Vitamin E Research Today is a free monthly online journal that collates and summarizes the latest research about Vitamin E, including details on benefits, dosage, supplements, antioxidants. | ||||||||
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Alpha-tocopherol modulates phosphatidylserine externalization in erythrocytes: relevance in phospholipid transfer protein-deficient mice.Klein A, Deckert V, Schneider M, Dutrillaux F, Hammann A, Athias A, Le Guern N, Pais de Barros JP, Desrumaux C, Masson D, Jiang XC, Lagrost L INSERM U498, IFR100, Université de Bourgogne, Dijon, France. OBJECTIVE: The aim of the present study was to assess the effect of alpha-tocopherol, the main vitamin E isomer on phosphatidylserine (PS) exposure at the surface of circulating erythrocytes, and to determine consequences on erythrocyte properties. METHODS AND RESULTS: In vitro alpha-tocopherol enrichment of isolated erythrocytes significantly decreased PS externalization as assessed by lower Annexin V-fluorescein isothiocyanate labeling. Plasma phospholipid transfer protein (PLTP) transfers vitamin E, and both alpha- and gamma-tocopherol accumulated in circulating erythrocytes from PLTP-deficient homozygous (PLTP-/-) mice as compared with wild-type mice. In agreement with in vitro studies, vitamin E-enriched erythrocytes from PLTP-/- mice displayed fewer externalized PS molecules than wild-type controls (-64%, P<0.05). The perturbation of phospholipid membrane asymmetry from PLTP-/- erythrocytes was accompanied by impairment of their procoagulant properties, with a 20% increase in clotting time as compared with wild-type controls (P<0.05). Less pronounced, however still significant, changes were observed in alpha-tocopherol content, procoagulant properties, and PS externalization in erythrocytes of PLTP-deficient heterozygotes. Finally, whole blood coagulation and circulating level of D-dimer, which reflects increased thrombus formation in vivo, were significantly decreased in PLTP-/- mice compared with wild-type mice. CONCLUSIONS: Vitamin E modifies PS externalization in circulating erythrocytes, thus modulating in vivo their PS-dependent procoagulant properties. Published 18 August 2006 in Arterioscler Thromb Vasc Biol, 26(9): 2160-7.
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