中文摘要：

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、20 mmol/L）苯分别染毒骨髓细胞2、4、6 h;tBHQ预处理组：骨髓细胞染苯前先行tBHQ（100 μmol/L）预处理12 h.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Ⅰ/Ⅱ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、20 mmol/L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、20 mmol/L苯染毒2 h及10、15、20 mmol/L苯染毒4 h和5、10、15、20 mmol/L苯染毒6 h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）;tB-HQ预处理组骨髓细胞内NQO1活力（1.62±0.16 mg pro^-1·min^-1）高于对照组（0.95±0.08 mg pro^-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.

英文摘要：

Objective To investigate the protective effect of tert-butylhydroquinone on bone marrow cells in rats from cytotoxicity induced by benzene in vitro. Methods The bone marrow cells in rats were divided into two groups randomizedly. Cells of the control group were stimulated by 0,5,10,15,20 mmol/L benzene for 2,4,6 hours respectively ,Cells of the tBHQ-pretreated group were treated by 100 μmol/L tBHQ for 12 hours followed by the same, conditions as the control group, The DNA damage was detected by single cell gel electrophoresis assay （SCGE） and cell apoptosis was examined by flow cytometry. The activities of NAD （P）H： quinone oxidoreduclase （NQO1） in bone marrow cells of rats were also measured before benzene treatment in two groups. Results In control group, the DNA damage and the apoptosis of bone marrow cells was increased with the growing concentration and time of bonzene treatment. The DNA migration and the lengths of DNA migration of the bone marrow cells in the rats under 5,10,15,20 mmol/L benzene treatment in the tBHQ preheated group were significantly lower than those in control group at the same time point （ P 〈 0.05）. The apoptosis of the bone marrow cells in the rats stimulated by 15,20 mmol/L bonzene for 2 hours and 10, 15,20 mmol/L benzene for 4 hours as well as 5, 10, 15,20 mmol/L benzene for 6 hours were also significantly lower than those in control group （ P 〈 0.05）. The activities of NQO1 in the bone marrow cells in the rats were increased after tBHQ treatment（ P 〈 0.01 ） （ 1.62 ± 0.16 min^-1·mg^-1 vs. the control group：0.95 ± 0.08 min^-1 · mg^-1 ）. Conclusion The benzene can induce the DNA damage and the apoptosis of bone marrow cells in rats in a time dependent and dose dependent manner to some extent. The tBHQ can protect the bone marrow cells in rats from the cytotoxicity induced by benzene, which can be partly explained by the increase of the NQO1 activity induced by tBHQ.