Effects of selenium on lipid peroxidation, DNA damage, and apoptosis induced by fluoride in human hepatocytes

The lipid peroxidation(LPO)level, reduced glutathione(GSH) content, DNA damage, apoptosis, and cell cycle in hepatocytes of each group were measured after hepatocytes were incubated with fluoride(80#mu#g/m) and /or selenium(1.73#mu#g/ml) for 12 hours in vitro. The LPO levels(2.88+-0.59 nM MDA/mg. prot),percentages of DNA damage (59.0%) and apoptotic hepatocytes(15.56%+-2.06%),and the number of cells in S phase(4.82%+-0.45%) were higher in the cells of the F group than these in the control group, but the GSH content(4.23+_0.78)#mu#g/mg. prot was lower in the F group than in the control group. These results suggest that flouride treatment has an increased toxicity to the cells. On the other hand, selnium can antagonize these aspects of toxicity of luoride through raising GSH content, reducing LPO level, percentages of DNA damage and apoptosis, and the number of cells in S phase. Fluoride treatment can cause hepatocyte damage, whereas selenium can antagonize lipid peroxiation, DNA damage, and apoptosis of hepatocytes induced by fluor