Effects of polystyrene nanoplastic gestational exposure on mice.

Airborne plastic particles have received increasing attention due to their ubiquity in the atmosphere and potential human health risks. Previous studies have demonstrated that early-life exposure to environmental toxicants is associated with abnormal metabolic function. However, the impact of exposure to polystyrene nanoplastics (PSNPs) through inhalation on the development of non-alcoholic fatty liver disease (NAFLD) in mothers and offspring remains unknown. In the present study, mice were gestationally exposed to PSNPs at different doses (0, 1, 5, and 25 µg µl-1) through inhalation to investigate health hazards to the dam at weaning and to adult offspring. Gestational exposure to PSNPs at high doses significantly induced hepatic steatosis in the dam and upregulated genes involved in de novo lipogenesis, fatty acids (FAs) uptake, and triacylglycerol (TG) synthesis in the monoacylglycerol acyltransferase pathway. Gestational exposure to high doses of PSNPs led to hepatic steatosis in adult female offspring but not male offspring, and expression levels of genes related to FAs uptake and TG synthesis in the glycerol 3-phosphate pathway were significantly elevated. Collectively, our data demonstrate that gestational exposure to airborne PSNPs induced different development processes of NAFLD in the dam and offspring, providing vital data about plastic particulate toxicology.

Prenatal exposure to diesel exhaust PM2.5 programmed non-alcoholic fatty liver disease differently in adult male offspring of mice fed normal chow and a high-fat diet.

Air pollution is one of the leading preventable threats to public health. Emerging evidence indicates that exposure to environmental stressors is associated with abnormal foetal development. However, how prenatal exposure to diesel exhaust PM2.5 (DEP) predisposes adult offspring to the development of non-alcoholic fatty liver disease (NAFLD) remains unclear. To examine this, C57BL/6J mice were exposed to DEP or a vehicle before conception and during pregnancy and fed normal chow or a high-fat diet. Then, the hepatic fatty accumulation in the adult male offspring and possible molecular mechanisms were assessed. Our data showed that prenatal exposure to DEP on normal chow led to hepatic steatosis in adult male offspring with normal liver function. However, prenatal DEP exposure relieved the hepatic steatosis and liver function in offspring of mice fed a high-fat diet. Furthermore, prenatal exposure to DEP on normal chow increased lipogenesis and worsened fatty acid oxidation. The counteractive effect of prenatal DEP exposure on high-fat-diet-induced hepatic steatosis was produced through upregulated adenosine 5'-monophosphate-activated protein kinase, and this improved lipogenesis and fatty acid oxidation. Collectively, prenatal exposure to DEP programmed the development of NAFLD differently in the adult male offspring of mice fed normal chow and a high-fat diet, showing the pleotrophic effects of exposure to adverse environmental factors in early life.