b) these esters can effectively function as antioxidants protecting against oxidative stress. |
| doi_str_mv | 10.1159/000052898 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pasca</sourceid><recordid>TN_cdi_pascalfrancis_primary_910025</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>70671769</sourcerecordid><originalsourceid>FETCH-LOGICAL-c414t-cbf5e317db7b03b74ecc0e399b1c62e4086b3d0cc7c51f532c35b022be44999d3</originalsourceid><addsrcrecordid>eNqF0c9r2zAUB3BRNtq03WHnwRArFHZwp1-2rOMIbVPISGEt7GYk-TlTm8ieJI_2v6-yhBTGYLpIoA9P7-mL0HtKLigt1ReSV8lqVR-gCRWMF4SwH2_QhHBZF5KL6ggdx_hASMa1OERHlDLGK1VPUHc_JP0IWPsW34Y-gU2u91gvtfMx4cWTa3VyvwF_TwFixOYZX8YU-iX4zQFCxM7ju9ltQfFsXGuPv2kb-uGnXgKewmqF585DPEVvO72K8G63n6D7q8u76ayYL65vpl_nhRVUpMKargROZWukIdxIAdYS4EoZaisGgtSV4S2xVtqSdiVnlpeGMGZACKVUy0_Q-bbuEPpfI8TUrF20uQ3toR9jI0klqazUfyEjinGiZIaf_oIP_Rh8HqLJfyiruuabap-3KI8eY4CuGYJb6_DcUNJsImr2EWX7cVdwNGtoX-UukwzOdkBHq1dd0N66uHeK5nTL174edVhC2F9fL27-vNMMbZfRh3-ibScv2V6rDw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>223768839</pqid></control><display><type>article</type><title>Uptake and Protection against Oxidative Stress by Estrogen Esters in THP-1 Human Macrophage Cell Lines</title><source>Karger Journals</source><source>MEDLINE</source><creator>Abplanalp, W. ; Ravi Subbiah, M.T.</creator><creatorcontrib>Abplanalp, W. ; Ravi Subbiah, M.T.</creatorcontrib><description>Estrogen replacement therapy offers protection from coronary artery disease in postmenopausal women. However, there is serious concern that long-term unopposed estrogen use increases the risk of breast and endometrial cancer through estrogen-receptor-driven mechanisms. In this communication, we have explored an alternate route of estrogen delivery to macrophages using hydrophobic derivatives that associate with lipoproteins. Unlike free estradiol (E 2 ), long-chain fatty acid esters of E 2 associate extensively with low-density lipoprotein (LDL). In THP-1 cells, E 2 esters accumulated to a significantly higher level when compared to E 2 in the presence of LDL. In the presence of oxidized LDL even greater amounts of E 2 esters accumulated in cells. In THP-1 cells, E 2 esters were capable of preventing the azo-bis-induced increase in oxidative stress (hydrogen peroxide formation). These studies suggest that (a) hydrophobic esters of estrogens that associate with LDL can be delivered to macrophages and (b) these esters can effectively function as antioxidants protecting against oxidative stress.</description><identifier>ISSN: 0378-7346</identifier><identifier>EISSN: 1423-002X</identifier><identifier>DOI: 10.1159/000052898</identifier><identifier>PMID: 11223698</identifier><identifier>CODEN: GOBIDS</identifier><language>eng</language><publisher>Basel, Switzerland: Karger</publisher><subject>Biological and medical sciences ; Cell Line ; Cells, Cultured ; Culture Media ; Estradiol - metabolism ; Estradiol - pharmacokinetics ; Female ; Hormones. Endocrine system ; Humans ; Lipoproteins, HDL - metabolism ; Lipoproteins, LDL - metabolism ; Macrophages - metabolism ; Medical sciences ; Original Paper ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Pharmacology. Drug treatments ; Probability ; Reference Values ; Sensitivity and Specificity</subject><ispartof>Gynecologic and obstetric investigation, 2001-01, Vol.51 (2), p.81-84</ispartof><rights>2001 S. Karger AG, Basel</rights><rights>2001 INIST-CNRS</rights><rights>Copyright 2001 S. Karger AG, Basel.</rights><rights>Copyright (c) 2001 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c414t-cbf5e317db7b03b74ecc0e399b1c62e4086b3d0cc7c51f532c35b022be44999d3</citedby><cites>FETCH-LOGICAL-c414t-cbf5e317db7b03b74ecc0e399b1c62e4086b3d0cc7c51f532c35b022be44999d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2423,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=910025$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11223698$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Abplanalp, W.