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Article: Enhancement of hypoxia-induced gene expression in fish liver by the aryl hydrocarbon receptor (AhR) ligand, benzo[a]pyrene (BaP)

TitleEnhancement of hypoxia-induced gene expression in fish liver by the aryl hydrocarbon receptor (AhR) ligand, benzo[a]pyrene (BaP)
Authors
Issue Date2008
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/aquatox
Citation
Aquatic Toxicology, 2008, v. 90 n. 3, p. 235-242 How to Cite?
AbstractFish in polluted coastal habitats commonly suffer simultaneous exposure to both hypoxia and xenobiotics. Although the adaptive molecular responses to each stress have been described, little is known about the interaction between the signaling pathways mediating these responses. Previous studies in mammalian hepatoma cell lines have shown that hypoxia-inducible factor (HIF)- and/or aryl hydrocarbon receptor (AhR)-activated gene expression is suppressed following co-exposure to hypoxia and the hallmark AhR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). However, whether similar crosstalk exists in the non-tumor liver tissues of fish and whether other non-TCDD ligands also play the same inhibitory role in this crosstalk remain unknown. Here, the in vivo hepatic mRNA expression profiles of multiple hypoxia- and AhR-responsive genes (later gene expression = mRNA expression of the gene) were examined in the orange-spotted grouper (Epinephelus coioides) upon single and combined exposures to hypoxia and benzo[a]pyrene (BaP). Combined exposure enhanced hypoxia-induced gene expression but did not significantly alter BaP-induced gene expression. Protein carbonyl content was markedly elevated in fish subjected to combined exposure, indicating accumulation of reactive oxygen species (ROS). Application of diethyldithiocarbamate (DDC) to hypoxia-treated grouper liver explants similarly exaggerated hypoxia-induced gene expression as in the combined stress tissues in vivo. These observations suggest that ROS derived from the combined hypoxia and BaP stress have a role in enhancing hypoxia-induced gene expression. © 2008 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/179095
ISSN
2015 Impact Factor: 3.557
2015 SCImago Journal Rankings: 1.671
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYu, RMKen_US
dc.contributor.authorNg, PKSen_US
dc.contributor.authorTan, Ten_US
dc.contributor.authorChu, DLHen_US
dc.contributor.authorWu, RSSen_US
dc.contributor.authorKong, RYCen_US
dc.date.accessioned2012-12-19T09:51:57Z-
dc.date.available2012-12-19T09:51:57Z-
dc.date.issued2008en_US
dc.identifier.citationAquatic Toxicology, 2008, v. 90 n. 3, p. 235-242en_US
dc.identifier.issn0166-445Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/179095-
dc.description.abstractFish in polluted coastal habitats commonly suffer simultaneous exposure to both hypoxia and xenobiotics. Although the adaptive molecular responses to each stress have been described, little is known about the interaction between the signaling pathways mediating these responses. Previous studies in mammalian hepatoma cell lines have shown that hypoxia-inducible factor (HIF)- and/or aryl hydrocarbon receptor (AhR)-activated gene expression is suppressed following co-exposure to hypoxia and the hallmark AhR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). However, whether similar crosstalk exists in the non-tumor liver tissues of fish and whether other non-TCDD ligands also play the same inhibitory role in this crosstalk remain unknown. Here, the in vivo hepatic mRNA expression profiles of multiple hypoxia- and AhR-responsive genes (later gene expression = mRNA expression of the gene) were examined in the orange-spotted grouper (Epinephelus coioides) upon single and combined exposures to hypoxia and benzo[a]pyrene (BaP). Combined exposure enhanced hypoxia-induced gene expression but did not significantly alter BaP-induced gene expression. Protein carbonyl content was markedly elevated in fish subjected to combined exposure, indicating accumulation of reactive oxygen species (ROS). Application of diethyldithiocarbamate (DDC) to hypoxia-treated grouper liver explants similarly exaggerated hypoxia-induced gene expression as in the combined stress tissues in vivo. These observations suggest that ROS derived from the combined hypoxia and BaP stress have a role in enhancing hypoxia-induced gene expression. © 2008 Elsevier B.V. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/aquatoxen_US
dc.relation.ispartofAquatic Toxicologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Metabolismen_US
dc.subject.meshBenzo(A)Pyrene - Toxicityen_US
dc.subject.meshGene Expression Profilingen_US
dc.subject.meshGene Expression Regulation - Drug Effects - Physiologyen_US
dc.subject.meshLiver - Drug Effects - Metabolismen_US
dc.subject.meshMetabolic Detoxication, Drug - Geneticsen_US
dc.subject.meshOrgan Culture Techniquesen_US
dc.subject.meshPerciformes - Metabolismen_US
dc.subject.meshProtein Carbonylation - Drug Effectsen_US
dc.subject.meshReactive Oxygen Species - Metabolismen_US
dc.subject.meshSuperoxide Dismutase - Metabolismen_US
dc.subject.meshWater Pollutants, Chemical - Toxicityen_US
dc.titleEnhancement of hypoxia-induced gene expression in fish liver by the aryl hydrocarbon receptor (AhR) ligand, benzo[a]pyrene (BaP)en_US
dc.typeArticleen_US
dc.identifier.emailWu, RSS: rudolfwu@hku.hken_US
dc.identifier.authorityWu, RSS=rp01398en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.aquatox.2008.09.004en_US
dc.identifier.pmid18945501-
dc.identifier.scopuseid_2-s2.0-55049133394en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-55049133394&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume90en_US
dc.identifier.issue3en_US
dc.identifier.spage235en_US
dc.identifier.epage242en_US
dc.identifier.isiWOS:000261776000010-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridYu, RMK=9278574900en_US
dc.identifier.scopusauthoridNg, PKS=13908200700en_US
dc.identifier.scopusauthoridTan, T=25230516600en_US
dc.identifier.scopusauthoridChu, DLH=25229992700en_US
dc.identifier.scopusauthoridWu, RSS=7402945079en_US
dc.identifier.scopusauthoridKong, RYC=7005290687en_US

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