Previous exposure of Day 4 embryos at the 8- to 16-cell stage to a mild and transient heat shock of 40°C for 80 min blocked the induction of apoptosis induced by a subsequent severe heat shock of 41 °C for 9 h. Such a phenomenon has been observed for others cells also. The biochemical mechanisms by which mild heat shock prevents apo-ptosis induced by a more severe heat shock presumably involves HSP70. Besides protecting cells from heat shock, HSP70 can protect cells against several apoptotic stimuli, including DNA damage, UV irradiation, serum withdrawal, and chemotherapeutic agents.
The mechanism by which HSP70 exerts its antiapoptotic action is not completely understood, but it can block multiple points along the apoptotic pathway. HSP70 and HSP72 inhibit poly-(ADP-ribose) polymerase cleavage. HSP70 also blocks cytochrome c release from mitochondria, processing of inactive procaspase-3, and SAPK/ JNK activation. In addition, disruption of murine heat shock factor 1 gene increased heat-induced apoptosis. The bovine embryo can produce higher amounts of HSP70 in response to heat shock as early as the 2-cell stage.