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首页> 外文期刊>Nanotoxicology >Differential effects of silver nanoparticles on DNA damage and DNA repair gene expression in Ogg1-deficient and wild type mice
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Differential effects of silver nanoparticles on DNA damage and DNA repair gene expression in Ogg1-deficient and wild type mice

机译：银纳米粒子对OGG1缺陷和野生型小鼠DNA损伤和DNA修复基因表达的差异效应

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Due to extensive use in consumer goods, it is important to understand the genotoxicity of silver nanoparticles (AgNPs) and identify susceptible populations. 8-Oxoguanine DNA glycosylase 1 (OGG1) excises 8-oxo-7,8-dihydro-2-deoxyguanine (8-oxoG), a pro-mutagenic lesion induced by oxidative stress. To understand whether defects in OGG1 is a possible genetic factor increasing an individual's susceptibly to AgNPs, we determined DNA damage, genome rearrangements, and expression of DNA repair genes in Ogg1-deficient and wild type mice exposed orally to 4mg/kg of citrate-coated AgNPs over a period of 7d. DNA damage was examined at 3 and 7d of exposure and 7 and 14d post-exposure. AgNPs induced 8-oxoG, double strand breaks (DSBs), chromosomal damage, and DNA deletions in both genotypes. However, 8-oxoG was induced earlier in Ogg1-deficient mice and 8-oxoG levels were higher after 7-d treatment and persisted longer after exposure termination. AgNPs downregulated DNA glycosylases Ogg1, Neil1, and Neil2 in wild type mice, but upregulated Myh, Neil1, and Neil2 glycosylases in Ogg1-deficient mice. Neil1 and Neil2 can repair 8-oxoG. Thus, AgNP-mediated downregulation of DNA glycosylases in wild type mice may contribute to genotoxicity, while upregulation thereof in Ogg1-deficient mice could serve as an adaptive response to AgNP-induced DNA damage. However, our data show that Ogg1 is indispensable for the efficient repair of AgNP-induced damage. In summary, citrate-coated AgNPs are genotoxic in both genotypes and Ogg1 deficiency exacerbates the effect. These data suggest that humans with genetic polymorphisms and mutations in OGG1 may have increased susceptibility to AgNP-mediated DNA damage.
机译：由于消费品广泛使用，重要的是要理解银纳米颗粒（AgNP）的遗传毒性并鉴定敏感群体。 8-氧基川DNA糖基糖基酶1（OGG1）促进8-氧代-7,8-二氢-2-脱氧（8- oxog），通过氧化应激诱导的促致诱变病变。要了解OGG1中的缺陷是否是可能的遗传因子增加个体易受侵略于agnps的遗传因素，我们确定了OGG1缺陷型和野生型小鼠中的DNA损伤，基因组重排和DNA修复基因的表达，并露出口服的4mg / kg柠檬酸盐涂层agnps在7d时期。在暴露的3和7D和7D暴露后检查DNA损伤。 AGNP诱导8-氧代，双链断裂（DSB），染色体损伤和双基因型中的DNA缺失。然而，在OGG1缺陷小鼠之前之前诱导8氧，在7-D处理后的8-氧气水平较高，曝光终止后持续更长时间。 AgNP下调DNA糖基酶OGG1，Neil1和Neil2在野生型小鼠中，但在OGG1缺陷小鼠中上调MyH，Neil1和Neil2糖基酶。 Neil1和Neil2可以修复8 oleg。因此，野生型小鼠中DNA糖基酶的AgNP介导的下调可能有助于遗传毒性，而OGG1缺陷小鼠的上调可以用作对AgNP诱导的DNA损伤的适应性反应。但是，我们的数据表明，OGG1对于AGNP诱导的损伤有效修复是必不可少的。总之，拟柠檬酸盐的AgNPS在基因型中是基因毒性，并且OGG1缺乏加剧了效果。这些数据表明，具有遗传多态性和OGG1中突变的人可能对AgNP介导的DNA损伤增加了易感性。

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