Polystyrene Nanoplastics Induce Mitochondrial Dysfunction and Hepatic Fibrosis via Oxidative Stress.

Authors

Shirong Qiang, Yongxiang Huang, Yujin Wang, Lianhang Jiao, Yuanhao Luo, Shuaiqi Li, Hong Gu, Zihuan Wang, Yue Zhang, Xuejuan Wu, Qiaohui Fan

Published in

Toxicology. Pages 154627. Nov 14, 2026. Epub Nov 14, 2026.

Abstract

Polystyrene Nanoplastics pose a significant threat via bioaccumulation and organ injury, yet their hepatic distribution and hepatotoxic mechanisms remain poorly understood. This study indicated that orally administered polystyrene nanoparticles accumulated in liver tissue, a distribution consistent with gastrointestinal absorption and portal venous delivery. Histological staining shows that the typical fibrotic changes are around the blood vessels of the liver, especially surrounding the central veins and interlobular arteries /veins in the portal tracts. Immunostaining verified elevated perivenous expression of fibrosis-related proteins alpha smooth muscle actin (α-SMA) and fibronectin positively linked to nanoparticle treatment. Further investigations showed that nanoparticles exposure caused intracellular oxidative stress response, damaged mitochondria, disrupted mitochondrial metabolic function, increased the expression of transforming growth factor-β/Smad protein (TGF-β/Smad) pathway-associated proteins together with hepatic stellate cell activation, and finally mediated liver fibrosis. This study provides new aspects of the liver toxicity associated with polystyrene nanoparticles.

PMID:
43034006
Bibliographic data and abstract were imported from PubMed on 15 Nov 2026.

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