The metabolism of exogenous and endogenous [14C] arachidonic 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 -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  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.
|Number of pages||6|
|Journal||Journal of Immunology|
|State||Published - Jan 1 1979|