Aim: To obtain pathophysiological meanings of lysophosphatidylcholine (LPC)through the investigation of the effects of LPC in Jurkat T cells .
Methods: We measured ROS generation, [Ca(2+)](i), and mitochondrial membrane potential (MMP)by fluorescent spectrometry in Jurkat T cells.
Results: We observed that LPC significantly increased the reactive oxygen species (ROS) level in human Jurkat T cells. Among structurally-related lysolipids and eleven synthetic LPCs with different acyl chain lengths, palmitoyl LPC increased ROS to the highest level. alpha-Tocopherol, an antioxidant, and rottlerin PKCdelta inhibitor were inhibitory effects on LPC-induced ROS generation. LPC rapidly depolarized MMP and markedly elevated [Ca(2+)](i) by Ca(2+) influx across the plasma membrane. However, LPC-induced ROS increase seemed to not be related with LPC-induced depolarization of MMP or [Ca(2+)](i) increase. G2A family G protein-coupled receptors (GPCR) for lysolipids were expressed in Jurkat T cells, however, evidence indicated that GPCR was not involved in LPC actions.
Conclusion: LPC induced several cellular changes in Jurkat T cells, including an increase of ROS generation in a PKCdelta-dependent and GPCR-independent manner, increase of [Ca(2+)](i) through Ca(2+) influx, and decrease of MMP. LPC-induced actions in Jurkat T cells represent novel action modes of LPC that do not involve GPCR and multiple independent changes of intracellular signaling molecules.