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Arachidonic and Eicosapentaenoic Acid Metabolism in Bovine Neutrophils and Platelets: Effect of Calcium Ionophore
Author(s) -
Taylor Stephen M.,
Laegreid William W.,
Heidel Jerry R.,
Straub Kenneth M.,
Liggitt H. Denny,
Silflow Ron M.,
Breeze Roger G.,
Leid R. Wes
Publication year - 1987
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.42.3.253
Subject(s) - arachidonic acid , ionophore , eicosapentaenoic acid , biochemistry , biology , leukotriene , leukotriene b4 , platelet , calcium , lipoxygenase , metabolite , phospholipase a2 , eicosanoid , fatty acid , cyclooxygenase , thromboxane , thromboxane b2 , enzyme , medicine , inflammation , immunology , polyunsaturated fatty acid , membrane , asthma
Substitution of dietary fatty acids has potential for altering the inflammatory response. The purpose of the present study was to define the metabolites of arachidonic acid (AA) and eicosapentaenoic acid (EPA) secreted by bovine peripheral blood neutrophils and platelets. High performance liquid chromatography was used to characterize cyclooxygenase and lipoxygenase metabolites secreted in response to the calcium ionophore A23187. Cells were prelabelled with 3 H‐AA or 3 H‐EPA prior to challenge with the calcium ionophore. Bovine neutrophils secreted leukotriene B 4 (LTB 4 ) and 5‐hydroxyeicosatet‐raenoic acid (5‐HETE) as the major metabolites of AA, as well as the corresponding leukotriene B 5 (LTB 5 ) and 5‐hydroxyeicosapentaenoic acid (5‐HEPE) metabolites of EPA. Peptidoleukotrienes derived from 3 H‐AA or 3 H‐EPA were not detected under these conditions. The major tritiated metabolites secreted from bovine platelets were: thromboxane A 2 , measured as the stable metabolite thromboxane B 2 (TXB 2 ); hydroxyhepta‐decatrienoic acid (HHT) and 12‐HETE derived from 3 H‐AA; and the omega‐3 analogs TXB 3 and 12‐HEPE, derived from 3 H‐EPA. Preferred substrate specificities existed amongst the AA‐ and EPA‐derived metabolites for the intermediary enzymes involved in the arachidonic acid cascade. These findings support the hypothesis that substitution of membrane‐bound AA by EPA has potential for modulation of the host inflammatory response following cellular phospholipid mobilization.