全氟辛烷
小桶
基因
生物途径
转录组
生物
信号转导
代谢途径
细胞生物学
计算生物学
生物化学
化学
基因表达
磺酸盐
有机化学
钠
作者
Tianrun Wang,Xuying Zhao,Tianze Liu,Jiguang Zhang,Jing Qiu,Mei Li,Rui Weng
出处
期刊:Chemosphere
[Elsevier]
日期:2023-04-06
卷期号:329: 138629-138629
被引量:3
标识
DOI:10.1016/j.chemosphere.2023.138629
摘要
Perfluorooctane sulfonate (PFOS) was widely used in industrial applications before it was listed as a persistent organic pollutant by the Conference of the Parties in the Stockholm Convention in 2009. Although the potential toxicity of PFOS has been studied, its toxic mechanisms remain largely undefined. Here, we investigated novel hub genes and pathways affected by PFOS to gain new conceptions of the toxic mechanisms of PFOS. Reduced body weight gain and abnormal ultra-structures in the liver and kidney tissues were spotted in PFOS-exposed rats, indicating successful establishment of the PFOS-exposed rat model. The transcriptomic alterations of blood samples upon PFOS exposure were analysed using RNA-Seq. GO analysis indicates that the differentially expressed gene-enriched GO terms are related to metabolism, cellular processes, and biological regulation. Kyoto encyclopaedia of gene and genomes (KEGG) and gene set enrichment analysis (GSEA) were conducted to identify six key pathways: spliceosome, B cell receptor signalling pathway, acute myeloid leukaemia, protein processing in the endoplasmic reticulum, NF-kappa B signalling pathway, and Fc gamma R-mediated phagocytosis. The top 10 hub genes were screened from a protein-protein interaction network and verified via quantitative real-time polymerase chain reaction. The overall pathway network and hub genes may provide new insights into the toxic mechanisms of PFOS exposure states.
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