Polyethylene Microplastics Induced Hepatic Oxidative Stress and Early Non-alcoholic Fatty Liver Disease in Wistar Rats

Background: Polyethylene microplastics (PE-MPs) are persistent environmental pollutants found extensively in various ecosystems. However, their specific impact on liver function remains inadequately investigated. Methods: Adult male wistar rats were orally exposed to PE-MPs (1-10 µm) at doses of 0.1, 1 and 5 mg/kg/day over 28 days. Attenuated total reflectance-fourier transform infrared spectroscopy (ATR-FTIR) and fluorescence microscopy identified accumulations of PE-MPs. Liver tissues were examined histologically using Haematoxylin and Eosin staining. Oxidative stress was measured by measuring malondialdehyde (MDA), superoxide dismutase (SOD) and reduced glutathione (GSH) levels. Transcriptomic analysis was performed to detect differentially expressed genes (DEGs). Functional enrichment analyses were conducted using gene ontology (GO) and kyoto encyclopaedia of genes and genomes (KEGG) pathways. Key genes were validated by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Result: Accumulation of PE-MPs was detected in liver tissue. Histological evaluation revealed dose-dependent liver injury, including inflammatory infiltration and periportal fibrosis. Elevated MDA levels indicated increased oxidative stress via lipid peroxidation (LPO). qRT-PCR investigation confirmed the upregulation of mitochondrial dysfunction-related genes (NDUFC, UQCRH, MT-CO2), pro-inflammatory genes (TNF-α, CXCL1, IL-1β) and fibrosis markers (IL-6, Col1A1, α-SMA). Transcriptomic analysis identified 189 DEGs linked with oxidative stress, inflammation and lipid metabolism pathways. Altogether, PE-MPs exposure induces oxidative stress, mitochondrial dysfunction, inflammation and fibrosis, contributing to non-alcoholic fatty liver disease (NAFLD) like hepatic alterations. This highlights the potential risk of PE-MPs as emerging environmental threats to liver health.