[Relationship between reactive oxygen species and apoptosis in HepG2 cells induced by sodium selenite].
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.


CONCLUSIONS
ROS may play a crucial role in sodium selenite-decreased cell viability and -induced apoptosis in HepG2 cells.
Zou
Yunfeng
Y
Department of Occupational and Environmental Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Yang
Jin
J
Liu
Xiaoyong
X
Yuan
Jing
J
D017209:Apoptosis / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D056945:Hep G2 Cells; D006801:Humans; D017382:Reactive Oxygen Species / Q000378:metabolism*; D018038:Sodium Selenite / Q000494:pharmacology*
D017382:Reactive Oxygen Species; D018038:Sodium Selenite