{"refrec":{"BRefID":256640,"RR":"<b>Lemaire, B.; Mignolet, E.; Debier, C.; Calderon, P.B.; Thomé, J.-P.; Rees, J.F.</b> (2016). High hydrostatic pressure influences the in vitro response to xenobiotics in <i>Dicentrarchus labrax</i> liver. <i>Aquat. Toxicol. 173</i>: 43-52. <a href=\"https://dx.doi.org/10.1016/j.aquatox.2016.01.004\" target=\"_blank\">https://dx.doi.org/10.1016/j.aquatox.2016.01.004</a>","BEntID":248649,"PublicFlag":1,"CheckedFlag":1,"wosflag":1,"vabbflag":null,"RefStringPartII":". <i>Aquat. Toxicol. 173</i>: 43-52. <a href=\"https://dx.doi.org/10.1016/j.aquatox.2016.01.004\" target=\"_blank\">https://dx.doi.org/10.1016/j.aquatox.2016.01.004</a>","DocTypID":8,"DocType":"Journal article","MarineFlag":1,"FreshFlag":0,"BrackishFlag":0,"TerrestrialFlag":0,"Authorstring":"Lemaire, B.; Mignolet, E.; Debier, C.; Calderon, P.B.; Thomé, J.-P.; Rees, J.F.","OrigTitleTranslFlag":0,"Authorstringtrunc":"Lemaire, B. <i>et al.</i>","Englishabstract":"Hydrostatic pressure (HP) increases by about 1 atmosphere (0.1 MPa) for each ten-meter depth increase in the water column. This thermodynamical parameter could well influence the response to and effects of xenobiotics in the deep-sea biota, but this possibility remains largely overlooked. To grasp the extent of HP adaptation in deep-sea fish, comparative studies with living cells of surface species exposed to chemicals at high HP are required. We initially conducted experiments with precision-cut liver slices of a deep-sea fish (<i>Coryphaenoides rupestris</i>), co-exposed for 15 h to the aryl hydrocarbon receptor (AhR) agonist 3-methylcholanthrene at HP levels representative of the surface (0.1 MPa) and deep-sea (5–15 MPa; <i>i.e.</i>, 500–1500 m depth) environments. The transcript levels of a suite of stress-responsive genes, such as the AhR battery <i>CYP1A</i>, were subsequently measured (Lemaire et al., 2012; <i>Environ. Sci. Technol.</i> 46, 10310–10316). Strikingly, the AhR agonist-mediated increase of <i>CYP1A</i> mRNA content was pressure-dependently reduced in <i>C. rupestris</i>. Here, the same co-exposure scenario was applied for 6 or 15 h to liver slices of a surface fish, <i>Dicentrarchus labrax</i>, a coastal species presumably not adapted to high HP. Precision-cut liver slices of <i>D. labrax</i> were also used in 1 h co-exposure studies with the pro-oxidant <i>tert</i>-butylhydroperoxide (tBHP) as to investigate the pressure-dependence of the oxidative stress response (<i>i.e.</i>, reactive oxygen production, glutathione and lipid peroxidation status). Liver cells remained viable in all experiments (adenosine triphosphate content). High HP precluded the AhR agonist-mediated increase of <i>CYP1A</i> mRNA expression in <i>D. labrax</i>, as well as that of <i>glutathione peroxidase</i>, and significantly reduced that of <i>heat shock protein 70</i>. High HP (1 h) also tended <i>per se</i> to increase the level of oxidative stress in liver cells of the surface fish. Trends to an increased resistance to tBHP were also noted. Whether the latter observation truly reflects a protective response to oxidative stress will be addressed in future co-exposure studies with both surface and deep-sea fish liver cells, using additional pro-oxidant chemicals. Altogether, data on <i>CYP1A</i> inducibility with <i>D. labrax</i> and <i>C. rupestris</i> support the view that high HP represses AhR signaling in marine fishes, and that only species adapted to thrive in the deep-sea have evolved the molecular adaptations necessary to counteract to some extent this inhibition.","AbstractOtherLang":null,"BibLvlCode":"AS","StandardTitle":"High hydrostatic pressure influences the in vitro response to xenobiotics in <i>Dicentrarchus labrax</i> liver","OrigTitleLangCode":"en","OrigTitleLangCodeExtended":"eng","OrigTitleLangID":15,"DateLastModified":{"date":"2024-12-10 01:33:17.368041","timezone_type":1,"timezone":"+01:00"},"UserAccessRight":null,"UserAccID":null,"AuthorKeywords":"Hydrostatic pressure; Precision-cut liver slices; CYP1A; Oxidativestress; Heat shock proteins; Fish","OtherDescriptors":null,"Notes":null,"AnaPub":2016,"MonPub":null,"DateUpdate":"2018-08-28","DateCreate":"2016-05-29","SecASFANote":null,"ConfID":null,"PeerRev":1,"VlizCoreFlag":1,"WoScode":"WOS:000372689900006","VABBcode":null,"OpenAcc":0,"DOI":"10.1016/j.aquatox.2016.01.004"},"refs":null,"anarec":{"AnaID":256640,"PubliDate":2016,"Pagination":"43-52","XtraPublOfAnaID":null,"ISBN":null,"Volume":"173","Issue":null,"BRefMon":null,"BRefMonRR":null,"BRefXtra":null,"BRefXtraRR":null,"SerBRefID":42203,"SerRR":"Aquatic Toxicology. Elsevier Science: Tokyo; New York; London; Amsterdam.  ISSN 0166-445X; e-ISSN 1879-1514","StandardTitleSer":"Aquatic Toxicology","ISSN":"0166-445X","AbbrevSer":"Aquat. 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