126 results on '"Véricel E"'
Search Results
2. N-3 Fatty Acids. Antithromboxane Activity. Effects on Redox Status of Blood Cells
- Author
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Lagarde, M., Croset, M., Véricel, E., Le Breton, G. C., Prigent, A. F., Calzada, C., Folco, Gian Carlo, editor, Samuelsson, Bengt, editor, Maclouf, Jacques, editor, and Velo, G. P., editor
- Published
- 1996
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3. DHA Metabolism: Targeting the Brain and Lipoxygenation
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Picq, M., Chen, P., Perez, M., Michaud, M., Véricel, E., Guichardant, M., and Lagarde, M.
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- 2010
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4. Pathophysiologic role of redox status in blood platelet activation. Influence of docosahexaenoic acid
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Lagarde, M., Calzada, C., and Véricel, E.
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- 2003
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5. Double lipoxygenation of polyunsaturated fatty acids of nutritional interest
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Guichardant, M., primary, Chen, P., additional, Liu, M., additional, Lo Van, A., additional, Jouvène, C., additional, Bernoud-Hubac, N., additional, Véricel, E., additional, and Lagarde, M., additional
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- 2020
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6. Pro- and antioxidant activities of docosahexaenoic acid on human blood platelets
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Véricel, E., Polette, A., Bacot, S., Calzada, C., and Lagarde, M.
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- 2003
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7. Role of polyunsaturated fatty acids in the inhibitory effect of human adipocytes on osteoblastic proliferation
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Maurin, A.C, Chavassieux, P.M, Vericel, E, and Meunier, P.J
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- 2002
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8. Minor Fatty Acids of the N-6 Series and Platelets
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Lagarde, M., Vericel, E., Guichardant, M., Durbin, S., Dechavanne, M., Galli, C., editor, and Fedeli, E., editor
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- 1987
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9. Very low dietary intake of n-3 fatty acids affects the immune function of healthy elderly people
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Bechoua, S., Dubois, M., Némoz, G., Chapuy, P., Véricel, E., Lagarde, M., and Prigent, A. F.
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- 1999
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10. Omega-3 Fatty Acids and Hemostasis
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Lagarde, M., Croset, M., Véricel, E., and Klör, H. U., editor
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- 1989
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11. Functional fluxolipidomics of polyunsaturated fatty acids and oxygenated metabolites in the blood vessel compartment
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Lagarde, M., primary, Calzada, C., additional, Jouvène, C., additional, Bernoud-Hubac, N., additional, Létisse, M., additional, Guichardant, M., additional, and Véricel, E., additional
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- 2015
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12. Glycoxidized HDL or HDL enriched with oxidized phospholipids inhibit human platelet aggregation
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Le, Q.H., primary, Véricel, E., additional, Lagarde, M., additional, Moulin, P., additional, and Calzada, C., additional
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- 2015
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13. Biological properties of a DHA-containing structured phospholipid (AceDoPC) to target the brain
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Lagarde, M., primary, Hachem, M., additional, Bernoud-Hubac, N., additional, Picq, M., additional, Véricel, E., additional, and Guichardant, M., additional
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- 2015
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14. Full characterization of PDX, a neuroprotectin/protectin D1 isomer, which inhibits blood platelet aggregation
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Chen, P., Fenet, B., Michaud, S., Tomczyk, N., Véricel, E., Lagarde, M., and Guichardant, M.
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- 2009
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- View/download PDF
15. Biological relevance of the 12-lipoxygenase pathway for platelet and lymphocyte functions
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Lagarde M, Catherine Calzada, Zakaroff A, Meskini N, Af, Prigent, and Véricel E
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Blood Platelets ,Leukotrienes ,Animals ,Humans ,Lymphocytes ,Mitogens ,Arachidonate 12-Lipoxygenase ,Lymphocyte Activation - Published
- 1999
16. Dose-effect and metabolism of docosahexaenoic acid: Pathophysiological relevance in blood platelets
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Lagarde, M., primary, Calzada, C., additional, Guichardant, M., additional, and Véricel, E., additional
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- 2013
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17. Functional lipidomics of oxidized products from polyunsaturated fatty acids
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Guichardant, M., primary, Chen, P., additional, Liu, M., additional, Calzada, C., additional, Colas, R., additional, Véricel, E., additional, and Lagarde, M., additional
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- 2011
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18. P86 Activation des plaquettes sanguines humaines par les lipoprotéines de faible densité glycoxydées in vitro et isolées de diabétiques de type 2
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Calzada, C., primary, Colas, R., additional, Le Coquil, E., additional, Ponsin, G., additional, Véricel, E., additional, Moulin, P., additional, and Lagarde, M., additional
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- 2008
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19. 2.E.2 Omega 3 fatty acids and eicosanoid metabolism
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Lagarde, M., primary, Achard, F., additional, Gilbert, M., additional, Lemaitre, D., additional, Calzada, C., additional, and Véricel, E., additional
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- 1997
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20. Involvement of lipid peroxidation in platelet signalling
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Lagarde, M., primary, Lemaitre, D., additional, Calzada, C., additional, and Véricel, E., additional
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- 1997
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21. Blood cell redox status and fatty acids
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Lagarde, M., primary, Véricel, E., additional, Chabannes, B., additional, and Prigent, A.F., additional
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- 1995
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22. Interactions between arachidonic and eicosapentaenoic acids during their dioxygenase-dependent peroxidation
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Lagarde, M., primary, Véricel, E., additional, Croset, M., additional, Calzada, C., additional, Bordet, J.C., additional, and Guichardant, M., additional
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- 1993
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23. Variations in the fatty acid composition of lipid classes from lipoproteins in elderly women
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Lecerf, J., primary, Rossignol, A., additional, Véricel, E., additional, Thiès, F., additional, Farnier, M., additional, and Lagarde, M., additional
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- 1993
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24. Chick Nutritional Encephalomalacia and Prostanoid Formation
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Véricel, E., primary, Budowski, P., additional, and Crawford, M.A., additional
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- 1991
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25. Effect of dietary supplementation with increasing doses of docosahexaenoic acid on neutrophil lipid composition and leukotriene production in human healthy volunteers.
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Stanke-Labesque F, Molière P, Bessard J, Laville M, Véricel E, and Lagarde M
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- 2008
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26. Functions and tocopherol content of blood platelets from elderly people after low intake of purified eicosapentaenoic acid
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Croset, M., primary, Véricel, E., additional, Rigaud, M., additional, Hanss, M., additional, Courpron, Ph., additional, Dechavanne, M., additional, and Lagarde, M., additional
- Published
- 1990
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27. Influence of very low dietary intake of marine oil on some functional aspects of immune cells in healthy elderly people.
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Bechoua S, Dubois M, Véricel E, Chapuy P, Lagarde M, and Prigent A
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- 2003
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28. B004 Effets sur la fonction plaquettaire et le statut redox d’une supplementation en acide docosahexaenoïque chez des hommes sains
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Caillet, E., Guillot, N., Laville, M., Calzada, C., Lagarde, M., and Vericel, E.
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- 2009
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29. 12(S)-Hydroperoxy-eicosatetraenoic acid increases arachidonic acid availability in collagen-primed platelets.
