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目的探讨叔丁基对苯二酚(tBHQ)对苯诱导的骨髓细胞毒性的保护作用。方法体外培养的大鼠骨髓细胞随机分为对照组和tBHQ预处理组,对照组:以不同浓度(0、5、10、15、20mmolL)苯分别染毒骨髓细胞2、4、6h;tBHQ预处理组:骨髓细胞染苯前先行tBHQ(100μmolL)预处理12h。单细胞凝胶电泳法检测骨髓细胞DNA损伤,流式细胞仪检测骨髓细胞凋亡率,2,6二氯靛酚还原法测定苯染毒前两组骨髓细胞内依赖还原型辅酶ⅠⅡ醌氧化还原酶(NQO1)的活力。结果对照组中随苯染毒浓度的增加、染毒时间的延长,骨髓细胞DNA损伤增强,细胞凋亡率增加。tBHQ预处理组中5、10、15、20mmolL苯染毒骨髓细胞的DNA迁移率和迁移度低于同浓度、同时间点的对照组,差异有统计学意义(P<0.05);15、20mmolL苯染毒2h及10、15、20mmolL苯染毒4h和5、10、15、20mmolL苯染毒6h骨髓细胞的凋亡率较同浓度、同时间点的对照组降低,差异有统计学意义(P<0.05);tBHQ预处理组骨髓细胞内NQO1活力(1.62±0.16mgpro-1·min-1)高于对照组(0.95±0.08mgpro-1·min-1),差异有统计学意义(P<0.01)。结论苯可诱导体外培养的大鼠骨髓细胞DNA损伤和细胞凋亡,并呈现一定的时间、剂量依赖性;tBHQ可诱导骨髓细胞NQO1活力增强,对苯诱导的骨髓细胞毒性有保护作用。
Objective To investigate the protective effect of t-butyl hydroquinone (tBHQ) on benzene-induced bone marrow cytotoxicity. Methods Rat bone marrow cells cultured in vitro were randomly divided into control group and tBHQ preconditioning group. Control group: BMSCs were exposed to different concentrations (0, 5, 10, 15, 20mmolL) Treatment group: Bone marrow cells pretreated with benzene before tBHQ (100μmolL) pretreatment 12h. Single cell gel electrophoresis was used to detect the DNA damage of bone marrow cells. Flow cytometry was used to detect the apoptosis rate of bone marrow cells. The 2,6-dichlorophenol-indophenol reduction method was used to determine the intracellular free-endoribonuclease-coenzyme I II quinone redox Enzyme (NQO1) activity. Results In the control group, with the increase of the concentration of benzene exposure and the prolongation of exposure time, the DNA damage of bone marrow cells increased and the apoptosis rate increased. In the tBHQ preconditioning group, the DNA mobility and migration of 5, 10, 15, 20mmolL benzene-contaminated bone marrow cells were lower than the same concentration at the same time point, the difference was statistically significant (P <0.05); 15,20mmolL The apoptosis rates of bone marrow cells exposed to benzene for 2h and 10,15,20mmolL benzene for 4h and 5,10,15,20mmolL benzene for 6h were lower than those of the control group at the same time points, with significant difference ( P <0.05). The activity of NQO1 in bone marrow cells (1.62 ± 0.16mgpro-1 · min-1) in tBHQ pretreatment group was significantly higher than that in control group (0.95 ± 0.08mgpro-1min-1) <0.01). Conclusion Benzene can induce DNA damage and apoptosis in cultured rat bone marrow cells in vitro and in a dose- and time-dependent manner. TBHQ can induce the enhanced NQO1 activity in bone marrow cells and protect the myeloid cells induced by benzene.