Cytotoxicity and Apoptosis Induction in Human HepG2 Hepatoma Cells by Decabromodiphenyl Ethane

Key words: 
• Apoptosis /
• Cytotoxicity /
• Decabromodiphenyl ethane /
• Flame retardants /
• Reactive oxygen species

Abstract: Objective To investigate the toxic effects of decabromodiphenyl ethane (DBDPE), used as an alternative to decabromodiphenyl ether in vitro.Methods HepG2 cells were cultured in the presence of DBDPE at various concentrations (3.125‐100.0mg/L) for 24, 48, and 72 h respectively and the toxic effect of DBDPE was studied.Results As 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 timeand 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.Conclusion DBDPE has cytotoxic and anti‐proliferation effect and can induce apoptosis in which ROS plays an important role