Journal Home Online First Current Issue Archive For Authors Journal Information 中文版

2007, Volume 1, Issue 3

Abstract

Keywords

Related Research

Back to Top

Frontiers of Medicine >> 2007, Volume 1, Issue 3 doi: 10.1007/s11684-007-0063-x

Relationship between reactive oxygen species and sodium-selenite-induced DNA damage in HepG2 cells

Department of Occupational and Environmental, Ministry of Education Key Laboratory of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China

Available online: 2007-09-05
HTML14 PDF 1 Collect 0

Next Previous

Abstract

Selenium compounds, as an effective chemopreventive agent, can induce apoptosis in tumor cells. Reactive oxygen species (ROS) are important mediators in apoptosis induced by various stimuli, which include chemopreventive agents. In this study, we investigated the relationship between ROS and the levels of DNA damage induced by selenite in HepG2 cells. After HepG2 cells were treated with selenite, there was a dose-dependent decrease in cell viability. The levels of ROS induced by selenite were measured by 2′, 7′-dichlorofluorescein diacetate (DCFH-DA) fluorescence, which shows a dose- and time-dependent increase in HepG2 cells. The levels of DNA damage in HepG2 increased in all cells treated with an increasing dose of selenite at 0, 2.5, 5, 10, and 20 μmol/L. N-acetylcysteine (NAC), a known antioxidant, increased cell viability and decreased ROS generation. Moreover, NAC effectively blocked DNA damage induced by selenite. These results revealed that ROS might play an important role in selenite-induced DNA damage that can be reduced by NAC treatment.

Related Research