Long-term exposure to polystyrene microplastics induces hepatotoxicity by altering lipid signatures in C57BL/6J mice.

It is estimated that the life of plastics is hundreds to thousands of years, their lasting properties making plastic debris absorbing toxic chemicals and degrading into microplastics (MPs). The purpose of this study was to explore the effects of exposure to different size (0.08 and 0.5 μm) polystyrene (PS) in mice. After 16 weeks of exposure, it was found that PS-MPs could be identified in the liver. No effect of PS-MPs treatment on body weight was observed. PS-MPs exposure disturbed lipids and lipid-like molecule metabolisms and perturbed the citrate cycle and oxidative phosphorylation. Meanwhile, isocitrate dehydrogenase (ICDHc), nicotinamide adenine dinucleotide -malate dehydrogenase (NAD-MDH), succinate dehydrogenase (SDH), α ketoglutarate dehydrogenase (α-KGDH) activities and adenosine triphosphate (ATP) level were obviously affected by PS-MPs treatment. In addition, significant differences were recorded in catalase (CAT) and malondialdehyde (MDA) levels, indicating that PS-MPs exposure induced an oxidative stress in the liver. In conclusion, our present study provided the first evidence of: (a) long-term exposure to PS-MPs lead to PS-MPs accumulated in the liver and results in liver injury; (b) long-term exposure to PS-MPs disturbs lipids and lipid-like molecule metabolisms; (c) long-term exposure to PS-MPs perturbs citrate cycle and oxidative phosphorylation and leads to oxidative stress in the liver. [Display omitted] • PS-MPs accumulates in the liver and induces liver injury in C57BL/6J mice. • PS-MPs alters lipid signatures in the liver. • ROS plays an important role in liver injury. • The production of ROS is related to abnormal lipid metabolism in the liver. [ABSTRACT FROM AUTHOR]