Cytotoxicity and apoptosis induction in human HepG2 hepatoma cells by decabromodiphenyl ethane.
- Author:
Ru Bao SUN
1
;
Zhu Ge XI
;
Jun YAN
;
Hong Lian YANG
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Bromobenzenes; toxicity; Cell Survival; drug effects; Dose-Response Relationship, Drug; Environmental Pollutants; toxicity; Hep G2 Cells; Humans; Reactive Oxygen Species; Time Factors
- From: Biomedical and Environmental Sciences 2012;25(5):495-501
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the toxic effects of decabromodiphenyl ethane (DBDPE), used as an alternative to decabromodiphenyl ether in vitro.
METHODSHepG2 cells were cultured in the presence of DBDPE at various concentrations (3.125-100.0 mg/L) for 24, 48, and 72 h respectively and the toxic effect of DBDPE was studied.
RESULTSAs evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and lactate dehydrogenase assays and nuclear morphological changes, DBDPE inhibited HepG2 viability in a time- and dose-dependent manner within a range of 12.5 mg/L to 100 mg/L and for 48 h and 72 h. Induction of apoptosis was detected at 12.5-100 mg/L at 48 h and 72 h by propidium iodide staining, accompanied with overproduction of reactive oxygen species (ROS). Furthermore, N-acetyl-L-cysteine, a widely used ROS scavenger, significantly reduced DBDPE-induced ROS levels and increased HepG2 cells viability.
CONCLUSIONDBDPE has cytotoxic and anti-proliferation effect and can induce apoptosis in which ROS plays an important role.
