Hyperpolarization by N-(3-oxododecanoyl)-l-homoserine-lactone, a quorum sensing molecule, in rat thymic lymphocytes.

To study the adverse effects of N-(3-oxododecanoyl)-l-homoserine-lactone (ODHL), a quorum sensing molecule, on mammalian host cells, its effect on membrane potential was examined in rat thymic lymphocytes using flow cytometric techniques with a voltage-sensitive fluorescent probe. As 3-300 μM ODHL elicited hyperpolarization, it is likely that it increases membrane K permeability because hyperpolarization is directly linked to changing K gradient across membranes, but not Na and Cl gradients. ODHL did not increase intracellular Ca concentration. ODHL also produced a response in the presence of an intracellular Zn chelator. Thus, it is unlikely that intracellular Ca and Zn are attributed to the response. Quinine, a non-specific K channel blocker, greatly reduced hyperpolarization. However, because charybdotoxin, tetraethylammonium chloride, 4-aminopyridine, and glibenclamide did not affect it, it is pharmacologically hypothesized that Ca-activated K channels, voltage-gated K channels, and ATP-sensitive K channels are not involved in ODHL-induced hyperpolarization. Although the K channels responsible for ODHL-induced hyperpolarization have not been identified, it is suggested that ODHL can elicit hyperpolarization in mammalian host cells, disturbing cellular functions.