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An evaluation of a hepatotoxicity risk induced by the microplastic polymethyl methacrylate (PMMA) using HepG2/THP-1 co-culture model
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Researchers tested the liver toxicity of polymethyl methacrylate (PMMA) microplastics using a lab model combining human liver and immune cells. The microplastics triggered inflammation and oxidative stress at concentrations as low as 0.1 mg/mL, activating pathways linked to cell death and chronic disease. Since the liver is a primary organ where microplastics accumulate after entering the body, these findings suggest that long-term microplastic exposure could contribute to liver damage and inflammation-driven diseases.
Inappropriate disposal of plastic wastes and their durability in nature cause uncontrolled accumulation of plastic in land/marine ecosystems, also causing destructive effects by bioaccumulating along the food chain. Microplastics may cause chronic inflammation in relation to their permanent structures, especially through oxidative stress and cytotoxic cellular damage, which could increase the risk of cancer development. The accumulation of microplastics in the liver is a major concern, and therefore, the identification of the mechanisms of their hepatotoxic effects is of great importance. Polymethyl methacrylate (PMMA) is a widely used thermoplastic. It has been determined that PMMA disrupts lipid metabolism in the liver in various aquatic organisms and causes reproductive and developmental toxicity. PMMA-induced hepatotoxic effects in humans have not yet been clarified. In our study, the toxic effects of PMMA (in the range of 3-10 μm) on the human liver were investigated using the HepG2/THP-1 macrophage co-culture model, which is a sensitive immune-mediated liver injury model. Cellular uptake of micro-sized PMMA in the cells was done by transmission electron microscopy. Determination of its effects on cell viability and inflammatory response, oxidative stress, along with gene and protein expression levels that play a role in the mechanism pathways underlying the effects were investigated. The results concluded that inflammation, oxidative stress, and disruptions in lipid metabolism should be the focus of attention as important underlying causes of PMMA-induced hepatotoxicity. Our study, which points out the potential adverse effects of microplastics on human health, supports the literature information on the subject.
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Using lab-grown human liver organoids, researchers showed that polystyrene microplastics caused liver cell damage even at concentrations found in the environment. The microplastics disrupted fat metabolism, increased harmful reactive oxygen species, and triggered inflammation in the liver tissue. This study provides early evidence that microplastic exposure could contribute to liver problems like fatty liver disease in humans.
The effects of concentration, duration of exposure, size and surface function of polymethyl methacrylate micro/nanoplastics on human liver cells
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Researchers tested the effects of polymethyl methacrylate micro- and nanoplastics on human liver cells, varying the particle concentration, exposure duration, size, and surface chemistry. They found that smaller particles and those with specific surface modifications caused greater cellular damage, including reduced viability and increased oxidative stress. The study suggests that the physical and chemical properties of microplastics play a critical role in determining their potential toxicity to human tissues.
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Polystyrene microplastics (0.1 µm) induced inflammatory responses and activated multiple inflammatory signalling pathways in mouse and human liver cell lines after 28 days of exposure. The study identified specific phosphorylation cascades through which PS MPs trigger hepatic inflammation, linking microplastic exposure to liver damage mechanisms.
Environmental microplastics and liver health: Brief review on human exposure and accumulation, hepatotoxicity mechanism, and intervention strategies
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This review links human exposure to microplastics, their accumulation in the liver and proposed mechanisms of liver toxicity, including oxidative stress, inflammation and cell death. Most of the evidence comes from cell, animal and organoid studies. It also discusses candidate interventions that are still at the research stage.
Microplastic-induced hepatic adverse effects evaluated in advanced quadruple cell human primary models following three weeks of repeated exposure
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Scientists tested the effects of microplastics on a sophisticated model of human liver cells over three weeks of repeated exposure, finding that certain microplastic types triggered inflammation and altered liver function. The advanced cell model, which combines four types of human liver cells, provides more realistic results than simpler lab tests. These findings add to growing evidence that microplastics accumulating in the liver could contribute to chronic inflammation and liver damage in humans.
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