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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
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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.
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Uptake and Accumulation of Polystyrene Microplastics in Zebrafish (Danio rerio) and Toxic Effects in Liver
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Researchers exposed zebrafish to polystyrene microplastics of two different sizes and tracked where the particles accumulated in the body. They found that smaller particles (5 micrometers) built up in the gills, liver, and gut, while larger particles (20 micrometers) mainly stayed in the gills and gut. The microplastics caused liver inflammation, oxidative stress, and disrupted fat metabolism, suggesting that ingested microplastics can damage internal organs in fish.
Microplastics and nanoplastics: Emerging drivers of hepatic pathogenesis and metabolic dysfunction
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This review examines emerging evidence linking micro- and nanoplastic exposure to liver disease, including metabolic dysfunction-associated liver disease, cirrhosis, and liver cancer. Researchers found that these particles may contribute to liver damage through oxidative stress, inflammation, and disruption of metabolic pathways. The study highlights the need for further research into how environmental plastic contamination may be influencing the rising rates of liver disease worldwide.
Microcystin-LR and polystyrene microplastics jointly lead to hepatic histopathological damage and antioxidant dysfunction in male zebrafish
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This study exposed zebrafish to a common water toxin (microcystin-LR) both alone and combined with polystyrene microplastics, and found that the microplastics made the liver damage significantly worse. The microplastics acted as carriers, increasing how much toxin accumulated in the fish liver and amplifying oxidative stress. This is relevant to human health because it shows microplastics can boost the harmful effects of other pollutants commonly found in drinking water sources.
Combined effects of microplastics and chemical contaminants on the organ toxicity of zebrafish ( Danio rerio )
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Researchers studied the combined effects of microplastics and chemical contaminants like PCBs and methylmercury on zebrafish organs over three weeks of exposure. They found that microplastics carrying adsorbed contaminants produced the most significant effects, particularly on the liver, compared to either microplastics or contaminants alone. The results indicate that microplastics may act as carriers that increase the delivery of harmful chemicals to organisms' tissues.
Micro- and Nanoplastics as Emerging Drivers of Liver Injury: Exposure, Evidence, and Mechanisms
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This review pulls together current research on tiny plastic particles (microplastics and nanoplastics) that we ingest or breathe in, showing they can travel through the body and accumulate in the liver. Lab studies suggest these particles may trigger inflammation, stress cells out, and disrupt normal liver function in ways that could contribute to fatty liver disease and scarring over time. That said, most of this evidence comes from animal and cell studies so far—scientists still need more direct human data to know exactly how much this matters for our health, but it's a good reason to be mindful of plastic exposure in food and water.
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