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Calzada, C, Véricel, E, Mitel, B, Coulon, L, and Lagarde, M
- Abstract
Lipid hydroperoxides have been reported to regulate cell function and eicosanoid formation. The aim of the present study was to determine the effect of 12(S)-hydroperoxy-eicosatetraenoic acid [12(S)-HPETE], the platelet 12-lipoxygenase-derived hydroperoxide of arachidonic acid (AA), on the availability of nonesterified AA, which represents a rate-limiting step in the biosynthesis of eicosanoids. The coincubation of human platelets with concentrations of 12(S)-HPETE below 50 nM and subthreshold concentrations (STC) of collagen (less than 0.24 microg/ml) significantly enhanced platelet aggregation and the formation of thromboxane B(2), the stable catabolite of the potent aggregating agent thromboxane A(2). In addition, the nonesterified endogenous AA concentration increased by 3-fold. Arachidonoyl-containing molecular species concentrations of 1,2-diacyl-glycero-3-phosphocholine, 1-alkyl-2-acyl-glycero-3-phosphocholine, and 1-alkenyl-2-acyl-glycero-3-phosphoethanolamine decreased specifically in response to 12(S)-HPETE, whereas no significant changes were observed within 1,2-diacyl-glycero-3-phosphoethanolamine and 1,2-diacyl-glycero-3-phosphoinositol molecular species. The 12(S)-HPETE-induced increase in nonesterified AA was fully prevented by arachidonoyl trifluoromethyl ketone, an inhibitor of cytosolic phospholipase A(2) (cPLA(2)), and cPLA(2) was translocated to membranes and phosphorylated in platelets incubated with 12(S)-HPETE.In conclusion, these results indicate that nanomolar concentrations of 12(S)-HPETE could play a significant role in controlling the level of endogenous AA and the formation of thromboxane, thereby potentiating platelet function.
- Published
- 2001
30. DHA Metabolism: Targeting the Brain and Lipoxygenation
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Chevallier-Michaud, Sabine, Picq, M., Chen, P., Perez, M., Michaud, M., Véricel, E., Guichardant, M., Lagarde, M., Institut des Sciences Moléculaires de Marseille (ISM2), Aix Marseille Université (AMU)-École Centrale de Marseille (ECM)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Lecor-Esitpa, Institut de Chimie et Biochimie Moléculaires et Supramoléculaires (ICBMS), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-École Supérieure de Chimie Physique Électronique de Lyon (CPE)-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)-École Centrale de Marseille (ECM)-Institut de Chimie du CNRS (INC), Université de Lyon-Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), and Institut National des Sciences Appliquées (INSA)-Université de Lyon-Institut National des Sciences Appliquées (INSA)-École Supérieure Chimie Physique Électronique de Lyon-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)
- Subjects
Docosahexaenoic Acids ,Platelet aggregation ,Lipoxygenase ,Neuroscience (miscellaneous) ,[CHIM.THER]Chemical Sciences/Medicinal Chemistry ,Article ,03 medical and health sciences ,chemistry.chemical_compound ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,Animals ,Humans ,ComputingMilieux_MISCELLANEOUS ,PDX ,030304 developmental biology ,chemistry.chemical_classification ,0303 health sciences ,Lysophosphatidylcholine ,Human blood ,biology ,Brain ,food and beverages ,Metabolism ,DHA ,Neurology ,Biochemistry ,chemistry ,Docosahexaenoic acid ,Phosphatidylcholines ,biology.protein ,030217 neurology & neurosurgery ,Polyunsaturated fatty acid - Abstract
Docosahexaenoic acid (DHA), the end-product of the metabolism of omega-3 family fatty acids, is the main polyunsaturated fatty acid of the brain, but its accumulation is incompletely understood. This paper reviews how it could accumulate through specific uptake of DHA-containing lysophosphatidylcholine (LysoPC-DHA). DHA migrates very easily from the sn-2 position of LysoPC, which could be considered as the physiological form of polyunsaturated LysoPC, to the sn-1 position, which is much more stable. An approach preventing migration by acetylating the sn-1 position, while retaining the main physico-chemical properties of the carrier, is described. Also, the double lipoxygenation and bond-isomerization of DHA into 10(S),17(S)-docosahexa-4Z,7Z,11E,13Z,15E,19Z-enoic acid, named PDX, by soybean lipoxygenase is described. As in other E,Z,E conjugated trienes, PDX is shown to inhibit human blood platelet aggregation at submicromolar concentrations.
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31. 35th Annual Meeting of the European Association for the Study of Diabetes
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Melander, A., Olsson, J., Lindberg, G., Salzman, A., Howard, T., Stang, P., Lydick, E., Emslie-Smith, A., Boyle, D. I. R., Evans, J. M. M., Macdonald, T. M., Bain, J., Sullivan, F., Juhl, C., Pørksen, N., Sturis, J., Hollingdal, M., Pincus, S., Veldhuis, J., Dejgaard, A., Schmitz, O., Kristensen, J. S., Frandsen, K. B., Bayer, Th., Müller, P., Dunning, B. E., Paladini, S., Gutierrez, C., Deacon, R., Valentin, M., Grunberger, G., Weston, W. M., Patwardhan, R., Rappaport, E. B., Sargeant, L. A., Wareham, N. J., Khaw, K. T., Zethelius, Björn, Lithell, Hans, Hales, C. Nicholas, Berne, Christian, Lakka, H.-M., Oksanen, L., Tuomainen, T.