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Exploring the Impacts of Polyethylene Microplastics on Rat Liver

2024 Score: 45 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Diwakar Maurya, Atul Katarkar, Pankaj M. Kulurkar, Santosh Deshpande, Kannan Krishnamurthi, Saravanadevi Sivanesan

Summary

Wistar rats exposed to polyethylene microplastics at 0.1–5 mg/kg for 4 weeks showed dose-dependent PE accumulation in liver tissue confirmed by fluorescence microscopy, with histopathological signs of liver injury despite no significant change in body weight.

Polymers
Body Systems
Models

Abstract The widespread presence of microplastics (MPs) has raised significant concerns due to their adverse impacts on organisms, public health, and ecological safety. Although hepatotoxic consequences of exposure to polystyrene microplastics (PS-MPs) have been studied recently, the potential effects of long-term accumulation of polyethylene microplastics (PE-MPs) in the liver remain unclear. In this study, we developed a rat model (Wistar) with doses of 0.1, 1, and 5 mg/kg of PE-MPs (with sizes ranging from 1–10 µM) over 4 weeks. As confirmed by FT-IR and fluorescence microscopy, PE-MPs exposure did not significantly affect body weight but led to dose-dependent accumulation in liver tissues. Histopathological assessment revealed signs of liver injury, accompanied by a significant dose-dependent increase in lipid peroxidation (LPO) in liver tissue extracts. Furthermore, transcriptomic profiling of the liver exposed to PE-MPs resulted in differentially expressed genes enriched in pathways linked to mitochondrial dysfunction, lipid and fatty acid metabolism, and non-alcoholic fatty liver disease (NAFLD). PE-MPs-induced LPO activates NAFLD pathways, which were further validated at the transcriptional level by involving genes affecting neutrophil infiltration, inflammation, and fibrosis. Thus, targeting the LPO pathway could serve as a potential avenue for intervention in PE-MPs-mediated liver toxicity.

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