Éditeur(s) : HAL CCSD Wiley
Résumé : International audience
MR and MDHD contributed equally to this work. Summary Painful vaso-occlusive crisis, a hallmark of sickle cell anaemia, results from complex, incompletely understood mechanisms. Red blood cell (RBC) damage caused by continuous endogenous and exogenous oxidative stress may precipitate the occurrence of vaso-occlusive crises. In order to gain insight into the relevance of oxidative stress in vaso-occlusive crisis occurrence , we prospectively compared the expression levels of various oxidative markers in 32 adults with sickle cell anaemia during vaso-occlusive crisis and steady-state conditions. Compared to steady-state condition, plasma levels of free haem, advanced oxidation protein products and myeloperoxi-dase, RBC caspase-3 activity, as well as the concentrations of total, neutrophil-and RBC-derived microparticles were increased during vaso-occlusive crises, whereas the reduced glutathione content was decreased in RBCs. In addition, natural anti-band 3 autoantibodies levels decreased during crisis and were negatively correlated with the rise in plasma advanced oxidation protein products and RBC caspase-3 activity. These data showed an exacerbation of the oxidative stress during vaso-occlusive crises in sickle cell anaemia patients and strongly suggest that the higher concentration of harmful circulating RBC-derived microparticles and the reduced anti-band 3 autoantibodies levels may be both related to the recruitment of oxidized band 3 into membrane aggregates.
ISSN: 0007-1048

inserm-01476067
http://www.hal.inserm.fr/inserm-01476067
http://www.hal.inserm.fr/inserm-01476067/document
http://www.hal.inserm.fr/inserm-01476067/file/2016%2C%20Hierso%20-%20Exacerbation%20of%20oxidative%20stress%20during%20sickle%20vaso-occlusive%20crisis.pdf
DOI : 10.1111/bjh.14476

Éditeur(s) : HAL CCSD
Résumé : International audience
Objective Oxidative stress, excess production of reactive oxygen species (ROS) and intense colonization of the respiratory tract by microorganisms are described in CF patients, leading to an influx in macrophages. This results in activation of NADPH oxidase that yields ROS, initiating the oxidative burst responsible for pathogen destruction. We showed that phagocytosis was altered in CF macrophages, yet oxidative status in this cell was not defined. The objective of this study is to draw a link between oxidative stress and plasma membrane integrity in CF macrophages, since lipid peroxidation is known to alter cell membrane. Methods Peripheral blood monocytes-derived macrophages were obtained from CF patients and healthy subjects. Plasma membrane fluidity was assessed with di4-ANEPPDHQ and oxidative status was measured with ROS indicating probes. Results In CF macrophages, membrane fluidity was increased whereas lipid peroxidation was diminished. Surprisingly, general oxidative status remained similar to the one observed in non-CF macrophages. Also, CF macrophages did not abolish chemically induced-oxidative stress. In non-CF macrophages, treatment with cholesterol slightly increased membrane fluidity whereas LPS treatment had no effect. Conclusion CF macrophages displayed an increased membrane fluidity associated with a decreased lipid peroxidation. This raises the hypothesis that membrane alteration in CF macrophages may be due to other mechanism than oxidative stress. Nevertheless, since the killing capacity of CF macrophage is defective, a deregulation of O•−2 production is very likely, suggesting alteration of NADPH oxidase or mitochondrial dysfunction
the 38th European Cystic Fibrosis Conference
Vienne, Austria

hal-01162769
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01162769
DOI : 10.1016/S1569-1993(15)30217-4

Éditeur(s) : Academic Press Ltd- Elsevier Science Ltd
Résumé : Antioxidant defences and induced oxidative stress tissue damage of the blue shrimp Litopenaeus stylirostris, under challenge with Vibrio nigriputchritudo, were investigated for a 72-h period. For this purpose, L stylirostris were first infected by immersion with pathogenic V. nigripulchritudo strain SFn1 and then antioxidant defences: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (Gpx), Total antioxidant status (TAS), glutathiones and induced tissue damage (MDA and carbonyl proteins) were determined in the digestive gland at 0, 12, 24, 48 and 72 h post-infection (h.p.i.). In the meantime, TAS was also measured in the blood. Infection level of the shrimps during the challenge was followed by determining V. nigripulchritudo prevalence and load in the haemolymph of the shrimps. Changes in all these parameters during the 72-h.p.i. period were recorded for control shrimps and shrimps previously fed for one month with probiotic Pediococcus aciditactici MA18/5M at 10(7) CFU g(-1) of feed. Our results showed that immersion with V nigripulchritudo led to maximal infection level in the haemolymph at 24 h.p.i. preceding the mortality peak recorded at 48 h.p.i. Significant decreases in the antioxidant defences were detected from 24 h.p.i. and beyond that time infection leaded to increases in oxidative stress level and tissue damage.. Compared to control group, shrimps fed the probiotic diet showed lower infection (20% instead of 45% at 24 h.p.i. in the control group) and mortality (25% instead of 41.7% in the control group) levels. Moreover, infected shrimp fed the probiotic compared to uninfected control shrimps exhibited very similar antioxidant status and oxidative stress level. Compared to the infected control group, shrimps fed the probiotic sustained higher antioxidant defences and lower oxidative stress level. This study shows that bacterial infection leads to oxidative stress in L. stylirostris and highlighted a beneficial effect of P. acidilactici, suggesting both a competitive exclusion effect leading to a reduction of the infection level and/or an enhancement of the antioxidant status of the shrimps. (C) 2010 Elsevier Ltd. All rights reserved.
Fish & Shellfish Immunology (1050-4648) (Academic Press Ltd- Elsevier Science Ltd), 2010-04 , Vol. 28 , N. 4 , P. 622-631

