Decreased cation channel activity and blunted channel-dependent eryptosis in neonatal erythrocytes.

Eryptosis or apoptosis-like death of erythrocytes is characterized by phosphatidylserine exposure and erythrocyte shrinkage, both typical features of nucleated apoptotic cells. Eryptosis is triggered by activation of nonselective Ca(2+)-permeable cation channels with subsequent entry of Ca(2+) and stimulation of Ca(2+)-sensitive scrambling of the cell membrane. The channels are activated and thus eryptosis is triggered by Cl(-) removal, osmotic shock, oxidative stress, or glucose deprivation.

Inhibition of erythrocyte "apoptosis" by catecholamines.

Osmotic shock, oxidative stress and Cl- removal activate a non-selective Ca2+-permeable cation conductance in human erythrocytes. The entry of Ca2+ leads to activation of a scramblase with subsequent exposure of phosphatidylserine at the cell surface. Phosphatidylserine mediates binding to phosphatidylserine receptors on macrophages which engulf and degrade phosphatidylserine exposing cells.