ROS-dependent Bax/Bcl2 and caspase 3 pathway-mediated apoptosis induced by zineb in human keratinocyte cells
There are a large number of agricultural workers who are exposed to pesticides through skin and inhalation. The best approach to identify altered molecular pathways during dermal exposure to pesticides is relevant to risk-associated concern about skin safety. In this study, we investigated the cytot...
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| Veröffentlicht in: | OncoTargets and therapy 2018-01, Vol.11, p.489-497 |
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| creator | Ali, Daoud Tripathi, Abhilasha Al Ali, Hussain Shahi, Yadvendra Mishra, Kamlesh K Alarifi, Saud Alkahtane, Abdullah A Manohardas, Salem |
| description | There are a large number of agricultural workers who are exposed to pesticides through skin and inhalation. The best approach to identify altered molecular pathways during dermal exposure to pesticides is relevant to risk-associated concern about skin safety. In this study, we investigated the cytotoxic effect of zineb, a fungicide, in human keratinocyte (HaCaT) cells. HaCaT cells were treated with zineb (1-40 µg/mL) for 24 hours. Cellular and molecular mechanisms of cell toxicity were investigated through MTT and neutral red-uptake assays. Zineb reduced viability of HaCaT cells and induced apoptosis in a concentration-dependent manner. Zineb increased levels of Bax and caspase 3 and inhibited the level of Bcl2, which subsequently induced apoptosis via the Bax/Bcl2 and caspase pathway. Therefore, zineb could have induced apoptosis through the mitochondrial pathway in HaCaT cells. Our study suggests that zineb is cytotoxic to HaCaT cells via the induction of apoptosis and oxidative stress in vitro. |
| doi_str_mv | 10.2147/OTT.S140358 |
| format | Article |
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The best approach to identify altered molecular pathways during dermal exposure to pesticides is relevant to risk-associated concern about skin safety. In this study, we investigated the cytotoxic effect of zineb, a fungicide, in human keratinocyte (HaCaT) cells. HaCaT cells were treated with zineb (1-40 µg/mL) for 24 hours. Cellular and molecular mechanisms of cell toxicity were investigated through MTT and neutral red-uptake assays. Zineb reduced viability of HaCaT cells and induced apoptosis in a concentration-dependent manner. Zineb increased levels of Bax and caspase 3 and inhibited the level of Bcl2, which subsequently induced apoptosis via the Bax/Bcl2 and caspase pathway. Therefore, zineb could have induced apoptosis through the mitochondrial pathway in HaCaT cells. Our study suggests that zineb is cytotoxic to HaCaT cells via the induction of apoptosis and oxidative stress in vitro.</description><identifier>ISSN: 1178-6930</identifier><identifier>EISSN: 1178-6930</identifier><identifier>DOI: 10.2147/OTT.S140358</identifier><identifier>PMID: 29416349</identifier><language>eng</language><publisher>New Zealand: Dove Medical Press Limited</publisher><subject>Agricultural laborers ; Apoptosis ; Crop diseases ; Cytotoxicity ; Deoxyribonucleic acid ; DNA ; DNA damage ; EDTA ; Fungicides ; Inflammation ; Lipid peroxidation ; Lipids ; Mammals ; Microscopy ; Original Research ; Oxidative stress ; Pesticides ; Proteins ; Skin ; Toxicity ; Workers</subject><ispartof>OncoTargets and therapy, 2018-01, Vol.11, p.489-497</ispartof><rights>COPYRIGHT 2018 Dove Medical Press Limited</rights><rights>2018. This work is licensed under https://creativecommons.org/licenses/by-nc/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2018 Ali et al. This work is published and licensed by Dove Medical Press Limited 