Ion fluxes and volume changes of the whole cell as well as of organelles be
long to the hallmarks of apoptosis; however, the molecular mechanism regula
ting these changes is only poorly characterized. Several ion channels in th
e plasma membrane, in particular the N-type K+ channel, the chloride channe
l cystic fibrosis conductance regulator, and an outward rectifying chloride
channel, as well as the mitochondrial permeability transition pore, have b
een implicated to be involved in signal transduction cascades regulating ap
optosis. Furthermore, Bcl-2-like proteins have been suggested to function,
at least in part, as ion channels, because they display some homology to ba
cterial pore-forming toxins. In contrast to the demonstration of the involv
ement of these different ion channels in apoptosis, the molecular consequen
ces regulated by these ion channels, and finally triggering apoptosis, are
almost completely unknown.