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Long-term polystyrene nanoplastic exposure disrupt hepatic lipid metabolism and cause atherosclerosis in ApoE-/- mice
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Long-term exposure to tiny polystyrene nanoplastics caused atherosclerosis (hardening of the arteries) in mice by disrupting fat metabolism in the liver and triggering inflammation and oxidative stress. This is one of the first studies to directly link nanoplastic exposure to cardiovascular disease development, raising concerns about heart health risks from the nanoplastics found in our food and environment.
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.
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Tiny plastic particles (nanoplastics), similar in size to what's already been found in human arteries, made clogged-artery disease significantly worse in mice by disrupting liver function, altering gut bacteria, and throwing off protective body chemicals—all at the same time. This matters because these mice were genetically similar to how many people process cholesterol, and the same disease patterns showed up when researchers compared their data to human artery disease samples, suggesting everyday plastic exposure could be a hidden contributor to heart disease risk in people, too.
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Researchers fed mice polystyrene microplastic beads and found that ingestion promoted fat accumulation and markers of cardiometabolic disease, including changes in cholesterol levels and inflammatory markers. The microplastics appeared to disrupt metabolic processes related to fat storage and energy regulation. The study suggests that dietary microplastic exposure may contribute to obesity and cardiovascular risk factors, adding a new dimension to concerns about microplastics in the food supply.
Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice
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Researchers found that polystyrene nanoplastics worsened liver damage in mice fed a high-fat diet by increasing oxidative stress, inflammation, and the infiltration of immune cells in liver tissue. The nanoplastic exposure accelerated the progression from fatty liver to hepatic fibrosis in the diet-induced model. The study suggests that nanoplastic exposure may compound the health risks associated with metabolic conditions affecting the liver.
Maternal Gestational and Lactational Exposure to Polystyrene Nanoplastics Triggers Vascular Injury and Lipid Deposition in Mouse Offspring
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Pregnant and nursing mice were given polystyrene nanoplastics in water. Their offspring showed lower body weight, organ damage, and blood vessel injury including fat buildup in the aorta, with some effects persisting into adulthood. Nanoplastics also caused fat accumulation in lab-grown blood vessel and immune cells.
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