Purpose. - The purpose of this preliminary study is to access whether moderate-intensity exercise training is associated with a chronic modification of the cellular response to a mechanical stress-induced with hypo-osmotic shock (regulatory volume decrease process) of 80 mosmoles.kg(-1).Materials and methods. - Wistar Kyoto male rats were subjected to a treadmill training protocol (Tr) (60 min per day, 5 days per week, 8 weeks, 15 degrees incline, 20m.min(-1)) or not (Sed). The rats were then sacrified and endothelial cells isolated from the thoracic and abdominal aortas.Results. - No significant group effect of hypo-osmotic shock was found. A RVD process was observed in cells from the Sed group, cell volume being significantly decreased 20 minutes after the shock (75% of initial volume). However, no RVD was found in cells from the Tr group. These preliminary results suggest that the increase in endothelial cell volume induced by hypo-osmotic shock is modified by chronic exercise as is the subsequent physiological response (RVD process). Therefore, we conclude that isolated endothelial cells from trained rat arteries would provide a good model to assess the effects of chronic exercise on cellular signaling. (C) 2014 Elsevier Masson SAS. All rights reserved.

Introduction: This study explored whether α-lactalbumine (cysteine-rich protein), an antioxidant food compound from milk protein (isolat P), increased myocardial function and/or pro/antioxidant protein in swine. We measured the effect of isolat P after one month of detraining (following 12 months of moderate chronic training), with and without a high fat diet. Methods: Male Göttingen swine (n=34, 18-24 weeks) were randomly assigned into sedentary (S) or exercise groups (E), fed with standard (N) or deleterious (D) diets. Only the D diet groups were supplemented with isolat P (+ or -). 6 groups were designed (NS-, NE-, DS-, DE-, DS+, DE+). Swine performed a treadmill training protocol that achieved 150 bpm for 60 min/day, 5 days/week for 12 weeks, and then detrained for 4 weeks. At the end of the program, myocardial tissues were analyzed for pro-oxydant NADPH oxydase (p47phox, p67phox) and eNOS expression by densitometry, as well as for antioxydant enzyme activities of SOD, CAT and GPx by spectrophotometry. Results: NADPH oxydase expression (p47phox only) (104.94±3.24 vs. 101.25±1.04 A.U., p<0.05) was higher in the DS- group than in NS-. eNOS expression tended to increase (77.33±2.90 UA vs. 71.70±1.07 UA) suggesting an eNOS decoupling. No difference was found between DS- and NS- for SOD, CAT or GPx activity, nor for p67phox expression. Training did not modify eNOS expression in N animals (75.18±2.14 UA vs. 71.70±1.07 UA, in NE- and NS- groups respectively, p>0.05). In DE- group eNOS expression is lower than in DS- (71.61±1.27 UA vs 77.33±2.90 UA, p<0.05). No modifications statistically observe for the others enzymes. DS+ group led to decreased expression of eNOS (DS- 77.33±2.90 AU vs. DS+: 71.24±2.7 AU, p<0.05) to reach a basal value, without modifying other enzymes. These results suggest an eNOS recoupling. Finally, in DE+ group, isolat P restored the basal activity and expression of enzymes eNOS, NADPHoxydase, SOD, CAT and GPx to similar values as in sedentary animal fed a standard diet (NS-). Conclusion: Addition of isolat P to high fat diet reverses eNOS decoupling induced by high fat diet. Isolat P may have an antioxidant role allowing antioxidant enzymes SOD, CAT and GPx to recover basal activity levels while NADPH oxydase increases with a high fat diet. After one month of detraining, the beneficial effects of chronic exercise had disappeared. Isolat P may slow down the detraining effect on eNOS but not upon antioxidant enzymes. Therefore, early isolat P association with exercise training may be an interesting preventive strategy against metabolic diseases.

Turbot Psetta maxima were exposed 5 days to the dissolved fraction of fuel oil number 2, then decontaminated over 30 days in clean sea water. Biliary metabolites and ethoxyresorufin‐O‐deethylase (EROD) activity were evaluated during and after the contamination. These results were compared with chromosomal damage measured by flow cytometry (FCM). Erythrocyte nuclear abnormality, micronuclei and immaturity were also evaluated over the exposure period. Biliary metabolites and EROD analyses showed a clear and early response: biliary metabolites were detected from the first day of contamination to the 14th day of depuration, EROD activity increased during the contamination period reached a maximum 3 days after the beginning of the decontamination and decreased to the control value after 1 month of depuration. FCM showed a bimodal response: a first increase of coefficient of variation of blood cell DNA content was observed during the contamination and a second one started after 14 days of depuration and was maintained for at least 2 weeks. Erythrocyte morphology analysis showed a strong increase in nuclear abnormality during the contamination period. These results confirm previous work and show that in the context of marine accidental pollution by heavy fuel oil, the measurements of chromosomal damage by FCM allow the detection of a genotoxic response in fishes.

Evaluating the ecological impact of an oil spill is a complex issue requiring coherently articulated examination of the sequence of interactions that link the cell, where contaminants exert their effects, to the ecosystem, where interactions with human activities arise. This sequence of interactions traverses the frontiers between scientific disciplines (chemistry, toxicology, physiology, and fisheries ecology). Using the common sole (Solea solea L.) as a model species for the coastal habitats polluted by the "Erika" oil spill, our research project attempted to define indices of functional integrity that characterised the consequences of fuel exposure at the different biological levels. The coupling of field observations with experimental laboratory work revealed how functional alterations which are readily observable within individuals and their organs are progressively obscured as investigation progresses towards more complex organisational levels. Some of the approaches and indices are proposed as instruments for evaluating the impact of contamination by hydrocarbons.

Flatfishes, turbots (Scophthalmus maximus), were injected intraperitoneally with two doses of fuel oil number 2. Biliary metabolites were evaluated by fixed fluorescence to verify the efficiency of intoxication. Ethoxyresorufin-O-deethylase (EROD) activity was compared with chromosomal damage measured by flow cytometry. The analysis of biliary metabolites showed a good dose–response relation and constitutes a clear reference for the subsequent measurements. Comparing flow cytometry and EROD results, a shorter delay of response for EROD activity was obtained, but chromosomal damage was significant only after 1 week. The persistence of the EROD response was shorter, while the genotoxic signal still persisted after 1 month. The measurement of chromosomal damage allowed a good differentiation between the two tested doses. In the case of EROD activity, the results were less clear. The results suggest that within a few weeks after exposure to fuel oil number 2, the measurements of chromosomal damage by flow cytometry can be used to detect a dose-dependant genotoxic response in fish.