Cation fluxes appear to play a key role in
palytoxin-induced signal. There are other cellular targets that have not been described as well as the biochemical signaling cascades that transmit
palytoxin-stimulated signals remain to be clarified. Since modifications of
cations, mainly
calcium, are generally associated to cell death or apoptosis, we wanted to further evaluate the effect of
palytoxin on cell death. Then, in vitro cytotoxic effects of
palytoxin were characterized on human
neuroblastoma cells. By using several techniques, we studied markers of cell death and apoptosis, such as cell detachment, mitochondrial membrane potential,
caspases, DNA damage, LDH leakage,
propidium iodide uptake,
F-actin depolymerization and inhibition of cellular proliferation. Results show that
palytoxin triggers a series of toxic responses; it inhibits cell proliferation, induces cell rounding, detachment from the substratum and
F-actin disruption. Among the apoptotic markers studied we only detected fall in mitochondrial membrane potential. Neither
caspases activation nor
chromatin condensation or DNA fragmentation were observed in
palytoxin-treated cells.