摘要目的 探讨叔丁基对苯二酚(tBHQ)对亚砷酸钠(NaAsO2)致细胞毒性和氧化损伤的拮抗作用。方法 Chang肝细胞用tBHQ[0(对照)、5、25μmol/L]预处理24h,再用5 μmol/L tBHQ和NaAsO2[0(对照)、30、40、50、60 μmol/L]共同作用24h,采用刃天青钠(Alamar blue)还原法检测细胞活力，结果用实验组Alamar blue还原率与对照组Alamar blue还原率的相对比值表示；Chang肝细胞用tBHQ[0(对照)、5、25 μmol/L]预处理24h,再用5μmol/L tBHQ和NaAso2[0(对照)、40、50 μmol/L]共同作用24h，采用荧光探针2′，7′-二乙酰二氯荧光素(DCFH-DA)检测细胞内活性氧(ROS)的生成，结果用实验组平均荧光强度与对照组平均荧光强度的相对比值表示。结果 30、40、50、60 μmol/L的NaAsO2暴露能够显著降低细胞活力，而tBHQ预处理(5、25 μmol/L)则可明显恢复细胞活力,NaAsO2和tBHQ两因素的主效应及其交互作用均有统计学意义（F值分别为566.57、55.09、14.50，P均＜0.05）；5、25 μmol/L tBHQ预处理的30、40、50、60 μmol/LNaAsO2组细胞活力(0.75±0.02、0.70±0.04、0.59±0.03、0.43±0.03和0.75±0.02、0.73±0.03、0.65±0.02、0.50±0.02)较相应NaAsO2单独作用组(0.70±0.03、0.64±0.03、0.43±0.03、0.33±0.01)显著升高（P均＜0.05），25 μmol/L tBHQ 预处理的50、60μmol/L NaAsO2组细胞活力高于相应5μmol/L tBHQ预处理组（P均＜0.05）。40、50 μmol/L的NaAsO2能显著诱导Chang肝细胞内ROS的产生，而tBHQ预处理(5、25 μmol/L)则可使NaAsO2诱导产生的细胞内ROS水平显著下降，NaAsO2和tBHQ两因素的主效应及其交互作用均有统计学意义（F值分别为181.78、60.55、4.93，P均＜0.05）;5、25 μmol/L tBHQ预处理的40、50 μmol/L NaAsO2组细胞内ROS水平(1.87±0.09、1.80±0.07和1.36±0.11、1.44±0.12)较相应NaAsO2单独作用组(2.30±0.18、2.18±0.17)显著降低(P 均＜ 0.05)，25 μmol/L tBHQ预处理的40、50 μmol/L NaAsO2组细胞内ROS水平低于相应5μmol/L tBHQ预处理组（P均＜ 0.05）。结论 tBHQ对NaAsO2诱导的细胞毒性和氧化损伤具有一定的拮抗作用。

abstractsObjective To study the protective effects of tert-butylhydroquinone(tBHQ) on sodium arsenite (NaAsO2)-induced cytotoxicity and oxidative injuries. Methods Chang liver cells were pretreated with tBHQ[0(control), 5, 25 μmol/L]for 24 h, and then co-treated with tBHQ(5 μmol/L) together with NaAsO2[0(control),30, 40, 50, 60 μmol/L] for another 24 h, and Alamar blue reduction rates were used to evaluate cell viability,the results were expressed as the relative ratio of Alamar blue reduction rates between the experimental group and the control group. On the other hand, Chang liver cells were pretreated with tBHQ[0(control), 5, 25 μmol/L] for24 h,and then co-treated with tBHQ(5 μmol/L) together with NaAsO2[0(control), 40, 50 μmol/L] for another 24 h,and the levels of cellular reactive oxygen species(ROS) were detected by staining cells with 2',7'-dichlorofluorescin diacetate(DCFH-DA), the results were expressed as the relative ratio of mean fluorescence intensity between the experimental group and the control group. Results Cell viability decreased dramatically by treatment with NaAsO2(30, 40, 50, 60 μmol/L), while relieved to some extent by pretreatment with 5, 25 μmol/L tBHQ, the main effects of NaAsO2 and tBHQ, as well as their interaction were all statistically significant(F =566.57, 55.09, 14.50,all P ＜ 0.05) ; the cell viability of NaAsO2(30, 40, 50, 60 μmol/L) pretreated with tBHQ(5, 25 mol/L) were 0.75 ±0.02, 0.70 ± 0.04, 0.59 ± 0.03, 0.43 ± 0.03 and 0.75 ± 0.02, 0.73 ± 0.03, 0.65 ± 0.02, 0.50 ± 0.02, respectively,all significantly higher than corresponding NaAsO2 alone groups(0.70 ± 0.03, 0.64 ± 0.03, 0.43 ± 0.03, 0.33 ±0.01, all P ＜ 0.05), the cell viability of NaAsO2(50, 60 μmol/L) pretreated with 25 μmol/L tBHQ was higher than corresponding 5 μmol/L tBHQ pretreatment groups(all P ＜ 0.05). On the other hand, 40, 50 μmol/L of NaAsO2 significantly induced hepatocellular ROS generation, while tBHQ(5, 25 μ mol/L) pretreatment significantly decreased NaAsO2-induced intracellular ROS levels, the main effects of NaAsO2 and tBHQ, as well as their interaction were all statistically significant (F =181.78, 60.55, 4.93, all P ＜ 0.05) ; the ROS levels of NaAsO2(40, 50 μ mol/L) pretreated with tBHQ(5, 25 μmol/L) were 1.87 ± 0.09, 1.80 ± 0.07 and 1.36 ± 0.11, 1.44 ± 0.12,all significantly decreased than corresponding NaAsO2 alone groups(2.30 ± 0.18, 2.18 ± 0.17, all P ＜ 0.05),the ROS levels of NaAsO2(40, 50 μmol/L) pretreated with 25 μmol/L tBHQ decreased than corresponding 5 μmol/L tBHQ pretreatment groups (all P ＜ 0.05). Conclusion tBHQ has a certain antagonism on arsenic induced cytotoxicity and oxidative injuries.