Vitamin E exerts antiaggregatory effects without inhibiting the enzymes of the arachidonic acid cascade in platelets |
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| Institution: | 1. Department of Human Physiology, Faculty of Basic Medical Sciences, College of Medicine, Delta State University, Abraka, Delta State, Nigeria;2. Department of Basic Medical Sciences, Achievers University, Owo, Ondo State, Nigeria;3. Department of Pharmacology and Therapeutics, Faculty of Basic Medical Sciences, College of Medicine, Delta State University, Abraka, Delta State, Nigeria;4. Department of Physiology, Faculty of Basic Medical Science, College of Medicine, University of Ibadan, Ibadan, Oyo State, Nigeria;5. Department of Science Laboratory Technology, Delta State Polytechnic, Ogwashi-Uku, Delta State, Nigeria;6. Department of Physiology, University of Medical Sciences, Ondo, Ondo State, Nigeria;7. Department of Pharmacology and Therapeutics, Faculty of Basic Medical Sciences, Rivers State University, Port Harcourt, Rivers State, Nigeria;1. Department of Epidemiology and Biostatistics, School of Health, Isfahan University of Medical Sciences, Isfahan, Iran;2. Student Research Committee, School of Health, Isfahan University of Medical Sciences, Isfahan, Iran;3. Department of Statistics, University of Isfahan, Isfahan, Iran;4. Cardiac Rehabilitation Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran;5. Hypertension Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran;6. Psychosomatic Research Center, Isfahan University of Medical Sciences, Isfahan, Iran;7. Isfahan Cardiovascular Research Center, Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran;8. Saw Swee Hock School of Public Health, National University of Singapore, Singapore;1. Department of Neurodegeneration, Hertie-Institute for Clinical Brain Research and German Center for Neurodegenerative Diseases, Tuebingen, Germany;2. Department of Neurology, Montreal General Hospital, Montreal, Quebec, Canada;3. The Parkinson''s Disease and Movement Disorders Center, Department of Neurology, Mayo Clinic, Scottsdale;4. Department of Neurology, Radboud university medical center, Donders Institute for Brain, Cognition and Behaviour, Nijmegen, Netherlands;5. Xuanwu Hospital of Capitol of Medical University, Beijing, Peoples Republic of China;6. Department of Neurology, Christian-Albrechts University, Kiel, Germany;7. Rush University Medical Center, Chicago, IL, USA;8. Neuroscience Research Australia and University of New South Wales, Randwick, Australia;9. Department of Epidemiology and Biostatistics, McGill University, Montreal, Quebec, Canada;10. Division of Neurology, Toronto Western Hospital, Toronto, Ontario, Canada;11. Department of Neurosciences, UC San Diego, La Jolla, California, USA;12. Institute for Neurodegenerative Disorders, New Haven, CT, USA;13. Department of Neurology, Philipps University of Marburg, Marburg, Germany;14. Department of Neurology, The Mount Sinai Hospital, New York, NY, USA;15. Department of Neurology, Innsbruck Medical University, Innsbruck, Austria;p. Penn Neurological Institute, Philadelphia, Pennsylvania, USA;1. Programa de Pós-Graduação em Ciências Farmacêuticas, Centro de Ciências da Saúde, Universidade Federal de Santa Maria, Santa Maria 97105-900, Brazil;2. Departamento de Farmácia Industrial, Universidade Federal de Santa Maria, Santa Maria 97105-900, Brazil;3. Programa de Pós-Graduação em Ciências Biológicas, Bioquímica Toxicológica, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria 97105-900, Brazil |
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| Abstract: | Vitamin E (α-tocopherol) and tocopherol acetate produced a slightly increased amount of thromboxane in treated compared to untreated platelets. In tocopherol acetate-treated platelets significantly more lipoxygenase products were produced. α-tocopherol induced an increased, but not significant, production of thromboxane B2 during blood clotting. α-tocopherol was not found to affect platelet phospholipase activity as determined by its effect on the release of labelled arachidonic acid from platelet phospholipids by challenging the platelets with calcium ionophore A23,187. α-tocopherol potentiated the incorporation of labelled arachidonate in the platelet phospholipids. Inspite of having no effect on the arachidonic acid cascade in platelets, α-tocopherol inhibited aggregation induced by several aggregating agents including A23,187. Inhibition of aggregation may be explained by the ability of α-tocopherol to inhibit intracellular mobilization of sequestered calcium from the dense tubular system to the cytoplasm. |
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