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DNA氧化损伤诱导的肿瘤发生中的作用，我们使用Ogg 1-，Mth 1-，Msh 2-或Trp 53-缺陷小鼠进行了KBrO 3诱导的肿瘤发生实验。与野生型和杂合子小鼠相比，我们观察到Msh 2或Trp 53缺陷小鼠小肠中肿瘤形成增强。这些结果表明，除了Mutyh，Msh 2和p53参与抑制氧化应激诱导的小鼠肠道肿瘤发生。与野生型小鼠相比，Ogg 1或Mth 1缺陷小鼠的肿瘤数量略有增加，这表明Ogg 1和Mth 1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.