Apoptosis, a type of programmed cell death, is a decisive mechanism in cell
processes such as homeostasis, development, and many diseases including ca
ncer. In mammals, the mechanisms that trigger and control the process of ap
optosis are complex, because it has been observed that many molecules might
be involved, acting in distinct ways and depending on the cellular type. T
he process of apoptosis is characterized by specific biochemical and morpho
logic changes. However, important specific messengers such as Ca2+ act in a
ctive proliferation as well as in apoptosis. At present, there is convincin
g evidence that a sustained increase in intracellular Ca2+ can activate cyt
otoxic mechanisms in various cells and tissues. Several ionic channels loca
ted in the cytoplasmic membrane might participate in the entry of calcium i
nto the cytosol during apoptosis. Among these ionic channels, the purinorec
eptors P2X and the channels of capacitative entry of calcium have been desc
ribed. Pro- and anti-apoptotic molecules such as bar and bcl-2, respectivel
y, have also been shown to participate in the process. We have recently fou
nd the activation of a Ca2+-permeable, nonselective cation channel of 23 pS
conductance in prostatic cancer (LNCaP) exclusively in cells previously in
duced to apoptosis. Our findings are discussed taking into account the diff
erent ion channels that might participate in programmed cell death in prost
ate cancer. (C) 2001 IMSS. Published by Elsevier Science Inc.