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c507t-b8fd75cd561fa5c6c1883907867c6805634391b4b856fd3f7cbc8f1dcafec05a3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5788927/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5788927/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,3849,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29416349$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ali, Daoud</creatorcontrib><creatorcontrib>Tripathi, Abhilasha</creatorcontrib><creatorcontrib>Al Ali, Hussain</creatorcontrib><creatorcontrib>Shahi, Yadvendra</creatorcontrib><creatorcontrib>Mishra, Kamlesh K</creatorcontrib><creatorcontrib>Alarifi, Saud</creatorcontrib><creatorcontrib>Alkahtane, Abdullah A</creatorcontrib><creatorcontrib>Manohardas, Salem</creatorcontrib><title>ROS-dependent Bax/Bcl2 and caspase 3 pathway-mediated apoptosis induced by zineb in human keratinocyte cells</title><title>OncoTargets and therapy</title><addtitle>Onco Targets Ther</addtitle><description>There are a large number of agricultural workers who are exposed to pesticides through skin and inhalation. The best approach to identify altered molecular pathways during dermal exposure to pesticides is relevant to risk-associated concern about skin safety. In this study, we investigated the cytotoxic effect of zineb, a fungicide, in human keratinocyte (HaCaT) cells. HaCaT cells were treated with zineb (1-40 µg/mL) for 24 hours. Cellular and molecular mechanisms of cell toxicity were investigated through MTT and neutral red-uptake assays. Zineb reduced viability of HaCaT cells and induced apoptosis in a concentration-dependent manner. Zineb increased levels of Bax and caspase 3 and inhibited the level of Bcl2, which subsequently induced apoptosis via the Bax/Bcl2 and caspase pathway. Therefore, zineb could have induced apoptosis through the mitochondrial pathway in HaCaT cells. Our study suggests that zineb is cytotoxic to HaCaT cells via the induction of apoptosis and oxidative stress in vitro.</description><subject>Agricultural laborers</subject><subject>Apoptosis</subject><subject>Crop diseases</subject><subject>Cytotoxicity</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA damage</subject><subject>EDTA</subject><subject>Fungicides</subject><subject>Inflammation</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Mammals</subject><subject>Microscopy</subject><subject>Original Research</subject><subject>Oxidative stress</subject><subject>Pesticides</subject><subject>Proteins</subject><subject>Skin</subject><subject>Toxicity</subject><subject>Workers</subject><issn>1178-6930</issn><issn>1178-6930</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkttrFDEUxgdR7EWffJeAIAWZbTKZ3F6EtniDwoJdn0Mml27qTDJOMur615ula90VyUPCye9858JXVS8QXDSoZefL1Wpxg1qICX9UHSPEeE0Fho_33kfVSUp3EFLKm_ZpddSIFlHciuOq_7y8qY0dbTA2ZHCpfp5f6r4BKhigVRpVsgCDUeX1D7WpB2u8ytYANcYxx-QT8MHMukS6Dfjlg-1KAKznQQXw1U4q-xD1Jlugbd-nZ9UTp_pkn-_u0-rL-3erq4_19fLDp6uL61oTyHLdcWcY0YZQ5BTRVCPOsYCMU6Yph6R0jgXq2o4T6gx2THeaO2S0clZDovBp9fZed5y70rIuk02ql-PkBzVtZFReHv4Ev5a38bskjHPRsCJwthOY4rfZpiwHn7YjqGDjnCQSQlAmCEEFffUPehfnKZTxZNO0RYsjSP5St6q30gcXS129FZUXhGMq2lZsyy7-Q5Vj7OB1DNb5Ej9IeL2XsLaqz-sU-zn7GNIh-OYe1FNMabLuYRkIyq2LZHGR3Lmo0C_39_fA_rEN_g3YY8F4</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Ali, Daoud</creator><creator>Tripathi, Abhilasha</creator><creator>Al Ali, Hussain</creator><creator>Shahi, Yadvendra</creator><creator>Mishra, Kamlesh K</creator><creator>Alarifi, Saud</creator><creator>Alkahtane, Abdullah A</creator><creator>Manohardas, Salem</creator><general>Dove Medical Press Limited</general><general>Taylor & Francis Ltd</general><general>Dove Medical Press</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180101</creationdate><title>ROS-dependent Bax/Bcl2 and caspase 3 pathway-mediated apoptosis induced by