PMID- 21660599 OWN - NLM STAT- MEDLINE DCOM- 20120316 LR - 20211020 IS - 1573-3017 (Electronic) IS - 0963-9292 (Linking) VI - 20 IP - 8 DP - 2011 Nov TI - Transcriptomic analyses in a benthic fish exposed to contaminated estuarine sediments through laboratory and in situ bioassays. PG - 1749-64 LID - 10.1007/s10646-011-0708-z [doi] AB - The transcription of contaminant response-related genes was investigated in juvenile Senegalese soles exposed to sediments from three distinct sites (a reference plus two contaminated) of a Portuguese estuary (the Sado, W Portugal) through simultaneous 28-day laboratory and in situ bioassays. Transcription of cytochrome P450 1A (CYP1A), metallothionein 1 (MT1), glutathione peroxidase (GPx), catalase (CAT), caspase 3 (CASP3) and 90 kDa heat-shock protein alpha (HSP90AA) was surveyed in the liver by real-time PCR. CASP3 transcription analysis was complemented by surveying apoptosis through the TUNEL reaction. After 14 days of exposure, relative transcription was either reduced or decreased in fish exposed to the contaminated sediments, revealing a disturbance stress phase during which animals failed to respond to insult. After 28 days of exposure all genes' transcription responded to contamination but laboratory and in situ assays depicted distinct patterns of regulation. Although sediments revealed a combination of organic and inorganic toxicants, transcription of the CYP1A gene was consistently correlated to organic contaminants. Metallothionein regulation was found correlated to metallic and organic xenobiotic contamination in the laboratory and in situ, respectively. The transcription of oxidative stress-related genes can be a good indicator of general stress but caution is mandatory when interpreting the results since regulation may be influenced by multiple factors. As for MT1, HSP90 up-regulation has potential to be a good indicator for total contamination, as well as the CASP3 gene, even though hepatocyte apoptosis depicted values inconsistent with sediment contamination, showing that programmed cell death did not directly depend on caspase transcription alone. FAU - Costa, Pedro M AU - Costa PM AD - IMAR-Instituto do Mar, Departamento de Ciencias e Engenharia do Ambiente, Faculdade de Ciencias e Tecnologia da Universidade Nova de Lisboa, 2829-516, Caparica, Portugal. pmcosta@fct.unl.pt FAU - Miguel, Celia AU - Miguel C FAU - Caeiro, Sandra AU - Caeiro S FAU - Lobo, Jorge AU - Lobo J FAU - Martins, Marta AU - Martins M FAU - Ferreira, Ana M AU - Ferreira AM FAU - Caetano, Miguel AU - Caetano M FAU - Vale, Carlos AU - Vale C FAU - DelValls, T A AU - DelValls TA FAU - Costa, Maria H AU - Costa MH LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20110610 PL - United States TA - Ecotoxicology JT - Ecotoxicology (London, England) JID - 9885956 RN - 0 (HSP90 Heat-Shock Proteins) RN - 0 (Water Pollutants, Chemical) RN - 0 (Xenobiotics) RN - 9038-94-2 (Metallothionein) RN - EC 1.11.1.6 (Catalase) RN - EC 1.11.1.9 (Glutathione Peroxidase) RN - EC 1.14.14.1 (Cytochrome P-450 CYP1A1) RN - EC 3.4.22.- (Caspase 3) SB - IM MH - Animals MH - Apoptosis/drug effects MH - Biological Assay MH - Caspase 3/genetics MH - Catalase/genetics MH - Cytochrome P-450 CYP1A1/genetics MH - Ecotoxicology/methods MH - Flatfishes/*genetics MH - Gene Expression Profiling MH - Geologic Sediments/*chemistry MH - Glutathione Peroxidase/genetics MH - HSP90 Heat-Shock Proteins/genetics MH - Hepatocytes/drug effects/pathology MH - Metallothionein/genetics MH - Portugal MH - Water Pollutants, Chemical/*toxicity MH - Xenobiotics/toxicity EDAT- 2011/06/11 06:00 MHDA- 2012/03/17 06:00 CRDT- 2011/06/11 06:00 PHST- 2011/05/29 00:00 [accepted] PHST- 2011/06/11 06:00 [entrez] PHST- 2011/06/11 06:00 [pubmed] PHST- 2012/03/17 06:00 [medline] AID - 10.1007/s10646-011-0708-z [doi] PST - ppublish SO - Ecotoxicology. 2011 Nov;20(8):1749-64. doi: 10.1007/s10646-011-0708-z. Epub 2011 Jun 10.