Droits : 2010 Elsevier Ltd All rights reserved.
http://archimer.ifremer.fr/doc/00003/11419/7984.pdf
DOI:10.1016/j.fsi.2009.12.024
http://archimer.ifremer.fr/doc/00003/11419/

Éditeur(s) : HAL CCSD Wiley
Résumé : International audience
High sea surface temperature accompanied by high levels of solar irradiance is responsible for the disruption of the symbiosis between cnidarians and their symbiotic dinoflagellates from the genus Symbiodinium. This phenomenon, known as coral bleaching, is one of the major threats affecting coral reefs around the world. Because an important molecular trigger to bleaching appears related to the production of reactive oxygen species (ROS), it is critical to understand the function of the antioxidant network of Symbiodinium species. In this study we investigated the response of two Symbiodinium species, from contrasting environments, to a chemically induced oxidative stress. ROS produced during this oxidative burst reduced photosynthesis by 30 to 50% and significantly decreased the activity of superoxide dismutase. Lipid peroxidation levels and carotenoid concentrations, especially diatoxanthin, confirm that these molecules act as antioxidants and contribute to the stabilization of membrane lipids. The comparative analysis between the two Symbiodinium species allowed us to highlight that Symbiodinium sp. clade A temperate was more tolerant to oxidative stress than the tropical S. kawagutii clade F. These differences are very likely a consequence of adaptation to their natural environment, with the temperate species experiencing conditions of temperature and irradiance much more variable and extreme.
ISSN: 0140-7791

hal-01546161
https://hal.archives-ouvertes.fr/hal-01546161
DOI : 10.1111/pce.12825

Éditeur(s) : HAL CCSD Wiley
Résumé : International audience
Painful vaso-occlusive crisis, a hallmark of sickle cell anaemia, results from complex, incompletely understood mechanisms. Red blood cell (RBC) damage caused by continuous endogenous and exogenous oxidative stress may precipitate the occurrence of vaso-occlusive crises. In order to gain insight into the relevance of oxidative stress in vaso-occlusive crisis occurrence, we prospectively compared the expression levels of various oxidative markers in 32 adults with sickle cell anaemia during vaso-occlusive crisis and steady-state conditions. Compared to steady-state condition, plasma levels of free haem, advanced oxidation protein products and myeloperoxidase, RBC caspase-3 activity, as well as the concentrations of total, neutrophil- and RBC-derived microparticles were increased during vaso-occlusive crises, whereas the reduced glutathione content was decreased in RBCs. In addition, natural anti-band 3 autoantibodies levels decreased during crisis and were negatively correlated with the rise in plasma advanced oxidation protein products and RBC caspase-3 activity. These data showed an exacerbation of the oxidative stress during vaso-occlusive crises in sickle cell anaemia patients and strongly suggest that the higher concentration of harmful circulating RBC-derived microparticles and the reduced anti-band 3 autoantibodies levels may be both related to the recruitment of oxidized band 3 into membrane aggregates.
ISSN: 0007-1048

hal-01668325
https://hal.univ-antilles.fr/hal-01668325
DOI : 10.1111/bjh.14476

Éditeur(s) : HAL CCSD Springer Verlag
Résumé : International audience
The implication of oxidative stress as primary mechanism inducing doxorubicin (DOX) cardiotoxicity is still questionable as many in vitro studies implied supra-clinical drug doses or unreliable methodologies for reactive oxygen species (ROS) detection. The aim of this study was to clarify whether oxidative stress is involved in compliance with the conditions of clinical use of DOX, and using reliable tools for ROS detection. We examined the cytotoxic mechanisms of 2 μM DOX 1 day after the beginning of the treatment in differentiated H9c2 rat embryonic cardiac cells. Cells were exposed for 2 or 24 h with DOX to mimic a single chronic dosage or to favor accumulation, respectively. We found that apoptosis was prevalent in cells exposed for a short period with DOX: cells showed typical hallmarks as loss of anchorage ability, mitochondrial hyperpolarization followed by the collapse of mitochondrial activity, and nuclear condensation. Increasing the exposure period favored a shift to necrosis as the cells preferentially exhibited early DNA impairment and nuclear swelling. In either case, measuring the fluorescence lifetime of 1-pyrenebutyric acid or the intensities of dihydroethidium or amplex red showed a consistent pattern in ROS production which was a slight increased level far from representative of an oxidative stress. Moreover, pre-treatment with dexrazoxane provided a cytoprotective effect although it failed to detoxify ROS. Our data support that oxidative stress is unlikely to be the primary mechanism of DOX cardiac toxicity in vitro.
ISSN: 0300-8177

