[Role of reactive oxygen species in sodium selenite induced DNA damage in HepG2 cells]

Wei Sheng Yan Jiu. 2006 May;35(3):291-3.
[Article in Chinese]

Abstract

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.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • DNA Damage*
  • Dose-Response Relationship, Drug
  • Hep G2 Cells
  • Humans
  • Reactive Oxygen Species / metabolism*
  • Sodium Selenite / pharmacology*

Substances

  • Reactive Oxygen Species
  • Sodium Selenite