High hydrostatic pressure influences the in vitro response toxenobiotics in Dicentrarchus labrax liver

Hydrostatic pressure (HP) increases by about 1 atmosphere (0.1 MPa) for each ten-meter depth increasein the water column. This thermodynamical parameter could well influence the response to and effects ofxenobiotics in the deep-sea biota, but this possibility remains largely overlooked. To grasp the extent of HPadaptation in deep-sea fish, comparative studies with living cells of surface species exposed to chemicalsat high HP are required. We initially conducted experiments with precision-cut liver slices of a deep-sea fish (Coryphaenoides rupestris), co-exposed for 15 h to the aryl hydrocarbon receptor (AhR) agonist3-methylcholanthrene at HP levels representative of the surface (0.1 MPa) and deep-sea (5–15 MPa; i.e.,500–1500 m depth) environments. The transcript levels of a suite of stress-responsive genes, such asthe AhR battery CYP1A, were subsequently measured (Lemaire et al., 2012; Environ. Sci. Technol. 46,10310–10316). Strikingly, the AhR agonist-mediated increase of CYP1A mRNA content was pressure-dependently reduced in C. rupestris. Here, the same co-exposure scenario was applied for 6 or 15 h toliver slices of a surface fish, Dicentrarchus labrax, a coastal species presumably not adapted to high HP.Precision-cut liver slices of D. labrax were also used in 1 h co-exposure studies with the pro-oxidant tert-butylhydroperoxide (tBHP) as to investigate the pressure-dependence of the oxidative stress response(i.e., reactive oxygen production, glutathione and lipid peroxidation status). Liver cells remained viable inall experiments (adenosine triphosphate content). High HP precluded the AhR agonist-mediated increaseof CYP1A mRNA expression in D. labrax, as well as that of glutathione peroxidase, and significantly reducedthat of heat shock protein 70. High HP (1 h) also tended per se to increase the level of oxidative stress inliver cells of the surface fish. Trends to an increased resistance to tBHP were also noted. Whether thelatter 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 CYP1A inducibility with D. labrax and C. rupestris support the view that high HPrepresses AhR signaling in marine fishes, and that only species adapted to thrive in the deep-sea haveevolved the molecular adaptations necessary to counteract to some extent this inhibition.