[Role of reactive oxygen species in sodium selenite induced DNA damage in HepG2 cells]
Yun-Feng Zou1, Pi-Ye Niu, Zhi-Yong Gong
1The MOE Key Lab of Environment and Health, Department of Occupational and Enviromental Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Objective:
To investigate the mechanisms of sodium selenite induced DNA damage in HepG2 cells.
Methods:
HepG2 cells were treated with the designed concentrations of sodium selenite and the selenite (10 micromol/L) added simultaneously with GSH (10 mmol) and NAC (5 mmol). Then the cell viability was detected by MTT, and the flurescent intensity of reactive oxygen species (ROS) was determined by flow cytometry, and DNA damage was detected by commet assay.
Results:
The level of ROS was increased after HepG2 was treated with 5, 10, 20 micromol/L sodium selenite for one hour, and the cell viability was decreased after 12 hours, and the DNA damage was enhanced. Compared with the control group, the difference was statistically significant (P < 0.05) . GSH and NAC effectively inhibited the ROS increased and cell viability decreased and DNA damage weakened.
Conclusion:
ROS may be the important reason that sodium selenite induced HepG2 cells DNA damage.
Related Concept Videos
01:38Nucleotide Excision Repair
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
01:08Nucleotide Excision Repair
02:36DNA Damage can Stall the Cell Cycle
02:36DNA Damage Can Stall the Cell Cycle
01:35Mutations
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...