硒与氟对人肝细胞凋亡和脂质过氧化的影响

目的　研究硒、氟对离体培养的人肝细胞凋亡和脂质过氧化的影响。方法　体外培养的人肝细胞分别接触一定剂量的氟和 /或硒 1 2h后 ,检测肝细胞凋亡小体百分率、细胞周期构成比、还原型谷胱甘肽 (GSH)含量和脂质过氧化物 (LPO)的水平以及培养液中LPO和乳酸脱氢酶 (LDH)、丙氨酸转氨酶 (ALT)和天冬氨酸转氨酶 (AST)的活性。结果　加氟组肝细胞凋亡小体百分率 (1 5 557±2 0 56) % ,S期细胞数 (4 82 3± 0 454) % ,肝组织和培养液中LPO水平 [分别为 (2 884± 0 589)和 (3 547± 0 561 )nmol/LMDA/mg prot) ,培养液中AST和LDH含量 (分别为 91 1± 36 4和 1 4 0 4± 7 6U/L) ,均明显高于对照组 [分别为 (1 0 31 3± 1 0 2 3) % ,(3 2 53± 0 743) % ,(1 473± 0 40 1 )nmol/LMDA/mg ,(1 694± 0 443)nmol/LMDA/mg,(54 5± 3 2 )U/L和 (1 2 6 4± 2 6)U/L] ,而氟组肝组织GSH含量则明显低于对照组 [分别为 (4 2 2 5± 0 781 ) μg/mg和 (7 595± 1 0 4 2 ) μg/mg) ;硒可通过升高GSH含量 ,降低LPO、AST、LDH水平和凋亡小体百分率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肝细胞凋亡和脂质过氧化

Effects of selenium and fluoride on apoptosis and lipid peroxidation in human hepatocytes

OBJECTIVE: To study the influence of selenium and fluoride on apoptosis and lipid peroxidation in human hepatocytes in vitro. METHODS: The apoptosis, cell cycle, GSH content and lipid peroxides (LPO) level in human hepatocytes, LPO level and LDH, AST and ALT activity in cell culture supernatants were investigated after hepatocytes were incubated with selenium and/or fluoride for around 12 hours periods in vitro. RESULTS: The percentage of hepatocyte apoptosis bodies (15.557 +/- 2.056)%, the number of cells in S phase (4.823 +/- 0.454)% and LPO level in liver tissue and supernatant [(2.884 +/- 0.589) and (3.547 +/- 0.561) nmol/L MDA/mg.prot, respectively], AST and LDH activity in supernatants (91.1 +/- 36.4 and 140.4 +/- 7.6 U/L, respectively) in the fluoride treated group was higher than the control group [(10.313 +/- 1.023)%, (3.253 +/- 0.743)%, (1.473 +/- 0.401) nmol/L MDA/mg.prot, (1.694 +/- 0.443) nmol/L MDA/mg.prot, (54.5 +/- 3.2) U/L and (126.4 +/- 2.6) U/L, respectively], The GSH content in live tissue [(4.225 +/- 0.781) microgram/mg.prot] is lower than control group [(7.595 +/- 1.042) microgram/mg.prot]. Selenium treatment reduced these kinds of toxicity of fluoride through raising GSH content, reducing LPO level, LDH and AST activity and percentage of apoptosis bodies. CONCLUSIONS: Selenium can antagonist apoptosis and lipid peroxidation of hepatocytes induced by fluoride.