zineb in human keratinocyte cells</title><author>Ali, Daoud ; Tripathi, Abhilasha ; Al Ali, Hussain ; Shahi, Yadvendra ; Mishra, Kamlesh K ; Alarifi, Saud ; Alkahtane, Abdullah A ; Manohardas, Salem</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c507t-b8fd75cd561fa5c6c1883907867c6805634391b4b856fd3f7cbc8f1dcafec05a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Agricultural laborers</topic><topic>Apoptosis</topic><topic>Crop diseases</topic><topic>Cytotoxicity</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA damage</topic><topic>EDTA</topic><topic>Fungicides</topic><topic>Inflammation</topic><topic>Lipid peroxidation</topic><topic>Lipids</topic><topic>Mammals</topic><topic>Microscopy</topic><topic>Original Research</topic><topic>Oxidative stress</topic><topic>Pesticides</topic><topic>Proteins</topic><topic>Skin</topic><topic>Toxicity</topic><topic>Workers</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ali, Daoud</creatorcontrib><creatorcontrib>Tripathi, Abhilasha</creatorcontrib><creatorcontrib>Al Ali, Hussain</creatorcontrib><creatorcontrib>Shahi, Yadvendra</creatorcontrib><creatorcontrib>Mishra, Kamlesh K</creatorcontrib><creatorcontrib>Alarifi, Saud</creatorcontrib><creatorcontrib>Alkahtane, Abdullah A</creatorcontrib><creatorcontrib>Manohardas, Salem</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>OncoTargets and therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ali, Daoud</au><au>Tripathi, Abhilasha</au><au>Al Ali, Hussain</au><au>Shahi, Yadvendra</au><au>Mishra, Kamlesh K</au><au>Alarifi, Saud</au><au>Alkahtane, Abdullah A</au><au>Manohardas, Salem</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ROS-dependent Bax/Bcl2 and caspase 3 pathway-mediated apoptosis induced by zineb in human keratinocyte cells</atitle><jtitle>OncoTargets and therapy</jtitle><addtitle>Onco Targets Ther</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>11</volume><spage>489</spage><epage>497</epage><pages>489-497</pages><issn>1178-6930</issn><eissn>1178-6930</eissn><abstract>There are a large number of agricultural workers who are exposed to pesticides through skin and inhalation. The best approach to identify altered molecular pathways during dermal exposure to pesticides is relevant to risk-associated concern about skin safety. In this study, we investigated the cytotoxic effect of zineb, a fungicide, in human keratinocyte (HaCaT) cells. HaCaT cells were treated with zineb (1-40 µg/mL) for 24 hours. Cellular and molecular mechanisms of cell toxicity were investigated through MTT and neutral red-uptake assays. Zineb reduced viability of HaCaT cells and induced apoptosis in a concentration-dependent manner. Zineb increased levels of Bax and caspase 3 and inhibited the level of Bcl2, which subsequently induced apoptosis via the Bax/Bcl2 and caspase pathway. Therefore, zineb could have induced apoptosis through the mitochondrial pathway in HaCaT cells. Our study suggests that zineb is cytotoxic to HaCaT cells via the induction of apoptosis and oxidative stress in vitro.</abstract><cop>New Zealand</cop><pub>Dove Medical Press Limited</pub><pmid>29416349</pmid><doi>10.2147/OTT.S140358</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | Taylor & Francis Open Access; DOVE Medical Press Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; PubMed Central |
| subjects | Agricultural laborers Apoptosis Crop diseases Cytotoxicity Deoxyribonucleic acid DNA DNA damage EDTA Fungicides Inflammation Lipid peroxidation Lipids Mammals Microscopy Original Research Oxidative stress Pesticides Proteins Skin Toxicity Workers |
| title | ROS-dependent Bax/Bcl2 and caspase 3 pathway-mediated apoptosis induced by zineb in human keratinocyte cells |
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