中文摘要：

[目的]研究三（2-氯乙基）磷酸酯[tris（2-chloroethyl）phosphate,TCEP]对肝细胞线粒体功能的影响。[方法]用0.00（溶剂对照组）、3.12、12.50、50.00和200.00 mg/L TCEP分别处理人正常肝细胞（L02细胞）和人肝癌细胞（Hep G2细胞）24 h和48 h。测定细胞活力、线粒体内活性氧水平、线粒体DNA拷贝数、线粒体膜电位和胞内游离钙（Ca2＋）水平以及胞内ATP的浓度。[结果]与相应溶剂对照组相比,在24 h,200.00 mg/L TCEP处理组L02细胞活力降低（P〈0.05）,≥12.50 mg/L TCEP处理组Hep G2细胞活力降低（P〈0.05）;在48 h,50.00 mg/L和200.00 mg/L TCEP处理组两种细胞活力降低（P〈0.05）。所有TCEP处理组两种细胞的线粒体DNA拷贝数均减少（P〈0.05或P〈0.01）。在24 h,所有TCEP处理组两种细胞的线粒体膜电位均下降（P〈0.05或P〈0.01）。在24 h,200.00 mg/L TCEP处理组两种细胞胞内游离Ca2＋水平均升高（P〈0.01）;在48 h,50.00 mg/L和200.00 mg/L TCEP处理组两种细胞胞内游离Ca2＋均升高（P〈0.01）。在24 h和48 h,200.00 mg/L TCEP处理组L02胞内ATP水平降低（P〈0.05）;在24 h,50.00 mg/L和200.00 mg/L TCEP处理组Hep G2胞内ATP浓度下降（P〈0.05或P〈0.01）。[结论]一定浓度的TCEP可致肝细胞线粒体损伤和线粒体功能指标异常,提示TCEP有肝细胞线粒体毒性。

英文摘要：

[ Objective ] To evaluate effects of tris（2-chloroethyl）phosphate （TCEP） on mitochondrial functions in liver cells. [ Methods ] At 24 and 48h after L02 and HepG2 cells were treated with 0.00 （solvent control group）, 3.12, 12.50, 50.00, 200.OOmg/L TCEP, we detected cell viability, mitochondrial reactive oxygen species （mtROS） levels, mitochondrial DNA copy numbrane, mitochondrial membrane potential, intracellular free Ca2＋ levels, and intracellular ATP level. [ Results ] Compared with the control group, TCEP decreased the cell viabilities of L02 cells in the 200 mg/L TCEP group （P 〈 0.05） and the cell viabilities of HepG2 cells in the ≥ 12.50mg/L TCEP groups （P〈0.05） at 24h; decreased the cell viabilities of L02 and HepG2 cells in the 50.00 and 200.00 mg/L TCEP groups at 48 h （P 〈 0.05）; reduced the mitochondrial DNA number of L02 and HepG2 cells in all treatment groups （P 〈 0.05 or P 〈 0.01）; decreased the mitochondrial membrane potential of L02 or HepG2 cells in all treatment groups at 24 h （P〈 0.05 or P 〈 0.01）; increased the intracellular free Ca2＋ concentrations of L02 and HepG2 cells only in the 200.00mg/L TCEP group at 24h and in the 50.00 and 200.00 mg/L groups at 48 h （P 〈 0.01）; decreased the intracellular ATP levels of L02 cells only in the 200.00 mg/L TCEP group at 24 and 48 h （P 〈 0.05） and in the 50.00 and 200.00 mg/L TCEP groups of HepG2 cells at 24 and 48 h （P 〈 0.05 or P 〈 0.01）. [ Conclusion ] A certain concentrations of TCEP could cause mitochondrial damage and abnormal changes in indices reflecting mitochondrial dysfunctions, implying that TCEP could induce mitochondrial toxicity in hepatocytes.