hal-01285736
https://hal-univ-perp.archives-ouvertes.fr/hal-01285736
DOI : 10.1007/s11010-016-2653-x

Éditeur(s) : HAL CCSD Wiley
Résumé : International audience
Oxidative stress and haemolysis-associated nitric oxide (NO) depletion plays a crucial role in the development of vasculopathy in sickle cell anaemia (SS). However it remains unknown whether oxidative stress and haemolysis levels influence vascular function in patients with sickle haemoglobin C disease (SC). Microvascular response to heat (using Laser Doppler flowmetry on finger), oxidative stress biomarkers, NO metabolites, endothelin-1 and haematological parameters were compared between patients with SS and SC. Vascular function, oxidative and nitrosative markers were also measured in healthy (AA) children. SS and SC had increased plasma advanced oxidation protein products (AOPP), malondialdehyde, plasma antioxidant activities and NO end products, compared to AA. SC had lower catalase activity compared to AA and SS. Haemolytic rate, glutathione peroxidase and nitrotyrosine concentrations were significantly increased in children with SS compared to SC and AA. SS and SC had impaired microvascular reactivity compared to AA. In SS, the plateau phase of the response to local thermal heating was negatively associated with nitrotyrosine and AOPP. No association between vascular function parameters and oxidative stress markers was observed in SC. Mild haemolysis in SC, compared to SS, may limit oxidative and nitrosative stress and could explain the better preserved microvascular function in this group.
ISSN: 0007-1048

hal-01668314
https://hal.univ-antilles.fr/hal-01668314
DOI : 10.1111/bjh.14693

Éditeur(s) : Agro Paris Tech
Résumé : P. acidilactici MA 18/5M is a dietary probiotic (BACTOCELL®) which has shown its efficiency on several terrestrial and aquatic species. The present thesis aimed to investigate more fully the effects of this probiotic on cultured penaeid shrimps. For this study, we chose a global approach by replacing the problem studied in a model of interactions between three compartments: the shrimp, its intestinal microflora and the probiotic. Having first defined how the probiotic should be administrated, we studied its effects under controlled laboratory conditions at several levels of Litopenaeus stylirostris biology: (i) Nutritional status and growth, (ii) associated bacterial microflora, and (iii) health status with respect to oxidative stress. Then the probiotic improves the growth of the shrimps and the feed conversion ratio. Our study shows that these effects are partially due to a better use of the feed, particularly of dietary carbohydrates, but also suggest an action on the metabolism, andor on the growth via a contribution of essential nutrients. On the other hand, although the intestinal bacterial communities seems little affected, we show an antagonism effect of the probiotic toward total and vibrionacea intestinal flora, as well as a decrease in the level of infection of shrimps during challenge with pathogenic V. nigripulchritudo. Beside, our works highlight that infection by this pathogen, led to a reduction in antioxidant defences, to a rise in oxidative damages, and to a release of mortalities within 48 hours. This oxidative stress following bacterial infection was better controlled by animals receiving the probiotic diet, and resistance of the shrimps to infection was significant improved. A nutritional hypothesis is proposed to explain such result, hypothesis based on a link between carbohydrate metabolism and antioxidant status. As a conclusion of these works, we can propose a first explanatory scenario for the effects of P. acidilactici on a penaeid shrimp. Finally probiotic's effects were assessed under a pilot scale in a commercial farm from New Caledonia currently affected by the "summer syndrome ". We confirm the improvements brought in term of zootechnical results, with in particular, a better resistance to this syndrome. This work was made possible thanks to a breeding method in floating cages, developed during this thesis, and therefore transferred, as an experimental tool, to the shrimp industry of New Caledonia.
Pediococcus acidilacticii MA18/5M est un probiotique bactérien (BACTOCELL®) qui a démontré son efficacité chez plusieurs espèces d'animaux terrestres et aquatiques. Cette thèse avait pour objectif d'investiguer plus en détails les effets de ce probiotique chez les crevettes pénéides d'élevage. Pour cette étude, nous avons choisi une approche globale replaçant la problématique dans un modèle d'interactions entre trois compartiments : la crevette, sa microflore intestinale et le probiotique. Après avoir défini les modalités d'administration, l'effet de P. acicilactici a été étudié, en conditions de laboratoire, chez la crevette Litopenaeus stylirostris, à différents niveaux: (i) statut nutritionnel et croissance, (ii) microflore bactérienne associée, et (iii) santé de l'animal à travers son statut antioxydant et son niveau de stress oxydant. Ainsi, le probiotique améliore la croissance des crevettes et l'indice de conversion de l'aliment. Notre étude montre que ces effets sont en partie liés à une meilleure utilisation de l'aliment, notamment des carbohydrates alimentaires, mais suggèrent aussi une action sur le métabolisme, et/ou sur la croissance via un apport de nutriments essentiels. D'autre part, bien que les communautés bactériennes intestinales semblent peu affectées, un effet d'antagonisme du probiotique vis-à-vis de la flore intestinale totale et vibrionacée a été montré, ainsi qu'une réduction du niveau d'infection des crevettes au cours de challenge avec le pathogène V. nigripulchritudo. Par ailleurs, nous mettons en évidence que l'infection par ce pathogène, conduit à un abaissement des défenses antioxydantes, à une élévation des dégâts oxydatifs, et au déclenchement de mortalités dans les 48 heures. Le probiotique atténue le niveau de ce stress oxydant, et améliore significativement la résistance des crevettes à l'infection. Une hypothèse nutritionnelle est proposée afin d'expliquer ce résultat, hypothèse reposant sur un lien entre le métabolisme des carbohydrates et le statut antioxydant. A l'issue de ces travaux, nous pouvons alors proposer un premier scénario explicatif des effets de P. acidilactici chez une crevette pénéide. Finalement le probiotique a été éprouvé à l'échelle pilote sur une ferme commerciale de Nouvelle-Calédonie affectée par le « syndrome d'été ». Nous confirmons les améliorations apportées en termes de résultats zootechniques, avec notamment une meilleure résistance au syndrome. Ce travail a été réalisé grâce une méthode d'élevage en cages flottantes, mis au point au cours de cette thèse, et qui a dés lors été transférée, comme outil expérimental, à la filière crevetticole Calédonienne.

