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Article: A proteome analysis of the arsenite response in cultured lung cells: evidence for in vitro oxidative stress-induced apoptosis

TitleA proteome analysis of the arsenite response in cultured lung cells: evidence for in vitro oxidative stress-induced apoptosis
Authors
Issue Date2004
PublisherPortland Press Ltd. The Journal's web site is located at http://www.biochemj.org/bj/default.htm
Citation
Biochemical Journal, 2004, v. 382 n. pt. 2, p. 641-650 How to Cite?
AbstractArsenite is well documented as a chemotherapeutic agent capable of inducing cell death. However, the cellular response at the molecular level has not been studied extensively. In the present study, we provide for the first time a proteomic analysis of rat LECs (lung epithelial cells) treated with arsenite, with the aim of identifying defence proteins, probably expressed to protect the cells during the course of arsenic-induced apoptosis. Comparative proteome analysis was conducted on LECs and LECs treated with 40 microM arsenite to identify global changes in their protein expression profiles. Over 1000 protein spots were separated by two-dimensional electrophoresis and visualized by silver staining. Seven proteins changed expression levels significantly and were identified by matrix-assisted laser-desorption ionization-time-of-flight mass spectrometry and database searching. The proteins up-regulated were mostly HSPs (heat-shock proteins) and antioxidative stress proteins, including HSP70, aldose reductase, haem oxygenase-1, HSP27, ferritin light chain and alphaB-crystallin. The glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase was down-regulated. Pretreatment with the thiol antioxidants glutathione or N-acetylcysteine before arsenite insult effectively abrogated the induction of these defence proteins and sustained cell viability, whereas antioxidants were protective only at earlier time points if they were added to cells after arsenite. Taken together, our results demonstrate that high levels of arsenite cause oxidative stress-induced apoptosis.
Persistent Identifierhttp://hdl.handle.net/10722/211356
ISSN
2015 Impact Factor: 3.562
2015 SCImago Journal Rankings: 2.582
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorLau, AT-
dc.contributor.authorHe, QY-
dc.contributor.authorChiu, JF-
dc.date.accessioned2015-07-08T09:33:42Z-
dc.date.available2015-07-08T09:33:42Z-
dc.date.issued2004-
dc.identifier.citationBiochemical Journal, 2004, v. 382 n. pt. 2, p. 641-650-
dc.identifier.issn0264-6021-
dc.identifier.urihttp://hdl.handle.net/10722/211356-
dc.description.abstractArsenite is well documented as a chemotherapeutic agent capable of inducing cell death. However, the cellular response at the molecular level has not been studied extensively. In the present study, we provide for the first time a proteomic analysis of rat LECs (lung epithelial cells) treated with arsenite, with the aim of identifying defence proteins, probably expressed to protect the cells during the course of arsenic-induced apoptosis. Comparative proteome analysis was conducted on LECs and LECs treated with 40 microM arsenite to identify global changes in their protein expression profiles. Over 1000 protein spots were separated by two-dimensional electrophoresis and visualized by silver staining. Seven proteins changed expression levels significantly and were identified by matrix-assisted laser-desorption ionization-time-of-flight mass spectrometry and database searching. The proteins up-regulated were mostly HSPs (heat-shock proteins) and antioxidative stress proteins, including HSP70, aldose reductase, haem oxygenase-1, HSP27, ferritin light chain and alphaB-crystallin. The glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase was down-regulated. Pretreatment with the thiol antioxidants glutathione or N-acetylcysteine before arsenite insult effectively abrogated the induction of these defence proteins and sustained cell viability, whereas antioxidants were protective only at earlier time points if they were added to cells after arsenite. Taken together, our results demonstrate that high levels of arsenite cause oxidative stress-induced apoptosis.-
dc.languageeng-
dc.publisherPortland Press Ltd. The Journal's web site is located at http://www.biochemj.org/bj/default.htm-
dc.relation.ispartofBiochemical Journal-
dc.rightsThe final version of record is available at [Journal URL].-
dc.subject.meshApoptosis - drug effects-
dc.subject.meshArsenites - antagonists & inhibitors - pharmacology-
dc.subject.meshLung - cytology - drug effects-
dc.subject.meshOxidative Stress - drug effects-
dc.subject.meshProteome - drug effects-
dc.titleA proteome analysis of the arsenite response in cultured lung cells: evidence for in vitro oxidative stress-induced apoptosis-
dc.typeArticle-
dc.identifier.emailLau, AT: andytylau@hotmail.com-
dc.identifier.emailHe, QY: qyhe@hkucc.hku.hk-
dc.identifier.emailChiu, JF: jfchiu@hkucc.hku.hk-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.pmid15175009-
dc.identifier.pmcidPMC1133821-
dc.identifier.hkuros91730-
dc.identifier.volume382-
dc.identifier.issuept. 2-
dc.identifier.spage641-
dc.identifier.epage650-
dc.publisher.placeUnited Kingdom-

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