摘要
目的 研究氟对人胚肝细胞 (L 0 2细胞 )氧化应激、DNA损伤及诱导凋亡的作用。方法 体外培养的L 0 2细胞接触 40、 80、 160 μg/ml氟化钠 2 4h ,检测L 0 2细胞脂质过氧化物 (LPO)水平 ,还原型谷胱甘肽 (GSH )含量 ,DNA损伤率 ,细胞凋亡率和周期构成比的情况。结果 氟可使L 0 2细胞LPO水平升高 ,GSH含量下降 ,并且二者均与氟浓度呈明显的剂量 效应关系 ;氟可使L 0 2细胞DNA损伤率、凋亡率和S期细胞数明显升高 ,高剂量氟组DNA损伤率和凋亡率与低剂量氟组之间存在显著性差异。结论 氟可致L 0 2细胞出现氧化应激 ,引起DNA损伤 ,诱导细胞凋亡 。
Objective To investigate the effects of flu or ide on oxidative stress, DNA damage and apoptosis in human embryo hepatocytes (L -02 cell). Methods The lipid peroxidation (LPO) level and reduced glutathi one (GSH) content, DNA damage,apoptosis and cell cycle in cells were measured a fter L-02 cell were incubated with 40, 80, and 160 μg/ml sodium fluoride for 2 4 h. Results Fluoride could increase the LPO level and reduce GSH co ntent in cells in the time- and dose-dependent manner. Fluoride could also enh ance the percentage of DNA damage, the percentage of apoptosis, and the cell num ber in S phase in the cells. The percentages of DNA damage and apoptosis in high -dose fluoride-treated group was significantly higher than in the low-dose fl uoride-treated group. Conclusion Fluoride can activate oxidati ve stress, DNA damage, and apoptosis of L-02 cell in a time- and dose-depende nt manner.
出处
《华中科技大学学报(医学版)》
CAS
CSCD
北大核心
2003年第6期585-588,共4页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
国家自然科学基金资助项目 (No .3 0 2 71155)