Droits : info:eu-repo/semantics/openAccess
http://archimer.ifremer.fr/doc/2009/these-6814.pdf
http://archimer.ifremer.fr/doc/00000/6814/

Éditeur(s) : Elsevier
Résumé : in this study we evaluated the effects of the probiotic Pediococcus acidilactici MA18/5M on shrimp, Litopenaeus stylirostris (also called Penaeus stylirostris), first on antioxidant defences and secondly on the oxidative stress status in the shrimps' haemolymph and digestive gland. We conducted two experiments with the same protocol in which shrimps were fed two diets for three weeks: a control diet and a probiotic diet containing 1 g of live P. acidilactici MA18/5M kg(-1). In the first experiment, the shrimps were found to be healthy over the trial period; no mortalities and non-detectable signs of infection were recorded. These resulted in high final survival rates (above 90% in both treatments). On the other hand, during the second trial, carried out at a period of increased risk for an outbreak of the summer syndrome, higher mortalities were recorded, associated with high V. nigripulchritudo prevalence and loads in the shrimp haemolymph. In healthy shrimps (trial 1), no detectable response of the antioxidant defence system and of oxidative stress bio-indicators were observed. However, feeding the probiotic significantly increased the total antioxidant status (TAS) and glutathione peroxidase activity, while all other parameters remained significantly unchanged. In the shrimps exposed to V nigripulchritudo (trial 2), the antioxidant response was characterized by higher antioxidant enzyme activities (superoxide dismutase and catalase) and higher oxidative stress level in the digestive gland (higher oxidized/reduced glutathione ratio, higher malonclialdehyde and carbonyl protein contents) compared to levels found in trial 1. However, shrimps fed the probiotic diet exhibited (i) significantly higher final survival rates (67 +/- 3%) compared to the control (47 +/- 4%) and (ii) a lower prevalence of V nigripulchritudo throughout the trial. Moreover, the antioxidant response and the oxidative stress level recorded in the digestive gland with shrimps submitted to the probiotic diet were lower. In the light of these results, we confirm that P acidilactici enrichment in shrimps' diet seems an effective way of reducing the susceptibility of shrimps to bacterial pathogens. (c) 2009 Elsevier B.V. All rights reserved.
Aquaculture (0044-8486) (Elsevier), 2009-09 , Vol. 294 , N. 3-4 , P. 306-313

Droits : 2009 Elsevier B.V. All rights reserved.
http://archimer.ifremer.fr/doc/2009/publication-6780.pdf
DOI:10.1016/j.aquaculture.2009.06.016
http://archimer.ifremer.fr/doc/00000/6780/

