Transcriptome sequencing reveals prenatal PFOS exposure on liver disorders

Perfluorooctane sulfonate (PFOS), a hepatic toxicant and a potential hepatocarcinogen, is commonly used in industrial products. The widespread contamination of PFOS in human maternal and cord blood has raised concerns about its potential risks to the fetus. It is believed that adverse environmental exposure during the critical period of embryo development can have long-lasting consequences in later life. In this report, we used transcriptome sequencing, followed by bioinformatics analysis, to elucidate the potential hepatotoxic and hepatocarcinogenic effects of prenatal PFOS exposure in the fetus. Our results demonstrated that prenatal PFOS exposure could activate the synthesis and metabolism of fatty acids and lipids, leading to liver damage and interference with liver development in the fetus. In addition, a number of cancer-promoting signaling pathways, including Wnt/β-catenin, Rac, and TGF-β, were found to be activated in the fetal liver. More importantly, hepatic transaminase activity, including aspartate aminotransferase and alanine transaminase activity, was induced in the liver of mice offspring after prenatal PFOS exposure. For the first time, our results demonstrate that the hepatotoxic effects of prenatal exposure to PFOS may predispose to a long-term liver disorder in the offspring. - Highlights: • Prenatal PFOS exposure causes liver damage in the fetus. • Prenatal PFOS exposure activates fetal metabolism of fatty acids and lipids. • Prenatal PFOS exposure stimulates cancer-promoting signaling pathways in fetus. • Prenatal PFOS exposure causes long term hepatotoxic effect in offspring.