Formation of thromboxane B2 and hydroxyarachidonic acids in purified human lymphocytes in the presence and absence of PHA.
The metabolism of exogenous and endogenous [14C] arachidonc acid was studied in purified human peripheral blood lymphocytes carefully freed of contaminating platelets. Formation of products co-migrating in a number of different solvent systems with 5-hydroxyarachidonic acid (5-HETE), thromboxane B2 (TB2), prostaglandins and probably 12-hydroxyarachidonic acid (12-HETE) was demonstrated. In cells prelabeled with [14C] arachidonic acid, phytohemagglutinin (PHA) produced substantial (3.5- to 12-fold) increases in 5-HETE, 12-HETE, and TB2 radiolabeling. The metabolism of exogenous [14C] arachidonic acid was much less affected by PHA. Since PHA releases cell-bound arachidonic acid, it appears that the response involving endogenous label is due to increased availability of free arachidonic acid rather than induction of arachidonic acid-metabolizing enzymes. Various inhibitors of arachidonic acid metabolism exerted similar effects in lymphocytes to those described previously in other tissues providing a possible basis for interpreting their inhibitory effects on mitogenesis, described in the preceding paper.
D001095:Arachidonic Acids / Q000037:antagonists & inhibitors / Q000096:biosynthesis* / Q000378:metabolism; D002469:Cell Separation; D006801:Humans; D008213:Lymphocyte Activation / Q000187:drug effects*; D008214:Lymphocytes / Q000378:metabolism; D010835:Phytohemagglutinins / Q000494:pharmacology*; D013929:Thromboxane B2 / Q000096:biosynthesis*; D013931:Thromboxanes / Q000096:biosynthesis*
D001095:Arachidonic Acids; D010835:Phytohemagglutinins; D013931:Thromboxanes; D013929:Thromboxane B2