AIM:To study the effect of fluoride on oxidative stress,DNA damage and apoptosis as well as cell cycle of ratoral mucosal cells and hepatocytes.METHODS:Ten male SD rats weighing 80～120 g wererandomly divided into control group and fluoride group,5 animals each group.The animals in fluoride group hadfree access to deionized water containing 150 mg/L so-dium fluoride(NaF).The animals in control group weregiven distilled water.Four weeks later,the animals werekilled.Reactive oxygen species(ROS)in oral mucosa andliver were measured by Fenton reaction,lipid peroxida-tion product,malondialdehyde(MDA),was detected bythiobarbituric acid(TBA)reaction,reduced glutathione(GSH)was assayed by dithionitrobenzoic acid(DTNB)reaction.DNA damage in oral mucosal cells and hepa-tocytes was determined by single cell gel(SCG)electro-phoresis or comet assay.Apoptosis and cell cycle in oralmucosal cells and hepatocytes were detected by flowcytometry.RESULTS:The contents of ROS and MDA in oral mucosaand liver tissue of fluoride group were significantly high-er than those of control group(P<0.01),but the level ofGSH was markedly decreased(P<0.01).The contents ofROS,MDA and GSH were(134.73±12.63) U/mg protein,(1.48±0.13)mmol/mg protein and(76.38±6.71)mmol/mg protein in oral mucosa respectively,and(143.45±11.76)U/mg protein,(1.444-0.12)mmol/mg protein and(78.83±7.72)mmol/mg protein in liver tissue respective-ly.The DNA damage rate in fluoride group was 50.20%in oral mucosal cells and 44.80% in hepatocytes,higherthan those in the control group(P<0.01).The apop-tosis rate in oral mucosal cells was(13.63±1.81)% influoride group,and(12.76±1.67)% in hepatocytes,higher than those in control group.Excess fluoride coulddifferently lower the number of oral mucosal cells andhepatocytes at G_0/G_1 and S G_2/M phases(P<0.05).CONCLUSION:Excess fluoride can induce oxidative stress and DNA damage and lead to apoptosis and cellcycle change in rat oral mucosal cells and hepatocytes. AIM: To study the effect of fluoride on oxidative stress, DNA damage and apoptosis as well as cell cycle of ratoral mucosal cells and hepatocytes. METHODS: Ten male SD rats weighing 80-120 g were randomly divided into control group and fluoride group, 5 animals each group. The animals in fluoride group had free access to deionized water containing 150 mg / L so-dium fluoride (NaF). the animals in control group were given distilled water. Four weeks later, the animals werekilled. Reactive oxygen species (ROS) in oral mucosa andliver were measured by Fenton reaction, lipid peroxida-tion product product, malondialdehyde (MDA), was detected by thiobarbituric acid (TBA) reaction, reduced glutathione (GSH) was assayed by dithionitrobenzoic acid (DTNB) reaction.DNA damage in oral mucosal cells and hepa-tocytes was determined by single cell gel (SCG) electro-phoresis or comet assay. Apoptosis and cell cycle in oral mucosal cells and hepatocytes were detected by flowcytometry .RESULTS: The contents of ROS and MDA in oral mucosaand live The contents of ROS, MDA and GSH were (134.73 ± 12.63) U / mg (P <0.01). The contents of ROS, MDA and GSH were significantly higher than those of control group (1.48 ± 0.13) mmol / mg protein and (76.38 ± 6.71) mmol / mg protein in oral mucosa respectively, and (143.45 ± 11.76) U / mg protein, 7.72) mmol / mg protein in liver tissue respective-ly.The DNA damage rate in fluoride group was 50.20% in oral mucosal cells and 44.80% in hepatocytes, higherthan those in the control group (P <0.01). The apop- tosis rate in oral mucosal cells was (13.63 ± 1.81)% influoride group, and (12.76 ± 1.67)% in hepatocytes higher than those in control group. Excess fluoride could be more dissimilarly lower the number of oral mucosal cells and hepaticocytes at G_0 / G_1 and S G_2 / M phases (P <0.05). CONCLUSION: Excess fluoride can induce oxidative stress and DNA damage and lead to apoptosis and cellcycle change in rat oral mucosal cells and hepatocytes.