摘要
[目的 ]研究硒对氟致离体培养人肝细胞脂质过氧化、DNA损伤及诱导凋亡的作用。 [方法 ]体外培养的正常人肝细胞分别接触 80 μg/ml氟化钠和 /或 1.73 μg/ml亚硒酸钠 12h后 ,检测细胞脂质过氧化物 (LPO)水平、还原型谷胱甘肽 (GSH)含量、细胞DNA损伤率、凋亡率和细胞周期构成比的情况。 [结果 ]氟组肝细胞LPO( 2 .88± 0 .5 9)nmolMDA/mg·prot、DNA损伤率 5 9.0 %、凋亡率 15 .5 6%± 2 .0 6%和S期细胞数 4.82 %± 0 .45 % ,均明显高于对照组 ,而GSH含量 ( 4 .2 3± 0 .78) μg/mg .prot则明显低于对照组 ;硒通过增加细胞GSH含量 ,降低LPO水平、DNA损伤率、凋亡率和S期细胞数而拮抗氟产生的毒性作用。 [结论 ]一定剂量的硒可拮抗氟所诱导的脂质过氧化、DNA损伤与细胞凋亡。
Objective] To evaluate the antagonistic effects of selenium on lipid peroxidation,DNA damage,and apoptosis induced by fluoride in human hepatocytes. [Methods] 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 μg/m) and/or selenium(1.73 μg/ml) for 12 hours in vitro. [Results] 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)μg/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, selenium can antagonize these aspects of toxicity of fluoride through raising GSH content,reducing LPO level,percentages of DNA damage and apoptosis,and the number of cells in S phase. [Conclusion] Fluoride treatment can cause hepatocyte damage,whereas selenium can antagonize lipid peroxidation,DNA damage,and apoptosis of hepatocytes induced by fluoride.
出处
《环境与职业医学》
CAS
北大核心
2004年第3期205-207,共3页
Journal of Environmental and Occupational Medicine
基金
国家自然科学基金资助项目 (编号 :30 2 71 1 55)
关键词
硒
氟
肝细胞
脂质过氧化
DNA损伤
细胞凋亡
selenium
fluoride
human hepatocytes
lipid peroxidation
DNA damage
apoptosis