</creatorcontrib><creatorcontrib>Ravi Subbiah, M.T.</creatorcontrib><title>Uptake and Protection against Oxidative Stress by Estrogen Esters in THP-1 Human Macrophage Cell Lines</title><title>Gynecologic and obstetric investigation</title><addtitle>Gynecol Obstet Invest</addtitle><description>Estrogen replacement therapy offers protection from coronary artery disease in postmenopausal women. However, there is serious concern that long-term unopposed estrogen use increases the risk of breast and endometrial cancer through estrogen-receptor-driven mechanisms. In this communication, we have explored an alternate route of estrogen delivery to macrophages using hydrophobic derivatives that associate with lipoproteins. Unlike free estradiol (E 2 ), long-chain fatty acid esters of E 2 associate extensively with low-density lipoprotein (LDL). In THP-1 cells, E 2 esters accumulated to a significantly higher level when compared to E 2 in the presence of LDL. In the presence of oxidized LDL even greater amounts of E 2 esters accumulated in cells. In THP-1 cells, E 2 esters were capable of preventing the azo-bis-induced increase in oxidative stress (hydrogen peroxide formation). These studies suggest that (a) hydrophobic esters of estrogens that associate with LDL can be delivered to macrophages and (b) these esters can effectively function as antioxidants protecting against oxidative stress.</description><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Cells, Cultured</subject><subject>Culture Media</subject><subject>Estradiol - metabolism</subject><subject>Estradiol - pharmacokinetics</subject><subject>Female</subject><subject>Hormones. Endocrine system</subject><subject>Humans</subject><subject>Lipoproteins, HDL - metabolism</subject><subject>Lipoproteins, LDL - metabolism</subject><subject>Macrophages - metabolism</subject><subject>Medical sciences</subject><subject>Original Paper</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Pharmacology. Drug treatments</subject><subject>Probability</subject><subject>Reference Values</subject><subject>Sensitivity and Specificity</subject><issn>0378-7346</issn><issn>1423-002X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqF0c9r2zAUB3BRNtq03WHnwRArFHZwp1-2rOMIbVPISGEt7GYk-TlTm8ieJI_2v6-yhBTGYLpIoA9P7-mL0HtKLigt1ReSV8lqVR-gCRWMF4SwH2_QhHBZF5KL6ggdx_hASMa1OERHlDLGK1VPUHc_JP0IWPsW34Y-gU2u91gvtfMx4cWTa3VyvwF_TwFixOYZX8YU-iX4zQFCxM7ju9ltQfFsXGuPv2kb-uGnXgKewmqF585DPEVvO72K8G63n6D7q8u76ayYL65vpl_nhRVUpMKargROZWukIdxIAdYS4EoZaisGgtSV4S2xVtqSdiVnlpeGMGZACKVUy0_Q-bbuEPpfI8TUrF20uQ3toR9jI0klqazUfyEjinGiZIaf_oIP_Rh8HqLJfyiruuabap-3KI8eY4CuGYJb6_DcUNJsImr2EWX7cVdwNGtoX-UukwzOdkBHq1dd0N66uHeK5nTL174edVhC2F9fL27-vNMMbZfRh3-ibScv2V6rDw</recordid><startdate>20010101</startdate><enddate>20010101</enddate><creator>Abplanalp, W.</creator><creator>Ravi Subbiah, M.T.</creator><general>Karger</general><general>S. Karger AG</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>3V.</scope><scope>7QO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20010101</creationdate><title>Uptake and Protection against Oxidative Stress by Estrogen Esters in THP-1 Human Macrophage Cell Lines</title><author>Abplanalp, W. ; Ravi Subbiah, M.T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c414t-cbf5e317db7b03b74ecc0e399b1c62e4086b3d0cc7c51f532c35b022be44999d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Biological and medical sciences</topic><topic>Cell Line</topic><topic>Cells, Cultured</topic><topic>Culture Media</topic><topic>Estradiol - metabolism</topic><topic>Estradiol - pharmacokinetics</topic><topic>Female</topic><topic>Hormones. Endocrine system</topic><topic>Humans</topic><topic>Lipoproteins, HDL - metabolism</topic><topic>Lipoproteins, LDL - metabolism</topic><topic>Macrophages - metabolism</topic><topic>Medical sciences</topic><topic>Original Paper</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Pharmacology. Drug treatments</topic><topic>Probability</topic><topic>Reference Values</topic><topic>Sensitivity and Specificity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Abplanalp, W.