Toxicity caused by the heavy metal Cadmium leads to liver diseases; this finding has generated interest among researchers. We detected DNA methylation using Whole Genome Bisulfite Sequencing (WGBS) to study the relationship between Cadmium exposure and liver damage. Forty-eight Sprague-Dawley rats were randomly divided into six groups, and given normal saline or 2.5, 5, 10, 20, and 40 mg/kg body weight per day CdCl2 by gavage. Twelve weeks later, their liver tissues were collected for pathological examination and DNA extraction. Increased exposure to Cadmium led to a reduction in the amount of weight gain as well as pathological degeneration and necrosis of liver cells of the rats. Using WGBS, we found that DNA methylation changes in the high-dose exposure group were more remarkable, and most of the changes occurred in the gene promoter region. GO enrichment analysis showed that the genes were enriched in the biological process of "response to stimulus." KEGG analysis revealed that metabolic pathways, like MAPK, PI3K-Akt and cAMP, had the largest number of enriched genes. Using Integrative Genomics Viewer (IGV), the demethylation of F2rl3 after Cadmium poisoning was established. This finding may explain why there are changes in liver metabolism after Cadmium poisoning.

中文翻译：

---

镉通过改变代谢途径中的 DNA 甲基化状态导致肝病

重金属镉引起的毒性导致肝脏疾病；这一发现引起了研究人员的兴趣。我们使用全基因组亚硫酸氢盐测序 (WGBS) 检测 DNA 甲基化，以研究镉暴露与肝损伤之间的关系。48 只 Sprague-Dawley 大鼠随机分为 6 组，分别给予生理盐水或 2.5、5、10、20 和 40 mg/kg 体重每天 CdCl2 灌胃。十二周后，收集他们的肝组织进行病理检查和 DNA 提取。镉暴露增加导致大鼠体重增加量减少以及肝细胞病理性变性和坏死。使用WGBS，我们发现高剂量暴露组DNA甲基化变化更为显着，且大部分变化发生在基因启动子区域。GO富集分析表明，基因在“对刺激作出反应”的生物过程中富集。KEGG 分析显示代谢途径，如 MAPK、PI3K-Akt 和 cAMP，具有最多数量的富集基因。使用 Integrative Genomics Viewer (IGV)，建立了镉中毒后 F2rl3 的去甲基化。这一发现或许可以解释镉中毒后肝脏代谢发生变化的原因。