Zhang Ming, Wang Aiguo, Xia Tao, He Ping
MOE Key Lab of Environment and Health, Department of Occupational and Environmental Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China.
Toxicol Lett. 2008 Jun 10;179(1):1-5. doi: 10.1016/j.toxlet.2008.03.002. Epub 2008 Mar 18.
The mechanisms underlying the neurotoxicity of fluorosis still remain obscure. To investigate DNA damage, cell-cycle distribution and expression of nuclear factor kappa B (NF-kappaB) induced by fluoride, the primary rat hippocampal neurons were incubated with various concentrations (20mg/l, 40 mg/l, and 80 mg/l) of sodium fluoride for 24 h in vitro. Our results showed that olive tail moments (OTMs) were significantly elevated in all fluoride-treated groups, while significant increases in the percentage of DNA in the tail were, respectively, observed at 40 mg/l and 80 mg/l levels of fluoride. An increase in the proportion of cells in S-phase was observed in response to the treatment of 40 mg/l and 80 mg/l fluoride. Gene expression of NF-kappaB was also enhanced by fluoride treatment in a dose-dependent manner. The results indicated that fluoride could induce S-phase cell-cycle arrest, up-regulation of NF-kappaB and DNA damage in primary rat hippocampal neurons.
氟中毒神经毒性的潜在机制仍不清楚。为了研究氟化物诱导的DNA损伤、细胞周期分布及核因子κB(NF-κB)的表达,将原代大鼠海马神经元在体外与不同浓度(20mg/L、40mg/L和80mg/L)的氟化钠孵育24小时。我们的结果显示,所有氟化物处理组的橄榄尾矩(OTM)均显著升高,而在40mg/L和80mg/L氟化物水平下分别观察到尾部DNA百分比显著增加。在40mg/L和80mg/L氟化物处理后,观察到S期细胞比例增加。氟化物处理还以剂量依赖的方式增强了NF-κB的基因表达。结果表明,氟化物可诱导原代大鼠海马神经元S期细胞周期停滞、NF-κB上调及DNA损伤。