Objective: To investigate the mechanism of sodium selenite-induced apoptosis in HepG2 cells.
Methods: HepG2 cells were treated with 0,2.5,5,10 and 20 micromol/L sodium selenite for different time, and NAC (5 micromol) was added simultaneously with selenite (10 micromol/L). Then the cell viability was detected by MTT, and the fluorescent intensity of ROS and the apoptosis rate was determined by flow cytometry.
Results: Compared with the control group, the levels of ROS were increased after HepG2 was treated with 5, 10 and 20 micromol/L sodium selenite for one hour, and the cell viability decreased after 12 hours, and the apoptosis rate of HepG2 was increased. After NAC was added with selenite, ROS was effectively inhibited. Subsequently cell viability was increased and the cell apoptosis rate was decreased.
Conclusion: ROS may play a crucial role in sodium selenite-decreased cell viability and -induced apoptosis in HepG2 cells.