Éditeur(s) : HAL CCSD IOS Press
Résumé : International audience
Sickle cell anemia (SCA) is an inherited red blood cells (RBC) disorder characterized by significantly decreased RBC deformability. The present study aimed to assess whether modulation of RBC Nitric Oxide Synthase (RBC-NOS) activation could affect RBC deformability in SCA.Blood of twenty-five SCA patients was treated for 1 hour at 37°C with Phosphate Buffered Saline (PBS) or PBS containing 1% of Dimethylsulfoxyde as control, L-arginine or N(5)-(1-Iminoethyl)-L-ornithine (L-NIO) to directly stimulate or inhibit RBC-NOS, insulin or wortmannin to indirectly stimulate or inhibit RBC-NOS through their effects on the PI3 Kinase/Akt pathway, and sodium nitroprusside (SNP) and 2-(4-Carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) as NO donor and NO scavenger, respectively. RBC deformability was measured by ektacytometry at 3 Pa.RBC deformability significantly increased after insulin treatment and significantly decreased after L-NIO and wortmannin incubation. The other conditions did not affect deformability. Significantly increased nitrotyrosine levels, a marker of enhanced free radical generation, were detected by immunohistochemistry in SNP and insulin treated samples.These data suggest that RBC deformability of SCA can be modulated by RBC-NOS activity but also that oxidative stress may impair effectiveness of RBC-NOS produced NO.
ISSN: 1386-0291

hal-01669738
https://hal.univ-antilles.fr/hal-01669738
DOI : 10.3233/CH-162042

Éditeur(s) : HAL CCSD Federation of American Society of Experimental Biology
Résumé : International audience
Testes of most male mammals present the particularity of being externalized from the body and are consequently slightly cooler than core body temperature (4-8 degrees C below). Although, hypothermia of the testis is known to increase germ cells apoptosis, little is known about the underlying molecular mechanisms, including cold sensors, transduction pathways, and apoptosis triggers. In this study, using a functional knockout mouse model of the cold and menthol receptors, dubbed transient receptor potential melastatine 8 (TRPM8) channels, we found that TRPM8 initiated the cold-shock response by differentially modulating cold- and heat-shock proteins. Besides, apoptosis of germ cells increased in proportion to the cooling level in control mice but was independent of temperature in knockout mice. We also observed that the rate of germ cell death correlated positively with the reactive oxygen species level and negatively with the expression of the detoxifying enzymes. This result suggests that the TRPM8 sensor is a key determinant of germ cell fate under hypothermic stimulation.Borowiec, A.-S., Sion, B., Chalmel, F., Rolland, A. D., Lemonnier, L., De Clerck, T., Bokhobza, A., Derouiche, S., Dewailly, E., Slomianny, C., Mauduit, C., Benahmed, M., Roudbaraki, M., Jegou, B., Prevarskaya, N., Bidaux, G. Cold/menthol TRPM8 receptors initiate the cold-shock response and protect germ cells from cold-shock-induced oxidation.
ISSN: 0892-6638

hal-01390973
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01390973
DOI : 10.1096/fj.201600257R
PUBMED : 27317670

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
Cnidarians living in symbiosis with photosynthetic dinoflagellates (commonly named zooxanthellae) are exposed to high concentrations of reactive oxygen species (ROS) upon illumination. To quench ROS production, both the cnidarian host and zooxanthellae express a full suite of antioxidant enzymes. Studying antioxidative balance is therefore crucial to understanding how symbiotic cnidarians cope with ROS production. We characterized glutathione peroxidases (GPx) in the symbiotic cnidarian Anemonia viridis by analysis of their isoform diversity, their activity distribution in the three cellular compartments (ectoderm, endoderm and zooxanthellae) and their involvement in the response to thermal stress. We identified a GPx repertoire through a phylogenetic analysis showing 7 GPx transcripts belonging to the A. viridis host and 4 GPx transcripts strongly related to Symbiodinium sp. The biochemical approach, used for the first time with a cnidarian species, allowed the identification of GPx activity in the three cellular compartments and in the animal mitochondrial fraction, and revealed a high GPx electrophoretic diversity. The symbiotic lifestyle of zooxanthellae requires more GPx activity and diversity than that of free-living species. Heat stress induced no modification of GPx activities. We highlight a high GPx diversity in A. viridis tissues by genomic and biochemical approaches. GPx activities represent an overall constitutive enzymatic pattern inherent to symbiotic lifestyle adaptation. This work allows the characterization of the GPx family in a symbiotic cnidarian and establishes a foundation for future studies of GPx in symbiotic cnidarians.
ISSN: 0300-9084

hal-01404424
http://hal.upmc.fr/hal-01404424
http://hal.upmc.fr/hal-01404424/document
http://hal.upmc.fr/hal-01404424/file/Pey_Characterization_of.pdf
DOI : 10.1016/j.biochi.2016.10.016

