Abstract
A specific diacylglycerol kinase inhibitor, at a concentration of 10(-5) M, consistently enhanced superoxide generation from human neutrophils stimulated with fMet-Leu-Phe, IgG, heat-aggregated IgG and opsonized zymosan. The concentration-response curve for fMet-Leu-Phe was displaced to the left and the maximum superoxide release was also consistently increased by R59022 whereas the diacylglycerol lipase inhibitor, RHC80267, 10(-5) M, had no significant effect. These results suggest that the diacylglycerol formed after fMet-Leu-Phe stimulation in human neutrophils is metabolized largely by the kinase and not the lipase, which implies that diacylglycerol is not the major source of arachidonate during signal-transduction.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cyclohexanones / pharmacology
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Diacylglycerol Kinase
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Diglycerides / metabolism
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Humans
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In Vitro Techniques
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Lipoprotein Lipase / metabolism
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N-Formylmethionine Leucyl-Phenylalanine / pharmacology*
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Neutrophils / metabolism*
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Phosphotransferases / antagonists & inhibitors*
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Protein Kinase C / metabolism
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Pyrimidinones / pharmacology*
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Receptors, Complement / physiology*
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Receptors, Complement 3b
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Receptors, Fc / physiology*
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Receptors, Formyl Peptide
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Receptors, Immunologic / physiology*
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Superoxides / metabolism*
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Thiazoles / pharmacology*
Substances
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Cyclohexanones
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Diglycerides
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Pyrimidinones
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Receptors, Complement
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Receptors, Complement 3b
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Receptors, Fc
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Receptors, Formyl Peptide
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Receptors, Immunologic
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Thiazoles
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Superoxides
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N-Formylmethionine Leucyl-Phenylalanine
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1,6-bis(cyclohexyloximinocarbonyl)hexane
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R 59022
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Phosphotransferases
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Diacylglycerol Kinase
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Protein Kinase C
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Lipoprotein Lipase