-P., Kontula, K., Salonen, J. T., Dekker, J. M., de Boks, P., de Vegt, F., Stehouwer, C. D. A., Nijpels, G., Bouter, L. M., Heine, R. J., Bruno, G., Cavallo-Perin, P., Bargero, G., D’Errico, N., Borra, M., Macchia, G., Pagano, G., Newton, R. W., Ruta, D. A., New, J. P., Wallace, C., Roxburgh, M. A., Young, R. J., Vaughan, N. J. A., Elliott, P., Brennan, G., Devers, M., MacAlpine, R., Steinke, D., Lawson, D. H., Decallonne, B., Casteels, K., Gysemans, C., Bouillon, R., Mathieu, C., Linn, Thomas, Strate, Christine, Schneider, Kerstin, Funda, D. P., Jirsa, M., Kozáková, H., Kaas, A., Kofronová, O., Tlaskalová-Hogenová, H., Buschard, K., Wanka, H., Hartmann, A., Kuttler, B., Rasmussen, S. B., Sørensen, T. S., Markholst, H., Petersen, J. S., Karounos, D., Dyrberg, T., Mabley, J. G., Haskó, G., Szabó, C., Seissler, J., Nguyen, T. B. T., Steinbrenner, H., Scherbaum, W. A., Cipriani, R., Gabriele, A., Sensi, M., Guidobaldi, L., Pantellini, F., Cerrito, M. G., Scarpa, S., Di Mario, U., Morano, S., Ceolotto, G., Iori, E., Baritono, E., Del Prato, S., Semplicini, A., Trevisan, R., Zerbini, G., Meregalli, G., Asnaghi, V., Tentori, F., Maestroni, A., Mangili, R., Marescotti, C., Vedovato, M., Tiengo, A., Tadjieva, J., Mankovsky, B. N., Van Aken, S., Raes, A., Vande Walle, J., Matthys, D., Craen, M., Hansen, H. P., Lund, S. S., Rossing, P., Jensen, T., Parving, H.-H., Andersen, S., Tarnow, L., Hansen, B. V., Trautner, C., Haastert, B., Ennenbach, N., Willich, S., Tabák, Á. Gy., Orchard, T. J., Spranger, J., Preissner, K. T., Schatz, H., Pfeiffer, A., Cantón, A., Burgos, R., Hernández, C., Lecube, A., Mesa, J., Segura, R. M., Mateo, C., Simó, R., Fathallah, L., Greene, D. A., Obrosova, I., Gilbert, R. E., Kelly, D. J., Cox, A. J., Berka-Wilkinson, J. L., Taylor, H. R., Panagiotopoulos, S., Lee, V., Jerums, G., Cooper, M. E., Hitman, G. A., Aganna, E., Ogunkolade, W. B., Rema, M., Deepa, R., Shanthi-Rani, C. S., Barakat, K., Kumarajeewa, T. R., Cassell, P. G., McDermott, M. F., Mohan, V., Ways, K., Bursell, S., Devries, T., Woodworth, J., Alatorre, C., King, G., Aiello, L. P., Karisen, A. E., Pavlovic, D., Nielsen, K., Jensen, J., Andersen, H. U., Pociot, F., Mandrup-Poulsen, T., Eizirik, D. L., Nerup, J., Lortz, S., Tiedge, M., Lenzen, S., Lally, F. J., Bone, A. J., Darville, M. I., Ho, Y.-S., Sternesjö, J., Sandler, S., Chen, M.-C., Schuit, F., Pipeleers, D. G., Merezak, S., Hardikar, A., Hoet, J. J., Remacle, C., Reusens, B., Bréant, B., Garofano, A., Czernichow, P., Kubota, N., Terauchi, Y., Miki, H., Tamemoto, H., Yamauchi, T., Nakano, R., Komeda, K., Eto, K., Tobe, K., Kimura, S., Kadowaki, T., Ide, T., Murakami, K., Tsunoda, M., Mochizuki, T., Ozanne, S. E., Nave, B. T., Wang, C. L., Dorling, M. W., Petry, C. J., Koopmans, S. J., van der Bent, C., Que, I., Radder, J. K., Sebokova, E., Sana, A. K., Klimes, I., Ruderman, N., Morviducci, L., Pastore, L., Morelli, S., Sagratella, E., Zorretta, D., Buongiomo, A., Tamburrano, G., Giaccari, A., Martinenghi, Sabina, De Angelis, Gabriella Cusella, Ravasi, Flavio, Bifari, Francesco, Bordignon, Claudio, Falqui, Luca, Kessler, A., Dransfeld, O., Sasson, S., Tomas, E., Zorzano, A., Eckel, J., Thorsby, P., Rosenfalck, A. M., Kjems, L., Hanssen, K. F., Madsbad, S., Birkeland, K. I., Hamilton-Wessler, M., Markussen, J., Bergman, R. N., Melki, V., Hanaire-Broutin, H., Bessières-Lacombe, S., Tauber, J.-P., Home, P. D., Lindholm, A., Riis, A., Rosenstock, J., Schwartz, S., Clark, C., Edwards, M., Donley, D., Swift, P., Mortensen, H. B., Lynggaard, H., Hougaard, P., Cull, C. A., Neil, H. A. W., Frighi, V., Manley, S. E., Holman, R. R., Turner, R. C., Steiner, G., Davis, W. A., Weeraratna, T., Bruce, D. G., Davis, T. M. E., Vergès, B., Duvillard, L., Pont, F., Florentin, E., Gambert, Ph., Benko, B., Ljubić, S., Turk, Z., Granić, M., März, W., Wollschläger, H., Klein, G., Neiss, A., Wehling, M., Huxtable, S. J., Saker, P. J., Walker, M., Frayling, T. M., Levy, J. C., O’Rahilly, S., Hattersley, A. T., McCarthy, M. I., Orecchio, A., Giacchini, A., Dominici, R., Canettieri, G., Trinti, B., Zani, M., Andreoli, M., Sciacchitano, S., de Silva, A. M., Whitecross, K., Pasco, J., Kotowicz, M., Nicholson, G., Zimmet, P., Boyko, E. J., Collier, G. R., Frittitta, L., Pizzuti, A., Argiolas, A., Graci, S., Goldfine, I. D., Bozzali, M., Ercolino, T., Costanzo, B., Iacoviello, L., Tassi, V., Trischitta, V., Wauters, M., Rankinen, T., Mertens, I., Chagnon, M., Bouchard, C., Van Gaal, L., Sivenius, K., Valve, R., Hakkarainen, V., Niskanen, L., Laakso, M., Uusitupa, M., Beridze, N., Japaridze, M., Kurashvili, R., Dundua, M., Kebuladze, G., Kazakhashvili, N., Offley-Shore, B., Thomas, B., Ghebremeskel, K., Crawford, M., Lowy, C., Eriksson, Ulf J., Martin Simán, C., Wisse, Bert, Gittenberger-de Groot, Adriana C., Wentzel, P., Eriksson, U. J., Wender-Ożegowska, E., Drews, K., Biczysko, R., Bronisz, A., Rość, D., Graczykowska-Koczorowska, A., Kotschy, M., Sokup, A., Kohnert, K. D., Besch, W., Strese, J., Frick, U., Zander, E., Kemer, W., Škrha, J., Kvasnička, J., Kalvodová, B., Hilgertová, J., Schatteman, K., Goossens, F., Scharpé, S., De Leeuw, I., Hendriks, D., Legakis, I. N., Panayiotou, D., Mountokalakis, Th. D., Enderle, M. D., Beckmann, P., Balletshofer, B., Rittig, K., Maerker, E., Volk, A., Meisner, C., Jacob, S., Matthaei, S., Häring, H. U., Rett, K., Ueda, K., Nakagawa, T., Shimajiri, Y., Kokawa, M., Matsumoto, E., Sasaki, H., Sanke, T., Nanjo, K., McKinnon, Caroline M., Macfarlane, Wendy M., Docherty, Kevin, Furukawa, N., Shirotani, T., Kishikawa, H., Kaneko, K., Araki, E., Shichiri, M., Prentki, M., Roduit, R., Susini, S., Buteau, J., Ejrnæs, A. M., Andersen, N. Aa., Osterhoff, M., Möhlig, M., Ortmann, J., Bikashaghi, F., Mayer, C., Bikashagi, F., Ackermans, M. T., Pereira Arias, A. M., Bisschop, P. H. L. T., Endert, E., Sauerwein, H. P., Romijn, J. A., Gastaldelli, A., Baldi, S., Pettiti, M., Natali, A., Frascerra, S., Camastra, S., Toschi, E., Ferrannini, E., Stingl, H., Krssak, M., Bischof, M. G., Krebs, M., Fürnsinn, C., Nowotny, P., Waldhäusl, W., Roden, M., Neeft, M., Meijer, A. J., Båvenholm, P., Pigon, J., Efendic, S., Kästenbauer, T., Sauseng, S., Sokol, G., Auinger, M., Irsigler, K., Abbott, C. A., Carrington, A. L., Faragher, B., Kulkarni, J., Van