Éditeur(s) : HAL CCSD
Résumé : International audience
The development of diabetic vascular complications is initiated, at least in part, by mitochondrial reactive oxygen species (ROS) production in endothelial cells. Hyperglycemia induces superoxide production in the mitochondria and initiates changes in the mitochondrial membrane potential that leads to mitochondrial dysfunction. Hydrogen sulfide (H2S) supplementation has been shown to reduce the mitochondrial oxidant production and shows efficacy against diabetic vascular damage in vivo. However, the half-life of H2S is very short and it is not specific for the mitochondria. We have therefore evaluated two novel mitochondria-targeted anethole dithiolethione and hydroxythiobenzamide H2S donors (AP39 and AP123 respectively) at preventing hyperglycemia-induced oxidative stress and metabolic changes in microvascular endothelial cells in vitro. Hyperglycemia (HG) induced significant increase in the activity of the citric acid cycle and led to elevated mitochondrial membrane potential. Mitochondrial oxidant production was increased and the mitochondrial electron transport decreased in hyperglycemic cells. AP39 and AP123 (30–300 nM) decreased HG-induced hyperpolarisation of the mitochondrial membrane and inhibited the mitochondrial oxidant production. Both H2S donors (30–300 nM) increased the electron transport at respiratory complex III and improved the cellular metabolism. Targeting H2S to mitochondria retained the cytoprotective effect of H2S against glucose-induced damage in endothelial cells suggesting that the molecular target of H2S action is within the mitochondria. Mitochondrial targeting of H2S also induced >1000-fold increase in the potency of H2S against hyperglycemia-induced injury. The high potency and long-lasting effect elicited by these H2S donors strongly suggests that these compounds could be useful against diabetic vascular complications. © 2016
Pharmacological Research

hal-01373947
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01373947
DOI : 10.1016/j.phrs.2016.08.019
PUBMED : 27565382

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
: Previously, we demonstrated that eicosapentaenoic acid enhanced ethanol-induced oxidative stress and cell death in primary rat hepatocytes via an increase in membrane fluidity and lipid raft clustering. In this context, another n-3 polyunsaturated fatty acid, docosahexaenoic acid (DHA), was tested with a special emphasis on physical and chemical alteration of lipid rafts. Pretreatment of hepatocytes with DHA reduced significantly ethanol-induced oxidative stress and cell death. DHA protection could be related to an alteration of lipid rafts. Indeed, rafts exhibited a marked increase in membrane fluidity and packing defects leading to the exclusion of a raft protein marker, flotillin. Furthermore, DHA strongly inhibited disulfide bridge formation, even in control cells, thus suggesting a disruption of protein-protein interactions inside lipid rafts. This particular spatial organization of lipid rafts due to DHA subsequently prevented the ethanol-induced lipid raft clustering. Such a prevention was then responsible for the inhibition of phospholipase C-γ translocation into rafts, and consequently of both lysosome accumulation and elevation in cellular low-molecular-weight iron content, a prooxidant factor. In total, the present study suggests that DHA supplementation could represent a new preventive approach for patients with alcoholic liver disease based upon modulation of the membrane structures.
ISSN: 0278-6915

hal-00860153
https://hal-univ-rennes1.archives-ouvertes.fr/hal-00860153
https://hal-univ-rennes1.archives-ouvertes.fr/hal-00860153/document
https://hal-univ-rennes1.archives-ouvertes.fr/hal-00860153/file/Sergent-et-al-incl-figures-accepted.pdf
DOI : 10.1016/j.fct.2013.07.061

Éditeur(s) : HAL CCSD American Society for Biochemistry and Molecular Biology
Résumé : International audience
2-Amino-9H-pyrido[2,3-b]indole (AαC) is a carcinogenic heterocyclic aromatic amine formed during the combustion of tobacco. AαC undergoes bioactivation to form electrophilic N-oxidized metabolites that react with DNA to form adducts, which can lead to mutations. Many genotoxicants and toxic electrophiles react with human serum albumin (albumin); however, the chemistry of reactivity of AαC with proteins has not been studied. The genotoxic metabolites, 2-hydroxyamino-9H-pyrido[2,3-b]indole (HONH-AαC), 2-nitroso-9H-pyrido[2,3-b]indole (NO-AαC), N-acetyloxy-2-amino-9H-pyrido[2,3-b]indole (N-acetoxy-AαC), and their [(13)C6]AαC-labeled homologues were reacted with albumin. Sites of adduction of AαC to albumin were identified by data-dependent scanning and targeted bottom-up proteomics approaches employing ion trap and Orbitrap MS. AαC-albumin adducts were formed at Cys(34), Tyr(140), and Tyr(150) residues when albumin was reacted with HONH-AαC or NO-AαC. Sulfenamide, sulfinamide, and sulfonamide adduct formation occurred at Cys(34) (AαC-Cys(34)). N-Acetoxy-AαC also formed an adduct at Tyr(332). Albumin-AαC adducts were characterized in human plasma treated with N-oxidized metabolites of AαC and human hepatocytes exposed to AαC. High levels of N-(deoxyguanosin-8-yl)-AαC (dG-C8-AαC) DNA adducts were formed in hepatocytes. The Cys(34) was the sole amino acid of albumin to form adducts with AαC. Albumin also served as an antioxidant and scavenged reactive oxygen species generated by metabolites of AαC in hepatocytes; there was a strong decrease in reduced Cys(34), whereas the levels of Cys(34) sulfinic acid (Cys-SO2H), Cys(34)-sulfonic acid (Cys-SO3H), and Met(329) sulfoxide were greatly increased. Cys(34) adduction products and Cys-SO2H, Cys-SO3H, and Met(329) sulfoxide may be potential biomarkers to assess exposure and oxidative stress associated with AαC and other arylamine toxicants present in tobacco smoke
ISSN: 0021-9258

