癌变·畸变·突变 ›› 2007, Vol. 19 ›› Issue (2): 89-092.doi: 10.3969/j.issn.1004-616x.2007.02.002

• 论著 • 上一篇    下一篇

热休克预处理可抑制N_甲基_N'_硝基_N_亚硝基胍对CHL细胞的遗传毒性

董正伟 胡 虎 刘广义 沈筱筠 杨 军   

  1. 1.浙江大学公共卫生学院毒理学研究所;2. 浙江大学医学院病理及病理生理教研室,浙江 杭州 310058
  • 收稿日期:2006-11-06 修回日期:2006-12-07 出版日期:2007-03-30 发布日期:2007-03-30
  • 通讯作者: 杨 军

Pre-heat Pre-heat Shock Protects CHL Cells from the Genotoxicity of N-methyl-N'-nitro-N-nitrosoguanidine

DONG Zheng-wei1,HU Hu2,LIU Guang-yi1,SHEN Xiao-jun1,YANG Jun1,   

  1. 1.Institute of Toxicology, School of Public Health, Zhejiang University;2.Department of Pathology & Pathophysiology, Zhejiang University, Hangzhou 310058,Zhejiang,China
  • Received:2006-11-06 Revised:2006-12-07 Online:2007-03-30 Published:2007-03-30
  • Contact: YANG Jun

摘要: 背景与目的: 探讨热休克是否可诱导中国仓鼠肺细胞(CHL)中γH2AX焦点的形成,以及热休克对N-甲基-N'-硝基-N-亚硝基胍(MNNG)诱导γH2AX焦点形成的影响。 材料与方法: 用MTT实验检测热休克处理后细胞的生存率,用免疫荧光及流式细胞术检测细胞的γH2AX焦点的形成。 结果: MTT结果表明热休克对CHL细胞有细胞毒性作用;免疫荧光实验发现热休克处理后细胞中γH2AX焦点数量与对照组相比无显著差异(P>0.05);流式细胞检测结果发现经过热休克预处理再经MNNG处理的细胞与只经过MNNG处理的细胞相比,γH2AX荧光强度由0.316±0.042下降为0.194±0.011,其差异有统计学意义(P<0.05)。 结论: 热休克可以使CHL细胞死亡,但是并不引起细胞的遗传毒性;热休克预处理可减少MNNG所诱导的γH2AX焦点的形成。

关键词: 热休克, γH2AX, DNA损伤, 遗传毒性

Abstract: BACKGROUND & AIM: To study whether heat shock could induce the formation of γH2AX foci in CHL cells, and the effect of heat shock on N-methyl-N'-nitro-N-nitrosoguanidine(MNNG)-induced γH2AX foci formation. MATERIALS AND METHODS: The cytotoxic effect of heat shock was evaluated by MTT test.The phosphorylation of γH2AX was assessed using immunofluorescent microscopy and flow cytometry. RESULTS: MTT test showed that heat shock decreased cell viability.There was no significant difference in the number of γH2AX foci between heat-shock treated group and control group as shown by immunofluorescent microscopy. Flow cytometry analysis revealed that pre-heat shock followed by MNNG treatment decreased the mean γH2AX fluorescent intensity from 0.316±0.042 in the MNNG-treatment alone group to 0.194±0.011. CONCLUSION: Heat shock did not induce γH2AX foci formation in CHL cells.In addition, heat shock could inhibit the phosphorylation of H2AX induced by MNNG.

Key words: heat shock, γH2AX, DNA damage, genotoxicity

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