Ross, E. R. E., Boulton, A. J. M., Armstrong, D. G., Hadi, S., Nguyen, H. C., Harkless, L. B., Jirkovská, A., Kasalicky, P., Hosová, J., Skibova, J., Uccioli, L., Caselli, A., Giacomozzi, C., Macellari, V., Giurato, L., Lardieri, L., Menzinger, G., Pham, H. T., Rosenblum, B. I., Lyons, T. E., Giurini, J. M., Smakowski, P., Chrzan, J. S., Habershaw, G. M., Veves, A., Foster, A. M., Bates, M., Doxford, M., Edmonds, M. E., Kecha, O., Winkler, R., Martens, H., Collette, J., Lefèbvre, P. J., Greiner, D., Geenen, V., Atlan-Gepner, C., Naspetti, M., Valéro, R., Barad, M., Lepault, F., Vialettes, B., Naquet, P., de Galan, B., Netea, M. G., Hancu, N., Smits, P., Van der Meer, J. W. M., Osterbye, T., Jørgensen, K. H., Tranum-Jensen, J., Fredman, P., Høy, M., Bokvist, K., Olsen, H. L., Horn, T., Gromada, J., Laub, R., Lohmann, T., Hahn, H. J., Adler, T., Emmrich, F., Rabuazzo, A. M., Lupi, R., Dotta, F., Patanè, G., Marselli, L., Realacci, M., Piro, S., Del Guerra, S., Santangelo, C., Navalesi, R., Purrello, F., Marchetti, P., de Vos, P., Visser, L., de Haan, B. J., Klok, P., van Schilfgaarde, R., Poppema, S., Juang, J.-H., Kuo, C.-H., Hsu, B. R.-S., Nacher, V., Pérez, M., Biarnés, M., Raurell, M., Soler, J., Montanya, E., Ritzel, R., Maubach, J., Büsing, M., Becker, T., Klempnauer, J., Hücking, K., Schmiegel, W. H., Nauck, M. A., Bouček, P., Saudek, F., Adamec, M., Kožitarová, R., Jedináková, T., Vlasáková, Z., Skibová, J., Bartoš, V., Maffi, P., Bertuzzi, F., Aldrighetti, L., Taglietti, M. V., Castelnuovo, A., Pozza, G., Di Carlo, V., Secchi, A., Renier, G., Mamputu, J.-C., Gillespie, J. S., McMaster, D., Mercer, C., Trimble, E. 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S., Saponara, C., Tartaglione, T., Cercone, S., Caputo, S., Meloni, T., Brunetti, D., Di Lazzaro, V., Xu, G., Jiang, H. Y., Shy, M. E., Sugimoto, K., Zhang, W.-X., Kuchmerovskaya, T., Donchenko, G., Shymansky, I., Kuchmerovsky, N., Pakyrbaeva, L., Cameron, N. E., Keegan, A., Cotter, M. A., Mirrlees, D., Smale, S. E., Biessels, G. J., Duis, S. E. J., Kamal, A., Gispen, W. H., Carrington, A., Carman, S., Smiarowski, H., Lavoie, D., Sawicki, D., Sabetta, A., Litchfield, J., Van Zandt, M., Sredy, J., Smirnova, V., Strokov, I., Ivanova, L., Ichunina, A., Nakamura, J., Nakayama, M., Hamada, Y., Chaya, S., Kato, K., Kasuya, Y., Mizubayashi, R., Miwa, K., Yasuda, Y., Kamiya, H., Hotta, N., Bíró, K., Kukorelli, T., Szilágyi, N., Kürthy, M., Komáromy, A., Mogyorosi, T., Nagy, K., Çakir, M., Baskal, N., Güllü, S., Elhan, A. H., Erdogan, G., Ziegler, D., Piolot, R., Neubauer, J., Senesi, B., Bonetti, R., Napolitano, A., Canepa, F., Ottonello, P., Schabmann, A., Giménez-Pérez, G., Arroyo, J. A., López, T., Ponz, E., Mauricio, D., Diem, P., Zanchin, L., Suter, S. L., Lefrandt, J. D., Smit, A., van Roon, A. M., Dullaart, R., Voita, D., Mackevics, V., Vitols, A., Lengyel, Cs., Farkas, Gy., Török, T., Légrády, P., Várkonyi, T. T., Kardos, A., Gingl, Z., Kempler, P., Rudas, L., Lonovics, J., Marchand, M., Stevens, L. K., Tarnás, Gy., Estrella, F., Christensen, N. J., Keresztes, K., Barna, I., Hermányi, Zs., Vargha, P., Bonnevie, L., Chanudet, X., Larroque, P., Tutuncu, N. Bascil, Deger, A., Batur, M. K., Yildirir, A., Onalan, O., Aksöyek, S., Kabakçι, G., Erbaş, T., Galicka-Latała, D., Surdacki, A., Gerritsen, J., TenVoorde, B. J., Heethaar, R. M., Tagawa, T. S., Kodama, M., Yoshioka, R., Yamasaki, Y., Didangelos, T., Athyros, V., Kontopoulos, A., Papageorgiou, A., Karamitsos, D., Lacigová, S., Rušavý, Z., Kárová, R., Perrild, H., Kay, L., Jørgensen, T., Bień, A. I., Witek, P., Geraldes, Elizabete, Rodrigues, D., Pereira, L., Doménech, A., Leitão, P., Anagnostopoulos, D., Foster, A. V. M., Nag, S., Barsoum, M., Lewis, G., Dunlop, N., Connolly, V., Bilous, R., Kelly, W., Chantelau, E., Gede, A., Sharman, D., O’Halloran, D., Best, C., Abbas, Z. G., Lutale, J., Gill, G. V., Jarvis, W. R., Archibald, L. K., Corcoran, S., Mansell, J., Pibworth, L., Terada, H., Shiba, T., Utugi, N., Utugi, T., Blum, M., Strobel, J., Höffken, K., Razvi, F. M., Kritzinger, E. E., Taylor, K., Jones, S., Illahi, W., Grüβer, M., Hartmann, P., Hoffstadt, K., van Leiden, H. A., Moll, A. C., Polak, B. C. P., Pietragalla, G. B., Maurino, M., Montanaro, M., Karadeniz, Ş., Tommasini, P., Quadrini, C., Demiraj, V., Rispoli, E., Ota, A., Takama, H., Saito, N., Hemández, C., Lepore, D., Antico, L., Giardina, B., Franconi, F., Michoud, E., Chamot, S., Riva, Ch., Hammes, H.-P., Renner, O., Breier, G., Lin, J., Alt, A., Betzholtz, C., Bretzel, R. G., Manti, R., Gallo, M., Molinar Hin, A., Brignardello, E., Boccuzzi, G., Li, Shanfang, Xiang, Kunsan, Zhang, Rugeng, Shangguan, Xinhong, Wu, Jianrong, Donnan, P. T., Broomhall, J., Hunter, K., Morris, A. D., Ioannidis, G., Peppa, M., Rontogianni, E., Kallifronas, M., Lekatsas, I., Chrysanthopoulou, G., Anthopoulos, L., Kesse, M., Thalassinos, N., Neves, C., Medina, J. L., Lopes, F., Yılmaz, M., Güvener, N., Güvener, M., Kocagöz, T., Böke, E., Paşaoglu, I., Bascil