Nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) mediated 
generation of reactive oxygen species (ROS) was originally identified as the 
powerful host defense machinery against microorganism in phagocytes. But recent 
reports indicated that some non-phagocytic cells also have the NADPH oxidase 
activity, and the ROS produced by it may act as cell signal molecule. But as far 
as today, whether the NADPH oxidase also plays similar role in phagocyte has not 
been paid much attention. Utilizing the undifferentiated HL-60 promyelocytic 
leukemia cells as a model, the aim of the present study was to determine whether 
NADPH oxidase plays a role on ROS generation in undifferentiated HL-60, and the 
ROS mediated by it was essential for cell's survival. For the first time, we 
verified that the release of ROS in undifferentiated HL-60 was significantly 
increased by the stimulation with Calcium ionophore or opsonized zymosan, which 
are known to trigger respiration burst in phagocytes by NADPH oxidase pathway. 
Diphenylene iodonium (DPI) or apocynin (APO), two inhibitors of NADPH oxidase, 
significantly suppressed the increasing of ROS caused by opsonized zymosan. Cell 
survival assay and fluorescence double dyeing with acridine orange and ethidium 
bromide showed that DPI and APO, as well as superoxide dismutase (SOD) and 
catalase (CAT) concentration-dependently decreased the viability of 
undifferentiated HL-60 cells, whereas exogenous H2O2 can rescue the cells from 
death obviously. Our results suggested that the ROS, generated by NADPH oxidase 
play an essential role in the survival of undifferentiated HL-60 cells.