hal-01169796
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01169796
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01169796/file/Manuscript_KP_JBC_REV_050515_final_TC.pdf
DOI : 10.1074/jbc.M115.646539
PUBMED : 25953894

Éditeur(s) : HAL CCSD
Résumé : International audience
Introduction: Diabetes mellitus results from the loss of tolerance to insulin and alters glycemia and the glycogen content. Oxidative stress and inflammation are linked to theses alterations, especially with insulin-resistance. The therapy management of diabetes includes nutritional recommendations. Several nutrients are developed to improve glycemia, oxidative stress, inflammation and glycogen content. More interestingly, ?-GOS exhibits anti-inflammatory and insulin-sensitive effects in vitro (Efstathiou and Fathi 2010) and in vivo (Boucher et al. 2003). Thus, ?-GOS is a potential functional food for the treatment of diabetes. But, less is known about the in vivo effect of ?-GOS on inflammatory, glycoxidation markers and glycogen content in diabetes. In this context, the aim of this work was to study the effect of ?-GOS developed by Sojasun technologies (from fermented soy product) compared to a synthetic ?-GOS produced by Sigma on inflammatory, glycoxidation markers and glycogen content in a streptozotocin-induced diabetic rat model. Methods: Twenty-four male Wistar streptozotocin-diabetic rat (STZ) were divided into three group: control group, supplemented with natural ?-GOS (20 mg/kg/day) group and supplemented with synthetic ?-GOS (20 mg/kg/day). The supplementation protocol duration was 8 weeks. At the end of the protocol, blood and skeletal muscle (gastrocnemius) were obtained to measure glucose , insulin, fructosamine in plasma and N-(carboxymethyl)lysine, glycogen synthase activity and glycogen content, in muscle. Results-Discussion: Diabetes was confirmed with the measure of insuline and glucose levels. All the diabetic groups had significantly higher glucose and insuline levels compared to control healthy group (data not shown). Insuline level in plasma and storage of glycogen in muscle were increased only in both ?-GOS groups. Fructosamine, TNF?and glycogen synthase activity was also decreased in the two supplemented groups (synthetic ?-GOS and natural ?-GOS). CML remained unchanged in all groups. Natural ?-OGT and synthetic ?-OGT only differed on muscular glucose level: only natural ?-OGT induced a significant decrease in muscular glucose. To conclude, our results suggest that ?-GOS alters positively glucose level, increases the glycogen content in diabetique population, improves glycemic control in the long term and decreases the inflammatory effects in streptozotocin-diabetic rat . Keywords: ?-GOS, inflammatory and glycoxidation markers, diabetes. Acknowledgment : Brittany region References Efstathiou, T. and D. Fathi. Sojasun Technologies. 2010 Boucher J et al. J Physiol Biochem. 59(3):169-73, 2003
5e congrès international de "Nutrition, Oxygen Biology and Medicine", Paris 5-7 juin 2013
Paris, France

hal-01159375
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01159375

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
Hemorheological abnormalities have been well characterized in sickle cell disease (SCD) and seem to modulate the clinical severity [1]. For instance, increased blood viscosity raises the risk for frequent vaso-occlusive crisis (VOC) and increased red blood cell (RBC) aggregates robustness (i.e., RBC disaggregation threshold) enhances the risks for acute chest syndrome (ACS) [2]. Moreover, patients with the most rigid RBCs are characterized by high hemolytic rate, which increases the risks to develop leg ulcers or glomerulopathy [3]. However, except few studies supporting an effect of alpha-thalassemia and oxidative stress [1] on RBC rheological properties of SCD patients, very few experiments focused on the genetic and cellular factors modulating blood rheology in this disease.
ISSN: 1079-9796

hal-01263890
https://hal.archives-ouvertes.fr/hal-01263890
https://hal.archives-ouvertes.fr/hal-01263890/document
https://hal.archives-ouvertes.fr/hal-01263890/file/Ferdinand%20et%20al.%20eNOS%20and%20RBC%20rheology%20in%20SCD_BCMD.pdf
PUBMED : 26142331

