Release and metabolism of arachidonic acid in human neutrophils. J Biol Chem 1981 Jul 25;256(14):7228-34
Date
07/25/1981Pubmed ID
6788763Scopus ID
2-s2.0-0019870093 (requires institutional sign-in at Scopus site) 207 CitationsAbstract
Dual radiolabel incorporation of [3H]arachidonic acid and [14C]palmitate or [14C]stearate by human neutrophils was employed to study both the release and metabolism of arachidonic acid. Results indicate the involvement of a phospholipase A2 mechanism causing [3H]arachidonate release from membrane phospholipid. Phosphatidylinositol and phosphatidylcholine were the sources of [3H]arachidonate; about twice as much radiolabeled phosphatidylinositol was degraded as phosphatidylcholine. Challenge of neutrophils with opsonized zymosan and calcium ionophores caused the release of [3H]arachidonate; however, ionophores but not opsonized zymosan led to the production of [3H]hydroxyicosatetraenoic acid and [3H]dihydroxyicosatetraenoic acid. These products were preferentially released by neutrophils into the extracellular milieu in contrast with free [3H]arachidonate which remained cell associated. One-third of the [3H]hydroxyicosatetraenoic acid but not [3H]dihydroxyicosatetraenoic acid was reincorporated into cellular lipid, primarily phospholipid. No significant production of [3H]prostaglandin or [3H]thromboxane was detected. In contrast to zymosan and ionophore, phorbol myristate acetate, another potent stimulant of neutrophil oxidative metabolism and degranulation, did not release [3H]arachidonate.
Author List
Walsh CE, Waite BM, Thomas MJ, DeChatelet LRMESH terms used to index this publication - Major topics in bold
Arachidonic AcidArachidonic Acids
Calcimycin
Carbon Radioisotopes
Humans
Kinetics
Lipids
Neutrophils
Palmitic Acid
Palmitic Acids
Phospholipids
Tritium
