Exposure to triphenyl phosphate during pregnancy: The role of gut-bile acids-liver axis on lipid metabolism in male offspring.

The widespread use of Triphenyl phosphate (TPhP) as a substitute flame retardant in various commercial products has raised global concerns for its health risks. Previously, we found that gestational and lactational TPhP exposure disturbed lipid metabolism and gut microbiota in offspring sex-dependently. In this study, we further explored the prenatal TPhP exposure on lipid metabolism in male offspring, and the role of gut-bile acids-liver axis in it.

Prenatal Triphenyl Phosphate Exposure and Hyperlipidemia in Offspring: Role of Trophoblast-Derived Extracellular Vesicle PPARγ.

Triphenyl phosphate (TPhP) is a widely used organophosphate flame retardant, the health risks of TPhP are a global concern. In this study, we found that prenatal TPhP exposure at human relevant concentration induced hyperlipidemia in male offspring, it increased serum levels of triglyceride, total cholesterol, and low-density lipoprotein cholesterol. Placental trophoblast-derived extracellular vesicles (T-EVs) could transport to the fetus through maternal-fetal circulation.

Effects of Xenobiotic Compounds on Preeclampsia and Potential Mechanisms.

Preeclampsia (PE) refers to a disease with new hypertension and albuminuria or other end-organ damage after 20 weeks of pregnancy. As a major complication of pregnancy, PE can increase the morbidity and mortality of pregnant women and fetuses and cause serious social burden. Recently, it has been found that exposure to xenobiotic compounds, especially endocrine disruptors in the environment, may contribute to the development of PE.