</creatorcontrib><creatorcontrib>Ravi Subbiah, M.T.</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>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Gynecologic and obstetric investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Abplanalp, W.</au><au>Ravi Subbiah, M.T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Uptake and Protection against Oxidative Stress by Estrogen Esters in THP-1 Human Macrophage Cell Lines</atitle><jtitle>Gynecologic and obstetric investigation</jtitle><addtitle>Gynecol Obstet Invest</addtitle><date>2001-01-01</date><risdate>2001</risdate><volume>51</volume><issue>2</issue><spage>81</spage><epage>84</epage><pages>81-84</pages><issn>0378-7346</issn><eissn>1423-002X</eissn><coden>GOBIDS</coden><abstract>Estrogen replacement therapy offers protection from coronary artery disease in postmenopausal women. However, there is serious concern that long-term unopposed estrogen use increases the risk of breast and endometrial cancer through estrogen-receptor-driven mechanisms. In this communication, we have explored an alternate route of estrogen delivery to macrophages using hydrophobic derivatives that associate with lipoproteins. Unlike free estradiol (E 2 ), long-chain fatty acid esters of E 2 associate extensively with low-density lipoprotein (LDL). In THP-1 cells, E 2 esters accumulated to a significantly higher level when compared to E 2 in the presence of LDL. In the presence of oxidized LDL even greater amounts of E 2 esters accumulated in cells. In THP-1 cells, E 2 esters were capable of preventing the azo-bis-induced increase in oxidative stress (hydrogen peroxide formation). These studies suggest that (a) hydrophobic esters of estrogens that associate with LDL can be delivered to macrophages and (b) these esters can effectively function as antioxidants protecting against oxidative stress.</abstract><cop>Basel, Switzerland</cop><pub>Karger</pub><pmid>11223698</pmid><doi>10.1159/000052898</doi><tpages>4</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0378-7346 |
| ispartof | Gynecologic and obstetric investigation, 2001-01, Vol.51 (2), p.81-84 |
| issn | 0378-7346 1423-002X |
| language | eng |
| recordid | cdi_pascalfrancis_primary_910025 |
| source | Karger Journals; MEDLINE |
| subjects | Biological and medical sciences Cell Line Cells, Cultured Culture Media Estradiol - metabolism Estradiol - pharmacokinetics Female Hormones. Endocrine system Humans Lipoproteins, HDL - metabolism Lipoproteins, LDL - metabolism Macrophages - metabolism Medical sciences Original Paper Oxidative Stress - drug effects Oxidative Stress - physiology Pharmacology. Drug treatments Probability Reference Values Sensitivity and Specificity |
| title | Uptake and Protection against Oxidative Stress by Estrogen Esters in THP-1 Human Macrophage Cell Lines |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T21%3A01%3A19IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pasca&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Uptake%20and%20Protection%20against%20Oxidative%20Stress%20by%20Estrogen%20Esters%20in%20THP-1%20Human%20Macrophage%20Cell%20Lines&rft.jtitle=Gynecologic%20and%20obstetric%20investigation&rft.au=Abplanalp,%20W.&rft.date=2001-01-01&rft.volume=51&rft.issue=2&rft.spage=81&rft.epage=84&rft.pages=81-84&rft.issn=0378-7346&rft.eissn=1423-002X&rft.coden=GOBIDS&rft_id=info:doi/10.1159/000052898&rft_dat=%3Cproquest_pasca%3E70671769%3C/proquest_pasca%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=223768839&rft_id=info:pmid/11223698&rfr_iscdi=true |