Antiproliferative effect of H2O2 against human acute myelogenous leukemia KG1 cell line

It has clearly been established that oxidative stress leads to perturbation of various cellular processes resulting in either inhibition of cell proliferation or cell death. In addition, there is a growing body of evidence indicating that reactive oxygen species (ROS) are required as signal molecules that regulate different physiological processes including survival or death. Free radicals, particularly ROS, have been proposed as general mediators for apoptosis and recent studies have established that the mode of cell death depends on the severity of the oxidative damage. In this study, we determined the effect of oxidative stress on cell proliferation and characterization of cell death in human KG1 cells treated with H2O2. Our results indicated that oxidative stress leads to a significant decrease in cell proliferation and induction of apoptosis. Moreover, our study suggests that antiproliferative and apoptotic cell death effects of H2O2 took place via activation of caspase-3, affecting the expression of Bcl-2 and Bax (an antiapoptotic and a proapoptotic factor, respectively), and through deactivation of catalase enzyme, leading to accumulation of intracellular ROS and depletion of intracellular ATP level.