The pro-apoptotic effect of hydroquinone in human neutrophils and eosinophils
Hydroquinone (HQ) is a benzene metabolite that is involved in hematopoiesis via its accumulation into bone marrow. HQ also acts as a toxic agent that influences various immune responses. Both neutrophils and eosinophils function as important leukocytes in immunological regulation and immune diseases...
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| Veröffentlicht in: | Toxicology in vitro 2011-02, Vol.25 (1), p.131-137 |
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| creator | Yang, Eun Ju Lee, Ji-Sook Yun, Chi-Young Kim, In Sik |
| description | Hydroquinone (HQ) is a benzene metabolite that is involved in hematopoiesis via its accumulation into bone marrow. HQ also acts as a toxic agent that influences various immune responses. Both neutrophils and eosinophils function as important leukocytes in immunological regulation and immune diseases. In this study, we examined the toxic effects of HQ on the apoptosis of human neutrophils and eosinophils isolated from the blood of healthy donors. HQ markedly increased the apoptosis of neutrophils and eosinophils in a concentration- and a time-dependent manner. The pro-apoptotic effect is involved in activation of caspase 9 and caspase 3. Reactive oxygen species (ROS) production was enhanced after HQ treatment in a dose-dependent manner. In addition, HQ upregulated the release of IL-8 and MCP-1 from neutrophils and eosinophils, respectively. Taken together, the results of this study demonstrated that HQ strongly induces the apoptosis of neutrophils and eosinophils through the caspase 9/3-dependent pathway and the increased ROS production. HQ exerts a cytotoxic effect in human neutrophils and eosinophils and may impair the regulation of immune responses. |
| doi_str_mv | 10.1016/j.tiv.2010.10.004 |
| format | Article |
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HQ also acts as a toxic agent that influences various immune responses. Both neutrophils and eosinophils function as important leukocytes in immunological regulation and immune diseases. In this study, we examined the toxic effects of HQ on the apoptosis of human neutrophils and eosinophils isolated from the blood of healthy donors. HQ markedly increased the apoptosis of neutrophils and eosinophils in a concentration- and a time-dependent manner. The pro-apoptotic effect is involved in activation of caspase 9 and caspase 3. Reactive oxygen species (ROS) production was enhanced after HQ treatment in a dose-dependent manner. In addition, HQ upregulated the release of IL-8 and MCP-1 from neutrophils and eosinophils, respectively. Taken together, the results of this study demonstrated that HQ strongly induces the apoptosis of neutrophils and eosinophils through the caspase 9/3-dependent pathway and the increased ROS production. HQ exerts a cytotoxic effect in human neutrophils and eosinophils and may impair the regulation of immune responses.</description><identifier>ISSN: 0887-2333</identifier><identifier>EISSN: 1879-3177</identifier><identifier>DOI: 10.1016/j.tiv.2010.10.004</identifier><identifier>PMID: 20946948</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Air Pollutants - toxicity ; Air Pollution, Indoor - adverse effects ; Apoptosis ; Apoptosis - drug effects ; Caspase 3 - metabolism ; Caspase 9 - metabolism ; Cell Survival - drug effects ; Chemokine CCL2 - metabolism ; Cytotoxicity ; Enzyme Activation - drug effects ; Enzyme Precursors - metabolism ; Eosinophils ; Eosinophils - drug effects ; Eosinophils - metabolism ; Humans ; Hydroquinone ; Hydroquinones - toxicity ; Interleukin-8 - metabolism ; Neutrophils ; Neutrophils - drug effects ; Neutrophils - metabolism ; Osmolar Concentration ; Reactive Oxygen Species - metabolism ; Time Factors ; Up-Regulation - drug effects</subject><ispartof>Toxicology in vitro, 2011-02, Vol.25 (1), p.131-137</ispartof><rights>2010 Elsevier Ltd</rights><rights>Copyright © 2010 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c450t-72403f4072ac3c9d28806a2cd056c9b3d18c43a8f4df6617ba56d7f85f65d8b3</citedby><cites>FETCH-LOGICAL-c450t-72403f4072ac3c9d28806a2cd056c9b3d18c43a8f4df6617ba56d7f85f65d8b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.tiv.2010.10.004$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20946948$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Eun Ju</creatorcontrib><creatorcontrib>Lee, Ji-Sook</creatorcontrib><creatorcontrib>Yun, Chi-Young</creatorcontrib><creatorcontrib>Kim, In Sik</creatorcontrib><title>The pro-apoptotic effect of hydroquinone in human neutrophils and eosinophils</title><title>Toxicology in vitro</title><addtitle>Toxicol In Vitro</addtitle><description>Hydroquinone (HQ) is a benzene metabolite that is involved in hematopoiesis via its accumulation into bone marrow. HQ also acts as a toxic agent that influences various immune responses. Both neutrophils and eosinophils function as important leukocytes in immunological regulation and immune diseases. In this study, we examined the toxic effects of HQ on the apoptosis of human neutrophils and eosinophils isolated from the blood of healthy donors. HQ markedly increased the apoptosis of neutrophils and eosinophils in a concentration- and a time-dependent manner. The pro-apoptotic effect is involved in activation of caspase 9 and caspase 3. Reactive oxygen species (ROS) production was enhanced after HQ treatment in a dose-dependent manner. In addition, HQ upregulated the release of IL-8 and MCP-1 from neutrophils and eosinophils, respectively. Taken together, the results of this study demonstrated that HQ strongly induces the apoptosis of neutrophils and eosinophils through the caspase 9/3-dependent pathway and the increased ROS production. HQ exerts a cytotoxic effect in human neutrophils and eosinophils and may impair the regulation of immune responses.