Analysis of High Pressure-Induced Apoptosis of Murine Erythroleukemia Cells

Abstract

Previously we showed the breakdown of mitochondrial membrane potential, cytochrome c release, caspase-3 activation, and DNA ladder in murine erythroleukemia (MEL) cells exposed to a pressure of 100 MPa. Here, to characterize pressure-induced apoptosis, the pathway of caspase-3 activation, morphological changes of the cells, and the spin-lattice relaxation time (T₁) of intracellular water were examined using 100 MPa-treated MEL cells. The results from caspase-inhibitors showed that both pathways via caspase-8 and mitochondria were involved in caspase-3 activation. Upon culture of pressure-treated cells, the plane surface of the membrane was observed using a scanning electron microscope. From the T₁ measurement, it was found that the efflux of intracellular water occurs in early stage of apoptosis, whereas the influx of water in its late stage.