Tutuncu, N., Oto, A., Karvonen, M. K., Koulu, M., Pesonen, U., Mercuri, M., Rauramaa, R., Rutter, M. K., Kestevan, P., McComb, J. M., Marshall, S. M., Sobieska, M., Wiktorowicz, K., Kanters, S. D. J. M., Banga, J. D., Algra, A., Frijns, C. J. M., Beutler, J. J., Fijnheer, R., Nicoloff, G., Baydanoff, S., Stanimirova, N., Petrova, Ch., Lario, S., Campistol, J. M., Cases, A., Clària, J., Iñigo, P., Esmatjcs, E., Sármán, B., Tóth, M., Kocsis, I., Somogyi, A., Bumbure, A., Jachimowicz, K., Samson, J., Tomasiak, M., Sobol, A., Stańczyk, L., Watala, C., Stradina, P., Wiśniewska-Jarosińska, M., Marciniak, D., Więcławska, B., Watała, C., Golański, J., Zinnat, R., Mahmud, I., Büyükasik, Yahya, Demiroğlu, H., Szczepanik, A., Skowroński, M., Murawska, A., Meeking, D. R., Allard, S., Munday, J., Chowienczyk, P., Shaw, K. M., Cummings, M. H., Šimková, R., Jirsa, M., Hadoke, P. W. F., McIntyre, C. A., Jones, G. C., Williams, B. C., Elliott, A. I., McKnight, J. A., Pernow, J., Bombonato, G. C., Finucci, G. F., Zotta, L., Senses, V., Ozyazgan, S., Ince, E., Tunçdemir, M., Oztürk, M., Sultuybek, G., Akkan, A. G., Özyazgan, S., Unlücerci, Y., Bekpınar, S., Meyer, M. F., Lee, B. C., Shore, A. C., Humphreys, J. M., Tooke, J. E., Dell’Omo, G., Giovannitti, G., Caricato, F., Mariani, M., Pedrinelli, R., Kiviet-Boehm, C., Schwelling, V., Matthäei, S., Pfohl, M., McInerney, D., Itoh, H., Ohno, T., Katoh, N., Baumgartner-Parzer, S., Artwohl, M., Graier, W., Ludwig, C., Tachi, Y., Bannai, C., Shinohara, M., Shimpuku, H., Ohura, K., Bertacca, A., Sasvári, M., Szaleczki, E., Pusztai, P., Boes, U., Klaus, E., Dittrich, P., Wagner, Z., Wittmann, I., Pótó, L., Wagner, L., Mazák, I., Nagy, J., Feletto, F., Taboga, C., Tonutti, L., Lizzio, S., Russo, A., Selmo, V., Ceriello, A., Lekakis, J., Papamichael, C. M., Stamatelopoulos, K., Stamatelopoulos, S., Yillar, D. O., Gay, M., Lillaz, E., Passaro, A., Vanini, A., Calzoni, F., D’Elia, K., Carantoni, M., Zuliani, G., Fellin, R., Solini, A., Chwatko, G., Bald, E., Dramais, A.-S., Wallemacq, P. E., Vandeleene, B., Ciaria, M. V., Ariano, M., Strom, R., Gibney, J., Weiss, U., Turner, B., O’Gorman, P., Watts, G., Powrie, J., Crook, M., Shaw, K., and Cummings, M.
- Published
- 1999
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32. Effects of small concentrations of eicosapentaenoic acid on platelets.
- Author
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LAGARDE, M., CROSET, M., VÉRICEL, E., and CALZADA, C.
- Published
- 1989
- Full Text
- View/download PDF
33. In vitro and in vivo bimodal effects of docosahexaenoic acid supplements on redox status and platelet function
- Author
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Lagarde M, Catherine Calzada, Guichardant M, and Véricel E
34. Comparative effects of linoleic acid and gamma-linolenic acid intake on plasma lipids and platelet phospholipids in elderly people
- Author
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Véricel, E., primary, Lagarde, M., additional, Mendy, F., additional, Courpron, Ph., additional, and Dechavanne, M., additional
- Published
- 1987
- Full Text
- View/download PDF
35. BLOOD PLATELET FUNCTIONS: INFLUENCE OF AGING
- Author
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Véricel, E, additional, Croset, M, additional, Courpron, Ph, additional, Dechavanne, M, additional, and Lagarde, M, additional
- Published
- 1987
- Full Text
- View/download PDF
36. IN VITRO AND IN VIVO EFFECT OF VITAMIN E ON NORMAL HUMAN PLATELETS. AGGREGATION AND ARACHIDONIC ACID (AA) METABOLISM
- Author
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Kockmann, V, additional, Véricel, E, additional, Croset, M, additional, and Lagarde, M, additional
- Published
- 1987
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- View/download PDF
37. Effets et métabolismes spécifiques des acides gras ω3
- Author
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Lagarde Michel and Véricel Evelyne
- Subjects
eicosapentaenoic and docosahexaenoic acids ,arachidonic acid ,inflammation ,cardiovascular protection ,Oils, fats, and waxes ,TP670-699 - Abstract
Omega 3 fatty acids are issued from linolenic acid (18:3ω3). Nutritional interest about ω3 fatty acids has begun since the epidemiological studies of Dyerberg et al. have shown a relationship between consumption of marine fats and reduction of cardiovascular diseases. Long-chain ω3 fatty acids, mainly eicosapentaenoic (20:5ω3 or EPA) and docosahexaenoic (22:6ω3 or DHA) acids, are considered to be the main bioactive components in marine sources. Other studies have confirmed that consumption of fish ou EPA\\DHA supplements may reduce mortality in patients who have suffered from myocardial infarction. Beneficial effects of ω3 fatty acids are also recognized in inflammatory disorders. The main mechanism involved for those effects is assumed to be the interference between long-chain ω3 fatty acids and the arachidonic acid (AA) metabolism in blood and vascular cells. In those cells, AA may be released from membrane phospholipids by phospholipase A2 and subsequently oxygenated into eicosanoids (overall called AA cascade). According to the cell, oxygenated products from AA include thromboxane (platelets), prostacyclin (endothelial cells) and leukotrienes (leukocytes). EPA and DHA can interfere with AA cascade by several ways to reduce the vascular risk. However, high intake of such fatty acids may increase lipid peroxidation and have deleterious effects, in particular in subjects suffering from oxidative stress, whereas law may exert “antioxidant” activity. We conclude that a moderate consumption of long-chain ω3 fatty acids can protect against cardiovascular dysfunction.
- Published
- 2004
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- View/download PDF
38. BLOOD PLATELET FUNCTIONS: INFLUENCE OF AGING
- Author
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Véricel, E, Croset, M, Courpron, Ph, Dechavanne, M, and Lagarde, M
- Published
- 1987
- Full Text
- View/download PDF
39. Biological relevance of double lipoxygenase products of polyunsaturated fatty acids, especially within blood vessels and brain.
