Nanoplastics, Liver Injury, and Oxidative Mechanisms: Translating Animal Models Into Human Risk Assessment

Micro- and nanoplastics (MNPs) have emerged as environmental contaminants of increasing concern due to their potential to disrupt biological systems. The liver, as a key organ in detoxification and metabolism, is particularly susceptible to MNP-induced injury. This scoping review aimed to synthesize experimental evidence from preclinical animal models to identify the principal hepatotoxic mechanisms induced by MNP exposure and evaluate the implications for human health. A systematic search was conducted in PubMed, Scopus, Web of Science, and OpenAlex databases. Eligible studies included original research assessing hepatic outcomes in animal models exposed to MNPs. Data were charted for polymer type, particle size, exposure route, exposure duration, and toxicological endpoints. The review followed PRISMA-ScR guidelines and included 34 studies. Consistent hepatotoxic signatures were identified, including oxidative stress, inflammation, lipid dysregulation, and apoptosis. Polystyrene, polyethylene, and polylactic acid were the most studied polymers, with exposure via oral gavage or aquatic immersion. Mitochondrial dysfunction and genotoxic markers were also reported. The mechanistic convergence suggests shared injury pathways across particle types and models. MNPs induce liver injury through oxidative, inflammatory, and metabolic mechanisms, supporting their classification as emerging hepatotoxicants. While translational gaps persist, these findings highlight urgent research needs and inform environmental health risk frameworks.