Caspase activation in high-pressure--induced apoptosis of murine erythroleukemia cells.

Abstract

Murine erythroleukemia cells were subjected to physicochemical stresses such as high pressure (60--110 MPa), heating (42--45 degrees C), and ultraviolet (UV) irradiation (5--25 kJ/cm(2)). After exposure to these stresses, the cells were cultured at 37 degrees C and atmospheric pressure. The number of the cells treated at 100 MPa, 45 degrees C, or 20 kJ/cm(2) remained constant or decreased at an early stage of culture. The nuclear morphology, agarose gel electrophoresis, and flow cytometry of these cells showed that they undergo apoptosis. The activity of caspase-3 was observed in cells subjected to each stress. In particular, caspase-3 was most readily activated by high pressure under our conditions. The caspase-3 activity and apoptosis exhibited a similar pressure dependence. It is important that both caspase-3 activation and apoptosis induced by high pressure were significantly suppressed by a caspase-3 inhibitor. These results suggest that high-pressure-induced apoptosis is also characterized by the activation of caspase-3, as seen with heat- and UV-induced apoptosis.