- Author
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Guichardant M, Véricel E, and Lagarde M
- Subjects
- Humans, Blood Vessels metabolism, Brain metabolism, Docosahexaenoic Acids metabolism, Lipoxygenases metabolism, alpha-Linolenic Acid metabolism
- Abstract
The double lipoxygenation of polyunsaturated fatty acids (PUFA) is possible with PUFA having at least three methylene-interrupted double bonds. Several PUFA of the omega-3/n-3 and -6 families may be converted through this route, and the products show interesting inhibitory effects on blood platelet function and cyclooxygenase activities. This review focuses on two main omega-3 PUFA of nutritional interest, namely docosahexaenoic acid (DHA/22:6n-3) and alpha linolenic acid (ALA/18:3n-3). The chemical configuration of the double lipoxygenase end-product from DHA (protectin DX) is compared with that of protectin D1 which is produced through a mono-lipoxygenation step followed by an epoxidation and epoxide hydrolysis process. The different metabolic pathways are discussed as well as the different biological activities of both protectins., (Copyright © 2018. Published by Elsevier B.V.)
- Published
- 2019
- Full Text
- View/download PDF
40. In vitro and in vivo bimodal effects of docosahexaenoic acid supplements on redox status and platelet function.
- Author
-
Lagarde M, Calzada C, Guichardant M, and Véricel E
- Abstract
Docosahexaenoic acid (DHA) is a prominent nutrient of marine lipids. Together with eicosapentaenoic acid, it is recognized as a protective molecule against atherosclerosis and thrombosis through the regulation of blood cell functions, especially platelets. Its high unsaturation index may however make it prone to peroxidation, which is usually considered as deleterious. This short review takes into consideration this possibility related to DHA concentrations both in vitro and in vivo. It is suggested that protective effects of DHA on platelet activation depend on the reduction of oxidative stress, and appear bimodal with the abolishment of such a protection when DHA is used at relatively high concentrations., (Copyright © 2016 Elsevier Ltd. All rights reserved.)
- Published
- 2018
- Full Text
- View/download PDF
41. Oxygenation of polyunsaturated fatty acids and oxidative stress within blood platelets.
- Author
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Lagarde M, Guichardant M, Bernoud-Hubac N, Calzada C, and Véricel E
- Subjects
- Animals, Arachidonate 12-Lipoxygenase genetics, Arachidonate 12-Lipoxygenase metabolism, Blood Platelets cytology, Cyclooxygenase 1 genetics, Cyclooxygenase 1 metabolism, Fatty Acids, Unsaturated genetics, Humans, Oxidation-Reduction, Blood Platelets metabolism, Fatty Acids, Unsaturated metabolism, Oxidative Stress physiology
- Abstract
The oxygenation metabolism of arachidonic acid (ArA) has been early described in blood platelets, in particular with its conversion into the potent labile thromboxane A
2 that induces platelet aggregation and vascular smooth muscle cells contraction. In addition, the primary prostaglandins D2 and E2 have been mainly reported as inhibitors of platelet function. The platelet 12-lipoxygenase (12-LOX) product, i.e. the hydroperoxide 12-HpETE, appears to stimulate platelet ArA metabolism at the level of its release from membrane phospholipids through phospholipase A2 (cPLA2 ) and cyclooxygenase (COX-1) activities, the first enzymes in prostanoid production cascade. Also, 12-HpETE may regulate the oxygenation of other polyunsaturated fatty acids (PUFA) by platelets, especially that of eicosapentaenoic acid (EPA). On the other hand, the reduced product of 12-HpETE, 12-HETE, is able to antagonize TxA2 action. This is even more obvious for the 12-LOX end-products from docosahexaenoic acid (DHA), 11- and 14-HDoHE. In addition, 12-HpETE plays a key role in platelet oxidative stress as observed in pathophysiological conditions, but may be regulated by DHA with a bimodal way according to its concentration. Other oxygenated products of PUFA, especially omega-3 PUFA, produced outside platelets may affect platelet functions as well., (Copyright © 2018. Published by Elsevier B.V.)- Published
- 2018
- Full Text
- View/download PDF
42. Moderate intake of docosahexaenoic acid raises plasma and platelet vitamin E levels in cystic fibrosis patients.
- Author
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Véricel E, Mazur S, Colas R, Delaup V, Calzada C, Reix P, Durieu I, Lagarde M, and Bellon G
- Subjects
- Adolescent, Adult, Child, Cross-Over Studies, Docosahexaenoic Acids pharmacology, Double-Blind Method, Drug Administration Schedule, Humans, Lipid Peroxidation, Male, Oxidative Stress genetics, Young Adult, Blood Platelets metabolism, Cystic Fibrosis blood, Docosahexaenoic Acids administration & dosage, Vitamin E blood
- Abstract
Patients with cystic fibrosis have increased oxidative stress and impaired antioxidant systems. Moderate intake of docosahexaenoic acid (DHA) may favor the lowering of oxidative stress. In this randomized, double-blind, cross-over study, DHA or placebo capsules, were given daily to 10 patients, 5mg/kg for 2 weeks then 10mg/kg DHA for the next 2 weeks (or placebo). After 9 weeks of wash-out, patients took placebo or DHA capsules. Biomarkers of lipid peroxidation and vitamin E were measured at baseline, and after 2 and 4 weeks of treatment in each phase. The proportions of DHA increased both in plasma and platelet lipids after DHA supplementations. The lipid peroxidation markers did not significantly decrease, in spite of a trend, after the first and/or the second dose of DHA but plasma and platelet vitamin E amounts increased significantly after DHA supplementation. Our findings reinforce the antioxidant potential of moderate DHA intake in subjects displaying increased oxidative stress., (Copyright © 2016 Elsevier Ltd. All rights reserved.)
- Published
- 2016
- Full Text
- View/download PDF
43. In vitro and in vivo bimodal effects of docosahexaenoic acid supplements on redox status and platelet function.
- Author
-
Lagarde M, Calzada C, Guichardant M, and Véricel E
- Abstract
Docosahexaenoic acid (DHA) is a prominent nutrient of marine lipids. Together with eicosapentaenoic acid, it is recognized as a protective molecule against atherosclerosis and thrombosis through the regulation of blood cell functions, especially platelets. Its high unsaturation index may however make it prone to peroxidation, which is usually considered as deleterious. This short review takes into consideration this possibility related to DHA concentrations both in vitro and in vivo. It is suggested that protective effects of DHA on platelet activation depend on the reduction of oxidative stress, and appear bimodal with the abolishment of such a protection when DHA is used at relatively high concentrations., (Copyright © 2016 Elsevier Ltd. All rights reserved.)
- Published
- 2016
- Full Text
- View/download PDF
44. Glutathione peroxidase 4 is reversibly induced by HCV to control lipid peroxidation and to increase virion infectivity.
