...
首页> 外文期刊>Archives of Toxicology >SnCl2-induced DNA damage and repair inhibition of MMS-caused lesions in V79 Chinese hamster fibroblasts
【24h】

SnCl2-induced DNA damage and repair inhibition of MMS-caused lesions in V79 Chinese hamster fibroblasts

机译:SnCl 2 诱导的V79中国仓鼠成纤维细胞DNA损伤及MMS损伤修复

获取原文
获取原文并翻译 | 示例
           

摘要

In order to clarify the molecular mechanisms of Sn2+ genotoxicity, we evaluated the induction of strand breaks, formamidopyrimidine DNA glycosylase (Fpg) and endonuclease III (Endo III) sensitive sites, and the interference with the repair of methyl methane sulfonate (MMS)-caused DNA damage in V79 Chinese hamster lung fibroblasts exposed to stannous chloride by comet assay. A concentration-related increase in the DNA damage induced by 2 h SnCl2 treatment at a concentration range of 50–1,000 μM was observed (r = 0.993; P < 0.01). Significantly elevated DNA migration in relation to the control level was detected at doses 100, 500 and 1,000 μM in normal alkaline and at doses 500 and 1,000 μM in modified (with Fpg and Endo III) comet assay. Although 50 μM SnCl2 concentration did not increase significantly the DNA migration by itself in comet assay, it was capable to inhibit the repair of MMS-induced DNA damage during the post-treatment period of 24 h. Our results demonstrate the genotoxic and comutagenic effects of stannous chloride in V79 cells. The inhibitory effect of Sn2+ on repair of MMS-induced DNA damage suggests that this metal can also interfere in DNA repair systems thus contributing to increased mutation by shifting the balance from error-free to error-prone repair processes.
机译:为了阐明Sn 2 + 遗传毒性的分子机制,我们评估了链断裂,甲酰胺基嘧啶DNA糖基化酶(Fpg)和内切核酸酶III(Endo III)敏感位点的诱导以及对修复的干扰彗星试验检测甲基磺酸甲酯(MMS)引起暴露于氯化亚锡的V79中国仓鼠肺成纤维细胞的DNA损伤在浓度范围为50–1,000μM的条件下,观察到2 h SnCl 2 处理引起的DNA损伤与浓度相关的增加(r = 0.993; P <0.01)。相对于对照水平,在正常碱性溶液中以100、500和1,000μM的剂量检测到DNA迁移,在改良(使用Fpg和Endo III)彗星分析中以500和1,000μM的剂量检测到。尽管50μMSnCl 2 的浓度在彗星试验中本身并未显着增加DNA迁移,但在处理后的24小时内它能够抑制MMS诱导的DNA损伤的修复。我们的结果证明了氯化亚锡在V79细胞中的遗传毒性和致癌作用。 Sn 2 + 对MMS诱导的DNA损伤修复的抑制作用表明,这种金属还可以干扰DNA修复系统,从而通过将平衡从无错变为易错而促进突变增加。维修过程。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号