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
Several epidemiologic studies have shown an interactive effect of heavy smoking and heavy alcohol drinking on the development of hepatocellular carcinoma. It has also been recently described that chronic hepatocyte death can trigger excessive compensatory proliferation resulting later in the formation of tumors in mouse liver. As we previously demonstrated that both benzo[a]pyrene (B[a]P), an environmental agent found in cigarette smoke, and ethanol possess similar targets, especially oxidative stress, to trigger death of liver cells, we decided to study here the cellular and molecular mechanisms of the effects of B[a]P/ethanol coexposure on cell death. After an 18-h incubation with 100nM B[a]P, primary rat hepatocytes were supplemented with 50mM ethanol for 5 or 8h. B[a]P/ethanol coexposure led to a greater apoptotic cell death that could be linked to an increase in lipid peroxidation. Plasma membrane remodeling, as depicted by membrane fluidity elevation and physicochemical alterations in lipid rafts, appeared to play a key role, because both toxicants acted with specific complementary effects. Membrane remodeling was shown to induce an accumulation of lysosomes leading to an important increase in low-molecular-weight iron cellular content. Finally, ethanol metabolism, but not that of B[a]P, by providing reactive oxygen species, induced the ultimate toxic process. Indeed, in lysosomes, ethanol promoted the Fenton reaction, lipid peroxidation, and membrane permeabilization, thereby triggering cell death. To conclude, B[a]P exposure, by depleting hepatocyte membrane cholesterol content, would constitute a favorable ground for a later toxic insult such as ethanol intoxication. Membrane stabilization of both plasma membrane and lysosomes might be a potential target for further investigation considering cytoprotective strategies.
ISSN: 0891-5849

hal-01018147
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01018147
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01018147/document
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01018147/file/Cooperative-interaction_final.pdf
PUBMED : 24681337

Éditeur(s) : HAL CCSD Wiley
Résumé : 13 pages, 4 figures, to be published on J. Am. Cer. Soc
International audience
Since crack propagation in oxide materials at low crack velocities is partly determined by chemical corrosion, proper knowledge of the crack tip chemistry is crucial for understanding fracture in these materials. Such knowledge can be obtained only from in situ studies because the processes that occur in the highly confined environment of the crack tip are very different from those that take place at free surfaces, or that can be traced post mortem. We report the occurrence of hydrous liquid condensate between the two fracture surfaces in the vicinity of the tip of tensile cracks in silica. Observations are performed in real-time by means of atomic force microscopy (AFM) at continuously controlled crack velocities in the regime of stress corrosion. Condensate formation and changes in extent and shape are demonstrated for a wide range of macroscopic humidity at different crack speeds. Its liquid character is confirmed by the study of AFM phase-contrast data. It is believed that this evidence of a nanoscale liquid hydrous phase at the crack tip will enable novel insights in the chemistry of failure of oxide materials.
ISSN: 0002-7820

hal-00424984
https://hal.archives-ouvertes.fr/hal-00424984
ARXIV : cond-mat/0509209
DOI : 10.1111/j.1551-2916.2005.00765.x

Éditeur(s) : PSIC 11 - 11th Pacific Science Inter-Congress : Pacific Countries and their Ocean: Facing Local and Global Changes / 2nd Symposium on French Research in the Pacific. March 2 - 6, 2009 Tahiti, French Polynesia.
Résumé : Meiofauna is a functional group made of small benthic metazoans 45 to 500µm in size. Although protista, foraminifera living in this kind of environment are often put in to the meiofauna. Meiofauna has been studied in New Caledonia for its double role as biological indicator for monitoring pond health status and as shrimp forage. Suitability of EOM (easily oxidized material), SOD(sediment oxygen demand),as new biochemical tools for monitoring shrimp pond health was assessed in an environmental survey aiming to assess the role of the water/sediment interface in the occurrence of the summer syndrome vibriosis. EOM, SOD and redox were correlated with shrimp survivals. Lowest meiofauna biomass and abundance were concomitantly found in the most polluted station. Proportion of abnormal tests over exceeding the one found in areas subjected to natural ecological stress were collected and were positively related to EOM and SOD and negatively to redox. Shrimp pond dominant species are common to estuaries and lagoons. But foraminifera abnormal behaviour indicates specific shrimp pond conditions

Droits : info:eu-repo/semantics/openAccess
http://archimer.ifremer.fr/doc/00198/30876/29244.pdf
http://archimer.ifremer.fr/doc/00198/30876/