Please use this identifier to cite or link to this item: https://doi.org/10.1152/physiolgenomics.00201.2005
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dc.titleTranscriptome kinetics of arsenic-induced adaptive response in zebrafish liver
dc.contributor.authorSiew, H.L.
dc.contributor.authorWinata, C.L.
dc.contributor.authorTong, Y.
dc.contributor.authorKorzh, S.
dc.contributor.authorWen, S.L.
dc.contributor.authorKorzh, V.
dc.contributor.authorSpitsbergen, J.
dc.contributor.authorMathavan, S.
dc.contributor.authorMiller, L.D.
dc.contributor.authorLiu, E.T.
dc.contributor.authorGong, Z.
dc.date.accessioned2014-10-27T08:44:08Z
dc.date.available2014-10-27T08:44:08Z
dc.date.issued2006-11-27
dc.identifier.citationSiew, H.L., Winata, C.L., Tong, Y., Korzh, S., Wen, S.L., Korzh, V., Spitsbergen, J., Mathavan, S., Miller, L.D., Liu, E.T., Gong, Z. (2006-11-27). Transcriptome kinetics of arsenic-induced adaptive response in zebrafish liver. Physiological Genomics 27 (3) : 351-361. ScholarBank@NUS Repository. https://doi.org/10.1152/physiolgenomics.00201.2005
dc.identifier.issn10948341
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/102062
dc.description.abstractArsenic is a prominent environmental toxicant and carcinogen; however, its molecular mechanism of toxicity and carcinogenicity remains poorly understood. In this study, we performed microarray-based expression profiling on liver of zebrafish exposed to 15 parts/million (ppm) arsenic [As(V)] for 8-96 h to identify global transcriptional changes and biological networks involved in arsenic-induced adaptive responses in vivo. We found that there was an increase of transcriptional activity associated with metabolism, especially for biosyntheses, membrane transporter activities, cytoplasm, and endoplasmic reticulum in the 96 h of arsenic treatment, while transcriptional programs for proteins in catabolism, energy derivation, and stress response remained active throughout the arsenic treatment. Many differentially expressed genes encoding proteins involved in heat shock proteins, DNA damage/repair, antioxidant activity, hypoxia induction, iron homeostasis, arsenic metabolism, and ubiquitin-dependent protein degradation were identified, suggesting strongly that DNA and protein damage as a result of arsenic metabolism and oxidative stress caused major cellular injury. These findings were comparable with those reported in mammalian systems, suggesting that the zebrafish liver coupled with the available microarray technology present an excellent in vivo toxicogenomic model for investigating arsenic toxicity. We proposed an in vivo, acute arsenic-induced adaptive response model of the zebrafish liver illustrating the relevance of many transcriptional activities that provide both global and specific information of a coordinated adaptive response to arsenic in the liver. Copyright © 2006 the American Physiological Society.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1152/physiolgenomics.00201.2005
dc.sourceScopus
dc.subjectArsenic toxicity
dc.subjectFish toxicogenomics
dc.subjectMicroarray expression profiling
dc.subjectOxidative stress
dc.typeArticle
dc.contributor.departmentBIOLOGICAL SCIENCES
dc.description.doi10.1152/physiolgenomics.00201.2005
dc.description.sourcetitlePhysiological Genomics
dc.description.volume27
dc.description.issue3
dc.description.page351-361
dc.description.codenPHGEF
dc.identifier.isiut000242340100015
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