摘要
瞄准：到学习，氧化应力， DNA 损坏和 apoptosis 以及房间上的氟化物的效果老鼠骑车口头的粘膜房间和 hepatocytes。方法：称 80-120 g 的十只男 SD 老鼠随机被划分成控制组和氟化物组， 5 个动物每个组。在氟化物组的动物免费使用包含 150 mg/L 氟化钠(NaF ) 的 deionized。在控制组的动物被给蒸溜水。四个星期以后，动物被打死。在口头的粘膜和肝的反应的氧种类(ROS ) 被 Fenton 反应测量，类脂化合物每氧化产品， malondialdehyde (MDA ) ，被 thiobarbituric 酸(TBA ) 检测反应，减少的谷胱甘肽(GSH ) 是由 dithionitrobenzoic 酸(DTNB ) 的 assayed 反应。在口头的粘膜房间和 hepatocytes 的 DNA 损坏被单个房间胶化(SCG ) 决定电气泳动或彗星试金。在口头的粘膜房间和 hepatocytes 的 Apoptosis 和房间周期被流动血细胞计数检测。结果：在口头的粘膜和氟化物组的肝织物的 ROS 和 MDA 的内容比控制组的那些显著地高(P 【
0.01 ) ，但是 GSH 的水平显著地被减少(P 【
0.01 ) 。 ROS ， MDA 和 GSH 的内容是( 134.73 +/- 12.63 ) U/mg 蛋白质，( 1.48 +/- 0.13 ) mmol/mg 蛋白质并且( 76.38 +/- 6.71 )在口头的粘膜的 mmol/mg 蛋白质分别地，并且( 143.45 +/- 11.76 ) U/mg 蛋白质，( 1.44 +/- 0.12 ) mmol/mg 蛋白质并且( 78.83 +/- 7.72 )在肝织物的 mmol/mg 蛋白质分别地。在氟化物组的 DNA 损坏率在口头的粘膜房间是 50.20% 并且 44.80% 在 hepatocytes，比那些高在控制组(P 【
0.01 ) 。在口头的粘膜房间的 apoptosis 率是(13.63 +/- 1.81 ) 在氟化物组的 % ，并且(12.76 +/- 1.67 ) 在 hepatocytes 的 % ，比那些高在控制组。过量氟化物能不同地在 G0/G1 和 S G2/M 阶段降低口头的粘膜房间和 hepatocytes 的数字(P 【
0.05 ) 。结论：过量氟化物罐头导致氧化应力和 DNA 损坏并且在老鼠导致 apoptosis 和房间周期变化口头的粘膜房间和 hepatocytes。
AIM： To study the effect of fluoride on oxidative stress, DNA damage and apoptosis as well as cell cycle of rat oral mucosal cells and hepatocytes.
METHODS： Ten male SD rats weighing 80N120 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 sodium fluoride （NaF）. The animals in control group were given distilled water. Four weeks later, the animals were killed. Reactive oxygen species （ROS） in oral mucosa and liver were measured by Fenton reaction, lipid peroxidation 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 hepatocytes was determined by single cell gel （SCG） electrophoresis or comet assay. Apoptosis and cell cycle in oral mucosal cells and hepatocytes were detected by flow cytometry.
RESULTS： The contents of ROS and MDA in oral mucosa and liver tissue of fluoride group were significantly higher than those of control group （P〈 0.01）, but the level of GSH was markedly decreased （P〈 0.01）. The contents of ROS, 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, （1.44：1：0.12） mmol/mg protein and （78.83±7.72） mmol/mg protein in liver tissue respectively. The DNA damage rate in fluoride group was 50.20% in oral mucosal cells and 44.80% in hepatocytes, higher than those in the control group （P 〈0.01）. The apop- tosis rate in oral mucosal cells was （13.63 ＋ 1.81） % in fluoride group, and （t2.76＋ 1.67） % in hepatocytes, higher than those in control group. Excess fluoride could differently lower the number of oral mucosal cells and hepatocytes at G0/G1 and S G2/M phases （P〈 0.05）.
CONCLUSION： Excess fluoride can induce oxidative stress and DNA damage and lead to apoptosis and cell cycle change in rat oral mucosal cells and hepatocytes.