- Author
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Brault C, Lévy P, Duponchel S, Michelet M, Sallé A, Pécheur EI, Plissonnier ML, Parent R, Véricel E, Ivanov AV, Demir M, Steffen HM, Odenthal M, Zoulim F, and Bartosch B
- Subjects
- Adult, Biomarkers, Biopsy, Case-Control Studies, Cell Line, Female, Gas Chromatography-Mass Spectrometry, Hepacivirus metabolism, Hepatitis C, Chronic enzymology, Hepatitis C, Chronic pathology, Humans, Liver enzymology, Liver pathology, Male, Middle Aged, Oxidative Stress, Phospholipid Hydroperoxide Glutathione Peroxidase, Reactive Oxygen Species metabolism, Virion metabolism, Glutathione Peroxidase metabolism, Hepacivirus pathogenicity, Hepatitis C, Chronic virology, Lipid Peroxidation, Liver virology, Virion pathogenicity
- Abstract
Objective: Inflammation and oxidative stress drive disease progression in chronic hepatitis C (CHC) towards hepatocellular carcinoma. HCV is known to increase intracellular levels of reactive oxygen species (ROS), but how it eliminates ROS is less well known. The role of the ROS scavenger glutathione peroxidase 4 (GPx4), induced by HCV, in the viral life cycle was analysed., Design: The study was performed using a replicative in vitro HCV infection model and liver biopsies derived from two different CHC patient cohorts., Results: A screen for HCV-induced peroxide scavengers identified GPx4 as a host factor required for HCV infection. The physiological role of GPx4 is the elimination of lipid peroxides from membranes or lipoproteins. GPx4-silencing reduced the specific infectivity of HCV by up to 10-fold. Loss of infectivity correlated with 70% reduced fusogenic activity of virions in liposome fusion assays. NS5A was identified as the protein that mediates GPx4 induction in a phosphatidylinositol-3-kinase-dependent manner. Levels of GPx4 mRNA were found increased in vitro and in CHC compared with control liver biopsies. Upon successful viral eradication, GPx4 transcript levels returned to baseline in vitro and also in the liver of patients., Conclusions: HCV induces oxidative stress but controls it tightly by inducing ROS scavengers. Among these, GPx4 plays an essential role in the HCV life cycle. Modulating oxidative stress in CHC by specifically targeting GPx4 may lower specific infectivity of virions and prevent hepatocarcinogenesis, especially in patients who remain difficult to be treated in the new era of interferon-free regimens., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/)
- Published
- 2016
- Full Text
- View/download PDF
45. Moderate oral supplementation with docosahexaenoic acid improves platelet function and oxidative stress in type 2 diabetic patients.
- Author
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Véricel E, Colas R, Calzada C, Lê QH, Feugier N, Cugnet C, Vidal H, Laville M, Moulin P, and Lagarde M
- Subjects
- Administration, Oral, Antioxidants pharmacology, Arachidonic Acid metabolism, Blood Platelets chemistry, Collagen pharmacology, Cross-Over Studies, Diabetes Mellitus, Type 2 blood, Diabetes Mellitus, Type 2 urine, Dinoprost analogs & derivatives, Dinoprost blood, Docosahexaenoic Acids pharmacology, Dose-Response Relationship, Drug, Double-Blind Method, F2-Isoprostanes urine, Fatty Acids blood, Female, Humans, Lipid Peroxidation drug effects, Membrane Lipids blood, Middle Aged, Phospholipids blood, Platelet Aggregation drug effects, Postmenopause, Thromboxane B2 analogs & derivatives, Thromboxane B2 blood, Thromboxane B2 urine, alpha-Tocopherol blood, Antioxidants therapeutic use, Blood Platelets drug effects, Diabetes Mellitus, Type 2 drug therapy, Dietary Supplements, Docosahexaenoic Acids therapeutic use, Lipids blood, Oxidative Stress drug effects
- Abstract
Platelets from patients with type 2 diabetes are characterised by hyperactivation and high level of oxidative stress. Docosahexaenoic acid (DHA) may have beneficial effects on platelet reactivity and redox status. We investigated whether moderate DHA supplementation, given as a triglyceride form, may correct platelet dysfunction and redox imbalance in patients with type 2 diabetes. We conducted a randomised, double-blind, placebo-controlled, two-period crossover trial (n=11 post-menopausal women with type 2 diabetes) to test the effects of 400 mg/day of DHA intake for two weeks on platelet aggregation, markers of arachidonic acid metabolism, lipid peroxidation status, and lipid composition. Each two week-period was separated from the other by a six-week washout. Daily moderate dose DHA supplementation resulted in reduced platelet aggregation induced by collagen (-46.5 %, p< 0.001), and decreased platelet thromboxane B2 (-35 %, p< 0.001), urinary 11-dehydro-thromboxane B2 (-13.2 %, p< 0.001) and F2-isoprostane levels (-19.6 %, p< 0.001) associated with a significant increase of plasma and platelet vitamin E concentrations (+20 % and +11.8 %, respectively, p< 0.001). The proportions of DHA increased both in plasma lipids and in platelet phospholipids. After placebo treatment, there was no effect on any parameters tested. Our findings support a significant beneficial effect of low intake of DHA on platelet function and a favourable role in reducing oxidative stress associated with diabetes.
- Published
- 2015
- Full Text
- View/download PDF
46. Glycoxidized HDL, HDL enriched with oxidized phospholipids and HDL from diabetic patients inhibit platelet function.
- Author
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Lê QH, El Alaoui M, Véricel E, Ségrestin B, Soulère L, Guichardant M, Lagarde M, Moulin P, and Calzada C
- Subjects
- Adult, Aged, Blood Platelets metabolism, Calcium metabolism, Dose-Response Relationship, Drug, Female, Humans, Male, Middle Aged, Signal Transduction drug effects, Young Adult, p38 Mitogen-Activated Protein Kinases metabolism, Blood Platelets drug effects, Diabetes Mellitus, Type 2 metabolism, Lipoproteins, HDL pharmacology, Phospholipids pharmacology, Platelet Activation drug effects, Platelet Aggregation drug effects
- Abstract
Context: High-density lipoproteins (HDL) possess atheroprotective properties including anti-thrombotic and antioxidant effects. Very few studies relate to the functional effects of oxidized HDL on platelets in type 2 diabetes (T2D)., Objective: The objective of our study was to investigate the effects of in vitro glycoxidized HDL and HDL from patients with T2D on platelet aggregation and arachidonic acid signaling cascade. At the same time, the contents of hydroxylated fatty acids were assessed in HDL., Results: Compared with control HDL, in vitro glycoxidized HDL had decreased proportions of linoleic (LA) and arachidonic (AA) acids in phospholipids and cholesteryl esters, and increased concentrations of hydroxy-octadecadienoic acids (9-HODE and 13-HODE) and 15-hydroxy-eicosatetraenoic acid (15-HETE), derived from LA and AA respectively, especially hydroxy derivatives esterified in phospholipids. Glycoxidized HDL dose-dependently decreased collagen-induced platelet aggregation by binding to scavenger receptor BI (SR-BI). Glycoxidized HDL prevented collagen-induced increased phosphorylation of platelet p38 MAPK and cytosolic phospholipase A2, as well as intracellular calcium mobilization. HDL enriched with oxidized phosphatidylcholine (PC), namely PC(16:0/13-HODE) dose-dependently inhibited platelet aggregation. Increased concentrations of 9-HODE, 13-HODE, and 15-HETE in phospholipids (2.1-, 2.1-, and 2.4-fold increase, respectively) were found in HDL from patients with T2D, and these HDL also inhibited platelet aggregation via SR-BI., Conclusions: Our results suggest that in vitro glycoxidized HDL as well as HDL from patients with T2D inhibit platelet aggregation, and suggest that oxidized LA-containing phospholipids may contribute to the anti-aggregatory effects of glycoxidized HDL and HDL from patients with T2D.
