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Conference Paper: Mycotoxin Zearalenone induced apoptosis in BEAS-2B cells through generation of ROS and activation of JNK and p38 MAPKs signalling pathways

TitleMycotoxin Zearalenone induced apoptosis in BEAS-2B cells through generation of ROS and activation of JNK and p38 MAPKs signalling pathways
Authors
Issue Date2012
PublisherSETAC Europe. The Abstracts Book's web site is located at http://berlin.setac.eu/scientific_programme/download_the_abstracts_book/?contentid=582
Citation
The 6th SETAC World Congress / 22nd Annual Meeting of SETAC Europe, Berlin, Germany, 20-24 May 2012. In Abstracts Book, 2012, pt. 5, p. 443, abstract WE 304 How to Cite?
AbstractHuman exposure to Zearalenone (ZEA, a non-steroidal estrogenic mycotoxin) through inhalation has raised considerable concern. However, the potential health risk and the mechanism of actions of ZEA are not well understood. In the present study, we used BEAS-2B, cultured human bronchial epithelial cells, as well as Cygb stably transfected BEAS-2B cells to study the cytotoxic effects and the toxic mechanisms of ZEA. Our results indicated that ZEA decreased cell viability, induced apoptosis and promoted ROS level in BEAS-2B cells. Oxidative stress was clearly evident, as shown by an elevated mRNA expression levels of oxidative stress markers (Hsp70 and Hsp27) and endogenous antioxidants (SOD2 and Gpx). Stable transfection of Cygb significantly increased the level of Cygb but reduced level of ROS and the percentage of apoptotic cells induced by ZEA. Cells pretreated with either p38 or JNK inhibitors showed no attenuation in ROS level, but the percentage of apoptotic cells was lower than cells treated with ZEA
DescriptionSession: ET05P - Ecotoxicology and ecosystem services: A southern perspective: WE 304
Persistent Identifierhttp://hdl.handle.net/10722/166241

 

DC FieldValueLanguage
dc.contributor.authorSo, MYen_US
dc.contributor.authorSha, Sen_US
dc.contributor.authorAntoniou, Men_US
dc.contributor.authorWu, SSen_US
dc.contributor.authorTan-Un, KCen_US
dc.date.accessioned2012-09-20T08:30:36Z-
dc.date.available2012-09-20T08:30:36Z-
dc.date.issued2012en_US
dc.identifier.citationThe 6th SETAC World Congress / 22nd Annual Meeting of SETAC Europe, Berlin, Germany, 20-24 May 2012. In Abstracts Book, 2012, pt. 5, p. 443, abstract WE 304en_US
dc.identifier.urihttp://hdl.handle.net/10722/166241-
dc.descriptionSession: ET05P - Ecotoxicology and ecosystem services: A southern perspective: WE 304-
dc.description.abstractHuman exposure to Zearalenone (ZEA, a non-steroidal estrogenic mycotoxin) through inhalation has raised considerable concern. However, the potential health risk and the mechanism of actions of ZEA are not well understood. In the present study, we used BEAS-2B, cultured human bronchial epithelial cells, as well as Cygb stably transfected BEAS-2B cells to study the cytotoxic effects and the toxic mechanisms of ZEA. Our results indicated that ZEA decreased cell viability, induced apoptosis and promoted ROS level in BEAS-2B cells. Oxidative stress was clearly evident, as shown by an elevated mRNA expression levels of oxidative stress markers (Hsp70 and Hsp27) and endogenous antioxidants (SOD2 and Gpx). Stable transfection of Cygb significantly increased the level of Cygb but reduced level of ROS and the percentage of apoptotic cells induced by ZEA. Cells pretreated with either p38 or JNK inhibitors showed no attenuation in ROS level, but the percentage of apoptotic cells was lower than cells treated with ZEA-
dc.languageengen_US
dc.publisherSETAC Europe. The Abstracts Book's web site is located at http://berlin.setac.eu/scientific_programme/download_the_abstracts_book/?contentid=582-
dc.relation.ispartof6th SETAC World Congress / SETAC Europe 22nd Annual Meetingen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleMycotoxin Zearalenone induced apoptosis in BEAS-2B cells through generation of ROS and activation of JNK and p38 MAPKs signalling pathwaysen_US
dc.typeConference_Paperen_US
dc.identifier.emailWu, SS: rudolfwu@hku.hken_US
dc.identifier.emailTan-Un, KC: kctanun@hkucc.hku.hken_US
dc.identifier.authorityWu, SS=rp01398en_US
dc.identifier.authorityTan-Un, KC=rp00787en_US
dc.description.naturepostprint-
dc.identifier.hkuros208584en_US
dc.identifier.hkuros208589-
dc.identifier.issuept. 5-
dc.identifier.spage443-
dc.identifier.epage443-
dc.publisher.placeBelgium-

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