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Effects of the lipid peroxidation product 4-hydroxynonenal on the aggregation of human platelets
Authors:J S Hurst  T F Slater  J Lang  G Juergens  H Zollner  H Esterbauer
Affiliation:1. Murdoch Childrens Research Institute, Royal Children''s Hospital, Parkville, Victoria, Australia;2. Department of Paediatrics, The University of Melbourne, Parkville, Victoria, Australia;3. Department of Clinical Haematology, Royal Children''s Hospital, Parkville, Victoria, Australia;4. Centre for Microscopy, Characterisation and Analysis, The University of Western Australia, Western Australia, Australia;1. Department of Blood Transfusion, the Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan, China;2. Department of Clinical Laboratory, the Affiliated Hospital of Luzhou Medical College, Luzhou, Sichuan, China;1. Instituto Nacional de Salud Pública, Cuernavaca, Morelos, Av. Universidad 655, Col. Sta María Ahuacatitlán, CP 62100 Cuernavaca, Morelos, Mexico;2. CONACYT, Instituto Nacional de Salud Pública (INSP), Av. Universidad 655, Col. Sta. María Ahuacatitlán, 62100 Cuernavaca, Morelos, Mexico;3. Departamento de Neuroquímica, Instituto Nacional de Neurología y Neurocirugía, Av. Insurgentes Sur No. 3877, Col. La Fama, Del. Tlalpan, Ciudad de México CP. 14269, Mexico;4. Departamento de Toxicología, CINVESTAV, Av. Instituto Politécnico Nacional 2508, Gustavo A. Madero, San Pedro Zacatenco, 07360 Ciudad de México, Mexico;1. Grupo de Biología y Toxicología Ambiental, Facultad de Ciencias, Universidad Nacional de Educación a Distancia, UNED, Senda del Rey 9, 28040 Madrid, Spain;2. Departamento de Ciencias y Técnicas Fisicoquímicas, Facultad de Ciencias, Universidad Nacional de Educación a Distancia, UNED, Senda del Rey 9, 28040 Madrid, Spain
Abstract:The stimulation by ADP or arachidonic acid of the aggregation of human platelets in plasma was inhibited by 4-hydroxynonenal (HNE). This reduction of aggregation was time related, and was increased by prolonged preincubation of the platelets with the aldehyde. HNE was more potent than its homologue 4-hydroxypentenal (HPE). HNE was less active in decreasing the aggregation induced by calcium ionophore A23187 or collagen in comparison with ADP. HNE was inactive against aggregation of platelet-rich plasma (PRP) stimulated by thrombin whereas it potently inhibited the aggregation of washed platelets in response to both thrombin and collagen. Platelets were found to degrade HNE, and mechanisms additional to covalent binding to glutathione are indicated by the results obtained. The aldehydes, including HNE, generated by platelets originated principally from arachidonic acid metabolism.
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