- Published
- 2015
- Full Text
- View/download PDF
47. Omega-3 polyunsaturated fatty acids and oxygenated metabolism in atherothrombosis.
- Author
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Guichardant M, Calzada C, Bernoud-Hubac N, Lagarde M, and Véricel E
- Subjects
- Animals, Atherosclerosis epidemiology, Atherosclerosis metabolism, Cardiovascular Agents adverse effects, Cardiovascular Agents metabolism, Docosahexaenoic Acids therapeutic use, Dose-Response Relationship, Drug, Eicosapentaenoic Acid therapeutic use, Fatty Acids, Omega-3 adverse effects, Fatty Acids, Omega-3 metabolism, Humans, Oxidation-Reduction, Risk Assessment, Risk Factors, Thrombosis epidemiology, Thrombosis metabolism, Treatment Outcome, alpha-Linolenic Acid therapeutic use, Atherosclerosis drug therapy, Cardiovascular Agents therapeutic use, Fatty Acids, Omega-3 therapeutic use, Thrombosis drug therapy
- Abstract
Numerous epidemiological studies and clinical trials have reported the health benefits of omega-3 polyunsaturated fatty acids (PUFA), including a lower risk of coronary heart diseases. This review mainly focuses on the effects of alpha-linolenic (ALA), eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids on some risk factors associated with atherothrombosis, including platelet activation, plasma lipid concentrations and oxidative modification of low-density lipoproteins (LDL). Special focus is given to the effects of marine PUFA on the formation of eicosanoids and docosanoids, and to the bioactive properties of some oxygenated metabolites of omega-3 PUFA produced by cyclooxygenases and lipoxygenases. The antioxidant effects of marine omega-3 PUFA at low concentrations and the pro-oxidant effects of DHA at high concentrations on the redox status of platelets and LDL are highlighted. Non enzymatic peroxidation end-products deriving from omega-3 PUFA such as hydroxy-hexenals, neuroketals and EPA-derived isoprostanes are also considered in relation to atherosclerosis. This article is part of a Special Issue entitled "Oxygenated metabolism of PUFA: analysis and biological relevance"., (Copyright © 2014 Elsevier B.V. All rights reserved.)
- Published
- 2015
- Full Text
- View/download PDF
48. Structure-function relationships of non-cyclic dioxygenase products from polyunsaturated fatty acids: poxytrins as a class of bioactive derivatives.
- Author
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Lagarde M, Véricel E, Liu M, Chen P, and Guichardant M
- Subjects
- Dioxygenases metabolism, Docosahexaenoic Acids metabolism, Docosahexaenoic Acids pharmacology, Fatty Acids, Omega-3 metabolism, Fatty Acids, Unsaturated metabolism, Humans, Molecular Structure, Platelet Aggregation drug effects, Stereoisomerism, Structure-Activity Relationship, alpha-Linolenic Acid metabolism, alpha-Linolenic Acid pharmacology, Docosahexaenoic Acids chemistry, Fatty Acids, Omega-3 chemistry, Fatty Acids, Unsaturated chemistry, alpha-Linolenic Acid chemistry
- Abstract
More and more attention is paid to omega-3 fatty acids because of their potential activities in preventing cardiovascular events. In this brief review, we focus on the lipoxygenase end-metabolites of two relevant nutrients belonging to the omega-3 family fatty acids: alpha-linolenic and docosahexaenoic acids, the latter being a prominent component of brain lipids. Dihydroxylated derivatives are described as well as their inhibitory effects on platelet aggregation and cyclooxygenase activities. We point out that only the dihydroxylated products with the trans,cis,trans/E,Z,E conjugated triene geometry exhibit those inhibitory activities. These properties being found with other polyunsaturated fatty acid oxygenated products sharing the same E,Z,E molecular motif, they have been collectively named poxytrins. From alpha-linolenic and docosahexaenoic acids, poxytrins are linotrins and protectin DX, respectively., (Copyright © 2014 Elsevier B.V. and Société française de biochimie et biologie Moléculaire (SFBBM). All rights reserved.)
- Published
- 2014
- Full Text
- View/download PDF
49. Docosahexaenoic acid, protectin synthesis: relevance against atherothrombogenesis.
- Author
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Lagarde M, Liu M, Véricel E, Calzada C, Chen P, Driss F, and Guichardant M
- Subjects
- Atherosclerosis blood, Atherosclerosis etiology, Blood Platelets drug effects, CD59 Antigens biosynthesis, Cholesterol, LDL blood, Diet, Dietary Fats blood, Dietary Fats pharmacology, Docosahexaenoic Acids blood, Docosahexaenoic Acids pharmacology, Humans, Leukocytes, Thrombosis blood, Antioxidants metabolism, Atherosclerosis prevention & control, CD59 Antigens blood, Dietary Fats therapeutic use, Docosahexaenoic Acids therapeutic use, Lipoxygenases blood, Thrombosis prevention & control
- Abstract
DHA is an abundant nutrient from marine lipids: its specific biological effects have been investigated in human volunteers, taking into consideration the dose effects. We report herein that, at dosages below 1 g/d, DHA proved to be effective in lowering blood platelet function and exhibited an 'antioxidant' effect. However, this was no longer the case following 1.6 g/d, showing then a U-shape response. The antioxidant effect has been observed in platelets as well as LDL, of which the redox status is assumed to be crucial in their relationship with atherosclerosis. Second, the oxygenated products of DHA, especially protectins produced by lipoxygenases, have been considered for their potential to affect blood platelets and leucocytes. It is concluded that DHA is an interesting nutrient to reduce atherothrombogenesis, possibly through complementary mechanisms involving lipoxygenase products of DHA.
- Published
- 2014
- Full Text
- View/download PDF
50. Lipidomics of essential fatty acids and oxygenated metabolites.
- Author
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Lagarde M, Bernoud-Hubac N, Calzada C, Véricel E, and Guichardant M
- Subjects
- Arachidonic Acid metabolism, Biological Availability, Endocannabinoids metabolism, Fatty Acids, Unsaturated pharmacokinetics, Humans, Linoleic Acid metabolism, Lipid Peroxidation, Oxygen metabolism, alpha-Linolenic Acid metabolism, Fatty Acids, Essential metabolism, Fatty Acids, Unsaturated metabolism
- Abstract
Polyunsaturated fatty acids in mammals may be oxygenated into a myriad of bioactive products through di- and monooxygenases, products that are rapidly degraded to control their action. To evaluate the phenotypes of biological systems regarding this wide family of compounds, a lipidomics approach in function of time and compartments would be relevant. The current review takes into consideration most of the diverse oxygenated metabolites of essential fatty acids at large and their immediate degradation products. Their biological function and life span are considered. Overall, this is a fluxolipidomics approach that is emerging., (© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)
- Published
- 2013
- Full Text
- View/download PDF
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