</description><subject>Air Pollutants - toxicity</subject><subject>Air Pollution, Indoor - adverse effects</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase 9 - metabolism</subject><subject>Cell Survival - drug effects</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Cytotoxicity</subject><subject>Enzyme Activation - drug effects</subject><subject>Enzyme Precursors - metabolism</subject><subject>Eosinophils</subject><subject>Eosinophils - drug effects</subject><subject>Eosinophils - metabolism</subject><subject>Humans</subject><subject>Hydroquinone</subject><subject>Hydroquinones - toxicity</subject><subject>Interleukin-8 - metabolism</subject><subject>Neutrophils</subject><subject>Neutrophils - drug effects</subject><subject>Neutrophils - metabolism</subject><subject>Osmolar Concentration</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Time Factors</subject><subject>Up-Regulation - drug effects</subject><issn>0887-2333</issn><issn>1879-3177</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtOwzAQRS0EoqXwAWyQd6xSxnbiOGKFEC-piE33luOH4qqNg51U6t-TPmDJajSjM1czB6FbAnMChD-s5r3fzikc-jlAfoamRJRVxkhZnqMpCFFmlDE2QVcprQCgEBQu0YRClfMqF1P0uWws7mLIVBe6PvReY-uc1T0ODjc7E8P34NvQWuxb3Awb1eLWDn0MXePXCavWYBvSSBz6a3Th1DrZm1OdoeXry_L5PVt8vX08Py0ynRfQZyXNgbkcSqo005WhQgBXVBsouK5qZojQOVPC5cZxTspaFdyUThSOF0bUbIbuj7Hd_jybernxSdv1WrU2DEkKDkxwSmEkyZHUMaQUrZNd9BsVd5KA3DuUKzk6lHuH-9HocNy5O6UP9caav41faSPweATs-OLW2yiT9rbV1vg4mpMm-H_ifwDJ-IKQ</recordid><startdate>20110201</startdate><enddate>20110201</enddate><creator>Yang, Eun Ju</creator><creator>Lee, Ji-Sook</creator><creator>Yun, Chi-Young</creator><creator>Kim, In Sik</creator><general>Elsevier Ltd</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>7U7</scope><scope>C1K</scope></search><sort><creationdate>20110201</creationdate><title>The pro-apoptotic effect of hydroquinone in human neutrophils and eosinophils</title><author>Yang, Eun Ju ; Lee, Ji-Sook ; Yun, Chi-Young ; Kim, In Sik</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c450t-72403f4072ac3c9d28806a2cd056c9b3d18c43a8f4df6617ba56d7f85f65d8b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Air Pollutants - toxicity</topic><topic>Air Pollution, Indoor - adverse effects</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase 9 - metabolism</topic><topic>Cell Survival - drug effects</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Cytotoxicity</topic><topic>Enzyme Activation - drug effects</topic><topic>Enzyme Precursors - metabolism</topic><topic>Eosinophils</topic><topic>Eosinophils - drug effects</topic><topic>Eosinophils - metabolism</topic><topic>Humans</topic><topic>Hydroquinone</topic><topic>Hydroquinones - toxicity</topic><topic>Interleukin-8 - metabolism</topic><topic>Neutrophils</topic><topic>Neutrophils - drug effects</topic><topic>Neutrophils - metabolism</topic><topic>Osmolar Concentration</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Time Factors</topic><topic>Up-Regulation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Eun Ju</creatorcontrib><creatorcontrib>Lee, Ji-Sook</creatorcontrib><creatorcontrib>Yun, Chi-Young</creatorcontrib><creatorcontrib>Kim, In Sik</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Toxicology in vitro</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Eun Ju</au><au>Lee, Ji-Sook</au><au>Yun, Chi-Young</au><au>Kim, In Sik</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The pro-apoptotic effect of hydroquinone in human neutrophils and eosinophils</atitle><jtitle>Toxicology in vitro</jtitle><addtitle>Toxicol In Vitro</addtitle><date>2011-02-01</date><risdate>2011</risdate><volume>25</volume><issue>1</issue><spage>131</spage><epage>137</epage><pages>131-137</pages><issn>0887-2333</issn><eissn>1879-3177</eissn><abstract>Hydroquinone (HQ) is a benzene metabolite that is involved in hematopoiesis via its accumulation into bone marrow. HQ also acts as a toxic agent that influences various immune responses. Both neutrophils and eosinophils function as important leukocytes in immunological regulation and immune diseases. In this study, we examined the toxic effects of HQ on the apoptosis of human neutrophils and eosinophils isolated from the blood of healthy donors. HQ markedly increased the apoptosis of neutrophils and eosinophils in a concentration- and a time-dependent manner. The pro-apoptotic effect is involved in activation of caspase 9 and caspase 3. Reactive oxygen species (ROS) production was enhanced after HQ treatment in a dose-dependent manner. In addition, HQ upregulated the release of IL-8 and MCP-1 from neutrophils and eosinophils, respectively. Taken together, the results of this study demonstrated that HQ strongly induces the apoptosis of neutrophils and eosinophils through the caspase 9/3-dependent pathway and the increased ROS production. 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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Air Pollutants - toxicity Air Pollution, Indoor - adverse effects Apoptosis Apoptosis - drug effects Caspase 3 - metabolism Caspase 9 - metabolism Cell Survival - drug effects Chemokine CCL2 - metabolism Cytotoxicity Enzyme Activation - drug effects Enzyme Precursors - metabolism Eosinophils Eosinophils - drug effects Eosinophils - metabolism Humans Hydroquinone Hydroquinones - toxicity Interleukin-8 - metabolism Neutrophils Neutrophils - drug effects Neutrophils - metabolism Osmolar Concentration Reactive Oxygen Species - metabolism Time Factors Up-Regulation - drug effects |
| title | The pro-apoptotic effect of hydroquinone in human neutrophils and eosinophils |
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