Long-term polystyrene nanoplastic exposure disrupt hepatic lipid metabolism and cause atherosclerosis in ApoE-/- mice.

Nanoplastics (NPs) exposure is usually linked with abnormal inflammation and oxidative stress, which are high-risk triggers of atherosclerosis; however, whether this exposure causes the development of atherosclerosis is vague. Here, we found that PS NPs co-exposure with ox-LDL induces significant accumulation of lipid, as well as oxidative stress and inflammation in RAW264.7 macrophages. Using an ultrasound biomicroscope (UBM), we observed the emergence of atherosclerotic plaques at the aortic arch of apolipoprotein knockout (ApoE-/-) mice after being exposed to PS NPs for three months. Oil-red O and hematoxylin-eosin (H&E) staining at the mice's aortic root also observed the deposition of lipids with plaque formation. Moreover, the development of atherosclerotic disease is associated with disturbances in lipid metabolism and oxidative stress damage in the mice liver. In conclusion, this study provides additional evidence to further understand the possible cardiovascular damage caused by NPs exposure. [Display omitted] • PS NPs co-exposure with ox-LDL induces significantly accumulation of lipid. • PS NPs co-exposure with ox-LDL induces oxidative stress and inflammation. • UBM technique indicated atherosclerotic plaques in PS NPs-exposed ApoE-/- mice. • Oil-red O and H&E staining also observed the deposition of lipids. • PS NPs exposure disturbs lipid metabolism and causes oxidative stress in the liver. [ABSTRACT FROM AUTHOR]