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) 201 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 LRAuthor
Michael J. Thomas PhD Professor in the Pharmacology and Toxicology department at Medical College of WisconsinMESH 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