Oxidative stress-induced tumorigenesis in the small intestines of various types of DNA repair-deficient mice

为了阐明DNA修复基因在抑制氧化DNA损伤诱导的肿瘤发生中的作用，我们使用Ogg1-、Mth1-、Msh2-或trp53缺陷小鼠进行了kbro3诱导的肿瘤发生实验。我们观察到，与野生型和杂合型小鼠相比，Msh2-或trp53缺陷小鼠的小肠肿瘤形成增强。这些结果表明，除Mutyh外，Msh2和p53也参与了小鼠氧化应激诱导的肠道肿瘤发生的抑制。与野生型小鼠相比，Ogg1-或Mth1缺陷小鼠的肿瘤数量略有增加，这表明Ogg1和Mth1可能在抑制氧化应激引起的肠道肿瘤发生中发挥有限的作用。

To elucidate the roles of DNA repair genes in the suppression of oxidative DNA damage-induced tumorigenesis, we performed KBrO3-induced tumorigenesis experiments using Ogg1-, Mth1-, Msh2- or Trp53-deficient mice. We observed an enhanced tumor-formation in the small intestines of Msh2- or Trp53-deficient mice, as compared with the wild type and heterozygous mice. These results indicate that in addition to Mutyh, Msh2 and p53 are involved in the suppression of oxidative stress-induced intestinal tumorigenesis in mice. The number of tumors was marginally increased in Ogg1- or Mth1-deficient mice, in comparison to the wild-type mice, suggesting that Ogg1 and Mth1 may play a limited role in the suppression of intestinal tumorigenesis caused by oxidative stress.