Sanduja S K, Trial J, Hall E R
Department of Internal Medicine, University of Texas Health Science Center, Houston 77030.
Biomed Biochim Acta. 1988;47(4-5):383-93.
A comparative analysis of prostaglandin production was carried out on human promyelocytic leukemia (HL-60) cells treated with either PMA or DMSO. When incubated with [1-14C]arachidonic acid these cells produced significant amounts of 6-keto prostaglandin F1 alpha, thromboxane B2, prostaglandin F2 alpha, prostaglandin E2, prostaglandin D2 and 12-hydroxy-5,8,10-heptadecatrienoic acid via the cyclooxygenase pathway. The major cyclooxygenase metabolite synthesized by these cells was prostaglandin F2 alpha. Its production increased significantly when the HL-60 cells were treated with PMA and decreased when treated with DMSO as compared to untreated control cells. This change in the production of prostaglandin F2 alpha appears to reflect alterations in cyclooxygenase activity. Another unidentified arachidonic acid metabolite was routinely observed in C18 high pressure liquid chromatography. The synthesis of this compound was inhibited by indomethacin. The unidentified metabolite was also seen in the human macrophage-like cell line U937.