CoA‐Dependent cleavage of arachidonic acid from phosphatidylcholine and transfer to phosphatidylethanolamine in homogenates of murine thymocytes

Increased turnover of the fatty acyl moieties of membrane phospholipids and in particular the metabolism of arachidonic acid play a central role in the early phase of ligand-receptor-mediated activation in many cell types. Alterations in the membrane lipid phase are thought to initiate changes in the membrane permeability to ions and the activation of membrane-bound enzymes [ 11. The synthesis of arachidonic acid metabolites by the cycle-oxygenase and lipoxygenase systems is also considered to be controlled by the availability of free arachidonic acid; this in turn is determined by the release of arachidonic acid from membrane-bound lipids [2-l]. In mitogen-induced activation of T lymphocytes, one of the early changes reported in activated cells is an increased incorporation of long-chain fatty acids into phosphatidylcholine and phosphatidylethanolamine [5]. In mitogen-activated human T cells an elevated release of arachidonic acid from. membrane phospholipids has been reported [6,7], coupled with a synthesis of arachidonic acid derivatives [8]. There is good evidence that phospholipid synthesising enzymes are activated in stimulated T cells [9] but we have been unable to detect significant phospholipase Aa activity in thymocytes using exogeneous substrate [lo]. The rapid incorporation of fatty acids