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Micro- and Nanoplastics as Drivers and Modulators of Hepatotoxicity in Zebrafish (Danio rerio): Interactions with Environmental Co-Contaminants and Molecular Mechanisms
Summary
This review pulls together years of zebrafish research showing that tiny plastic particles (microplastics and nanoplastics) build up in the liver and cause real damage—including cell death, inflammation, and disrupted fat and sugar processing. Making things worse, these plastic particles can act like tiny rafts that carry other pollutants (heavy metals, pesticides, toxins) deeper into the body, amplifying liver injury. While this study was done in fish, it adds to growing evidence that plastic pollution could pose similar risks to human liver health, since our livers work in fundamentally similar ways.
Micro- and nanoplastics (MNPs) have emerged as pervasive contaminants in aquatic ecosystems, raising concerns regarding their biological impacts on aquatic organisms. The liver plays a central role in metabolism, detoxification, and immune regulation, making it particularly vulnerable to MNP-induced toxicity. Importantly, MNPs also function as vectors and modulators of co-occurring environmental contaminants, including heavy metals, pesticides, antibiotics, PFASs, algal toxins, and polycyclic aromatic hydrocarbons (PAHs), thereby influencing contaminant bioavailability and hepatic toxicity. This narrative review synthesizes current evidence on hepatic alterations induced by micro- and nanoplastic exposure in zebrafish (Danio rerio), with emphasis on histopathological changes and underlying mechanisms. Relevant peer-reviewed studies were identified through systematic searches of Web of Science, Scopus, PubMed, and ScienceDirect, covering the period 2013–2026, and screened according to predefined inclusion criteria focusing on hepatic endpoints in zebrafish exposed to micro- and nanoplastics. Across the available literature, MNPs consistently accumulate in hepatic tissue and induce structural alterations, including hepatocellular vacuolization, steatosis, inflammatory infiltration, and necrosis. Mechanistically, these pathological changes are closely linked to oxidative stress, impairment of antioxidant defense systems, reprogramming of lipid and glucose metabolism, and activation of inflammatory and regulated cell death signaling pathways. In addition, interactions with co-occurring environmental contaminants—such as heavy metals, pesticides, antibiotics, and algal toxins—frequently exacerbate hepatic injury through synergistic toxicological mechanisms. Disruption of the gut–liver axis and intestinal microbiota has also emerged as an important contributor to systemic metabolic and inflammatory responses. Overall, zebrafish studies demonstrate that the liver represents a critical target organ for MNP toxicity. Future research should prioritize environmentally realistic exposure scenarios, standardized particle characterization, and integrated multi-omics approaches to improve ecological and human health risk assessment.