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何云, 庄志雄, 张锦周, 杨琨, 甘德秀. DNA修复酶hMSH2缺陷与细胞遗传不稳定性[J]. 中国公共卫生, 2003, 19(10): 1202-1204.
引用本文: 何云, 庄志雄, 张锦周, 杨琨, 甘德秀. DNA修复酶hMSH2缺陷与细胞遗传不稳定性[J]. 中国公共卫生, 2003, 19(10): 1202-1204.
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HE Yun, ZHUANG Zhi-xiong, ZHANG Jin-zhou, . hMSH2 deficiency of DNA repair enzyme and cell genetic stability[J]. Chinese Journal of Public Health, 2003, 19(10): 1202-1204.
Citation: HE Yun, ZHUANG Zhi-xiong, ZHANG Jin-zhou, . hMSH2 deficiency of DNA repair enzyme and cell genetic stability[J]. Chinese Journal of Public Health, 2003, 19(10): 1202-1204.
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DNA修复酶hMSH2缺陷与细胞遗传不稳定性

hMSH2 deficiency of DNA repair enzyme and cell genetic stability

    摘要
  • 摘要:
      目的   研究hMSH2酶缺陷与细胞遗传不稳定性的关系。
      方法   测定hMSH2酶正常细胞HLF与hMSH2酶缺陷细胞人胚肺成纤维细胞(HLFS)在甲基甲磺酸(MMS)染毒后的半数抑制浓度(IC50)、核异常率及微核率。
      结果   HLF细胞24hIC50约为7.90μmol/L, 人胚肺成纤维细胞(HLFS)细胞24hIC50约为89.13μmol/L; 2种细胞的微核率均随染毒剂量的增加而升高, 且呈正相关(P < 0.05);2种细胞中、高剂量组与对照组相比, 微核率均有显著性差异(P < 0.05或P < 0.01), 而低剂量组均无显著性差异(P > 0.05);HLFS细胞微核率总体上较HLF细胞高, 但是2者之间无显著性差异(P=0.08), 染毒与转染之间无交互效应。核异常率没有随MMS染毒剂量的增加而升高的趋势; 不同染毒剂量组HLFS的核异常率均明显高于HLF细胞(P < 0.01);2种细胞染毒剂量组与对照组相比核异常率在统计学上均无显著性差异(P > 0.05)。
      结论   DNA修复酶hMSH2缺陷导致烷化耐受、核异常率及微核率增加, 提示hMSH2酶缺陷可增加细胞遗传不稳定性。

     

    Abstract:
      Objective   To study the relationship between hMSH2-deficiency and cell genetic instability.
      Methods   After being administered by methyl methanesulphonate (MMS), 50% inhibitory concentration (IC50) of cell viability, rates of abnormal nuclei and that of micronuclei (MN) were detected in HLF and HLFS.
      Results   The IC50 and HLF to MMS in 24 hours was 7.9 0 μmol/L, while that of HLFS was 89.13 μmol/L.Six dose groups of both HLF and HLFS were assessed, in which there were positive dose-effect relationships between the rates of micronuclei and doses (P < 0.05).The rates of micronuclei were different significantly (P < 0.05 or P < 0.01) between middle and high dose groups v.s control group in either HLF or HLFS. The rates of micronuclei were different significantly between HLF and HLFS in 4μmol/L and 8μmol/L group, while that in 1 μmol/L and 2 μmol/L group showed no difference. The rates of micronuclei in HLFS seem higher than that in HLF, but no statistically significant difference was observed, while no interaction between administration and transfection (P > 0.05) was found. In all of the dose groups, the rates of abnormal nuclei in HLFS were higher significantly than that in HLF (P=0.000). There was no significant difference in rates of abnormal nuclei between administering group and control group. Intotal, the rates of abnormal nuclei in HLFS were higher than that in HLF significantly (P < 0.01).In term of forming abnormal nuclei, there were no interation between administration and transfection and no dose-effect relationship between rates of abnormal nuclei and doses.
      Conclusion   The hMSH2 deficiency of DNA repair enzyme resulted in alkylation tolerance, rates of abnormal nuclei and micronuclei increasing, which suggested that hMSH2 deficiency may increase the cellular genetic instability.

     

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