Effect of exercise training on respiration and reactive oxygen species metabolism in eel red muscle.

International audienceThis paper deals with the effects of exercise training on oxygen consumption (MO(2)) and ROS metabolism in the red muscle of trained and untrained female silver eels. Their critical swimming speed (U(crit)) was determined before and after a 4-day training (10h of swimming at 70% of U(crit) and 14 h at 50%, every day). The U(crit) of trained eels increased significantly (by about 7%). The in vitro MO(2) and ROS production by the red fibres were higher (not significant) in trained than in untrained eels, but the ROS production/MO(2) ratio was alike in both groups. The antioxidant-enzyme activities and lipoperoxidation index in trained eels were both lower than those of the untrained ones. These biochemical changes related to the increase in U(crit) suggest that such a training session could maintained or even increased aerobic power of the red muscle without deleterious impact by ROS. These regulations could play a role in the eel's swimming performance efficiency

Involvement of respiratory chain in the regulatory volume decrease process in turbot hepatocytes.

International audienceRegulatory volume decrease (RVD) constitutes a fundamental process that turbot (Scophthalmus maximus) hepatocytes are able to perform when exposed to hypo-osmotic stress. RVD is an integrative mechanism that involves various elements of the cellular machinery. Among others, ATP is an essential protagonist: released following hypo-osmotic shock, it acts as an auto/paracrine factor to trigger other signalling events. The origin of this ATP remains unclear and, to the best of our knowledge, no information exists about the role of mitochondrial respiration in RVD. Therefore, we propose to analyse the potential link between RVD and the respiratory chain, with a focus on ATP release and exocytosis. Using inhibitors of mitochondrial respiration, RVD was shown to be dependent on respiratory chain activity. However, we demonstrated an indirect role of mitochondrial respiration: ATP could be synthesized and then stored in intracellular vesicles until the moment cells release it to face hypo-osmotic swelling. However, the involvement of exocytosis in this process needs to be further investigated

Activation of the MAPKs ERK1/2 by cell swelling in turbot hepatocytes.

International audienceBACKGROUND INFORMATION: Activation of MAPKs (mitogen-activated protein kinases), in particular ERK1/2 (extracellular-signal-regulated kinase 1/2), has been reported to take place in a large variety of cell types after hypo-osmotic cell swelling. Depending on cell type, ERK1/2 phosphorylation can then serve or not the RVD (regulatory volume decrease) process. The present study investigates ERK1/2 activation after aniso-osmotic stimulations in turbot hepatocytes and the potential link between phosphorylation of these proteins and RVD. RESULTS: In turbot hepatocytes, Western-blot analysis shows that a hypo-osmotic shock from 320 to 240 mOsm kg(-1) induced a rapid increase in ERK1/2 phosphorylation, whereas a hyper-osmotic shock from 320 to 400 mOsm kg(-1) induced no significant change in the phosphorylation of these proteins. The hypo-osmotic-induced ERK1/2 phosphorylation was significantly prevented when hypo-osmotic shock was performed in the presence of the specific MEK (MAPK/ERK kinase) inhibitor PD98059 (100 microM). In these conditions, the RVD process was not altered, suggesting that ERK1/2 did not participate in this process in turbot hepatocytes. Moreover, the hypo-osmotic-induced activation of ERK1/2 was significantly prevented by breakdown of extracellular ATP by apyrase (10 units ml(-1)), by inhibition of purinergic P2 receptors by suramin (100 microM) or by calcium depletion using EGTA (1 mM) and thapsigargin (1 microM). CONCLUSIONS: In turbot hepatocytes, hypo-osmotic swelling but not hyper-osmotic shrinkage induced the activation of ERK1/2. However, these proteins do not seem to be involved in the RVD process. Their hypo-osmotic-induced activation is partially due to cascades of signalling events triggered by the binding of released ATP on purinergic P2 receptors and requires the presence of calcium

Volume regulation following hyposmotic shock in isolated turbot (Scophthalmus maximus) hepatocytes.

International audienceRegulatory volume decrease (RVD) following hyposmotic stimulation was studied in isolated turbot, Scophthalmus maximus, hepatocytes. Exposed to a reduced osmolality (from 320 to 240 mosm kg(-1)), cells first swelled and then exhibited a RVD. Volume regulation was significantly inhibited in presence of NPPB, 9-AC, acetazolamide, DIDS and barium. Taken together, these results could suggest that RVD operated via separate K+ and Cl- channels and probably Cl-/HCO3(-) exchanger in turbot hepatocytes. The K+/Cl- cotransporter could also be involved as furosemide and DIOA strongly inhibited the process whereas NEM, a K+/Cl- cotransporter activator, added under isosmotic conditions, led to cell shrinkage. RVD in turbot hepatocytes appeared also to depend on proteins p38 MAP kinase and tyrosine kinase but not on proteins ERK 1/2. Arachidonic acid and leukotrienes could also be involved since inhibition of synthesis of both these compounds by quinacrine and NDGA, respectively, inhibited the volume regulation. Likewise, Ca2+ has been proved to be an essential messenger as RVD was prevented in absence of Ca2+. Finally, this work provides bases for novel studies on cell volume regulation in marine teleosteans

Crustal strain-dependent serpentinisation in the Porcupine Basin, offshore Ireland

Highlights • Low upper mantle seismic velocity indicates mantle hydration in the Porcupine Basin. • Crustal stretching factors suggest crustal break up in the Porcupine Basin. • Fault-controlled mantle hydration explains across-axis mantle velocity variations. • Along-axis variations in mantle hydration control the development of low-angle faults. Abstract Mantle hydration (serpentinisation) at magma-poor rifted margins is thought to play a key role in controlling the kinematics of low-angle faults and thus, hyperextension and crustal breakup. However, because geophysical data principally provide observations of the final structure of a margin, little is known about the evolution of serpentinisation and how this governs tectonics during hyperextension. Here we present new observational evidence on how crustal strain-dependent serpentinisation influences hyperextension from rifting to possible crustal breakup along the axis of the Porcupine Basin, offshore Ireland. We present three new P-wave seismic velocity models that show the seismic structure of the uppermost lithosphere and the geometry of the Moho across and along the basin axis. We use neighbouring seismic reflection lines to our tomographic models to estimate crustal stretching ( ) of ∼2.5 in the north at 52.5° N and >10 in the south at 51.7° N. These values suggest that no crustal embrittlement occurred in the northernmost region, and that rifting may have progressed to crustal breakup in the southern part of the study area. We observed a decrease in mantle velocities across the basin axis from east to west. These variations occur in a region where is within the range at which crustal embrittlement and serpentinisation are possible ( 3–4). Across the basin axis, the lowest seismic velocity in the mantle spatially coincides with the maximum amount of crustal faulting, indicating fault-controlled mantle hydration. Mantle velocities also suggest that the degree of serpentinisation, together with the amount of crustal faulting, increases southwards along the basin axis. Seismic reflection lines show a major detachment fault surface that grows southwards along the basin axis and is only visible where the inferred degree of serpentinisation is >15%. This observation is consistent with laboratory measurements that show that at this degree of serpentinisation, mantle rocks are sufficiently weak to allow low-angle normal faulting. Based on these results, we propose two alternative formation models for the Porcupine Basin. The first involves a northward propagation of the hyperextension processes, while the second model suggests higher extension rates in the centre of the basin than in the north. Both scenarios postulate that the amount of crustal strain determines the extent and degree of serpentinisation, which eventually controls the development of detachments faults with advanced stretching