摘要
Reactive oxygen species (ROS), including the hydroxyl radical ( · OH), are known to be potential modulators of apoptosis. However, the biochemical mechanisms underlying apoptosis induced by ·OH, namely how the radical induces a cell to die, are poorly understood. The present work highlights the changes of the energy/redox status during apoptosis by exogenous ·OH treatment. HeLa cells were induced to undergo typical apoptosis by ·OH generated directly via the Fe 2+ mediated Fenton reaction. The thermodynamics study indicated that the ·OH treatment increased the cellular heat output in the first hours, and then the cellular thermodynamics shifted to endothermic. The data demonstrates that the mitochondria are actively involved in ·OH treatment induced apoptosis, with the cellular oxygen consumption rapidly decreasing after the ·OH treatment for only 0.5 h. But DNA fragmentation, which is the major characteristic of apoptosis, took place 16 h after ·OH treatment. The results suggest that alteration of the energy/redox metabolism and the energy/redox status may be the primary causes among the early events of ·OH induced apoptosis.
Reactive oxygen species (ROS), including the hydroxyl radical ( · OH), are known to be potential modulators of apoptosis. However, the biochemical mechanisms underlying apoptosis induced by ·OH, namely how the radical induces a cell to die, are poorly understood. The present work highlights the changes of the energy/redox status during apoptosis by exogenous ·OH treatment. HeLa cells were induced to undergo typical apoptosis by ·OH generated directly via the Fe 2+ mediated Fenton reaction. The thermodynamics study indicated that the ·OH treatment increased the cellular heat output in the first hours, and then the cellular thermodynamics shifted to endothermic. The data demonstrates that the mitochondria are actively involved in ·OH treatment induced apoptosis, with the cellular oxygen consumption rapidly decreasing after the ·OH treatment for only 0.5 h. But DNA fragmentation, which is the major characteristic of apoptosis, took place 16 h after ·OH treatment. The results suggest that alteration of the energy/redox metabolism and the energy/redox status may be the primary causes among the early events of ·OH induced apoptosis.
