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Exposure to Di(2‐Ethylhexyl) Phthalate Increases the Internalization of Polystyrene Microplastics by Human Hepatocellular Carcinoma Cells and Leads to Cell Damage
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Researchers found that the common plasticizer DEHP significantly increased the uptake of polystyrene microplastics by human liver cancer cells in laboratory experiments. The smallest microplastic particles (100 nanometers) had the highest uptake rate, and DEHP exposure boosted internalization especially for the larger particles. The study raises concerns that co-exposure to plasticizers and microplastics, which commonly occur together in the environment, could amplify cellular damage beyond what either pollutant causes alone.
Microplastics (MPs) and the plasticizer di(2-ethylhexyl) phthalate (DEHP) frequently co-occur, presenting substantial health risks to both humans and animals. While animal studies indicate adverse effects from exposure to MPs and DEHP, their potential toxicity in humans remains uncertain. This study examines the response of human hepatocellular carcinoma (HepG2) cells to concurrent exposure to synthetic spherical polystyrene (PS) particles and DEHP. We analyzed the effect of particle size on the internalization of PS-MPs using HepG2 spheres as a 3D model. The results showed that MPs at 100 nm had the highest internalization efficiency, which gradually decreased as the particle size increased to 1 and 5 μm. In addition, DEHP significantly improved the internalization of MPs, especially for 5 μm particles, which showed a 26% increase in internalization efficiency. We also evaluated changes in physiological activity. Co-exposure to MPs and DEHP resulted in significantly higher cytotoxicity than exposure to MPs alone, with a 20% reduction in cell viability. Larger particle sizes led to greater cellular damage, indicated by a 20% increase in reactive oxygen species (ROS) and a 40% rise in lactate dehydrogenase (LDH) release, suggesting membrane rupture. This study offers new insights into the potential toxicity of short-term exposure to MPs and DEHP, using HepG2 spheres to closely replicate in vivo conditions.
More Papers Like This
Transcriptome Sequencing and Metabolite Analysis Revealed the Single and Combined Effects of Microplastics and Di-(2-ethylhexyl) Phthalate on Mouse Liver
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Mice exposed to microplastics, the plasticizer DEHP, or both together showed liver damage including oxidative stress, cell death, and disrupted metabolism. The combined exposure was worse than either pollutant alone, activating cancer-related genes and impairing the liver's ability to process fats and amino acids. Since DEHP is commonly found alongside microplastics in the environment, these findings suggest that real-world exposure to contaminated plastics could pose a greater liver health risk than previously estimated.
Co-exposure to polystyrene nanoplastics and di(2-ethylhexyl) phthalate: Effects and mechanistic insights into hepatic lipid metabolism in mice
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In mice, exposure to tiny plastic particles (nanoplastics) combined with a plastic chemical called DEHP caused more liver fat buildup and liver damage than either alone. Tests in liver cells showed this involved a specific stress pathway, and blocking that pathway reduced the fat buildup caused by the combined exposure.
Di-(2-ethylhexyl) phthalate exacerbated the toxicity of polystyrene nanoplastics through histological damage and intestinal microbiota dysbiosis in freshwater Micropterus salmoides
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Researchers studied the combined effects of polystyrene nanoplastics and the plasticizer DEHP on juvenile largemouth bass through dietary and waterborne exposure. They found that DEHP worsened the toxic effects of nanoplastics, causing greater tissue damage in the liver and intestines and significant disruption of the gut microbiome. The study suggests that nanoplastics carrying adsorbed chemical pollutants may pose amplified risks to freshwater fish health.
The combined toxicity of polystyrene nano/micro-plastics and triphenyl phosphate (TPHP) on HepG2 cells
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This study found that polystyrene nanoplastics and microplastics made a common flame retardant chemical (TPHP) more toxic to human liver cells than the chemical alone. The nanoplastics absorbed the flame retardant and delivered it to cells, causing increased oxidative stress, mitochondrial damage, and cell death. Smaller nanoplastics caused more harm than larger microplastics, suggesting that as plastics break down into smaller pieces, their ability to carry toxic chemicals into human cells increases.
Di(2‐ethylhexyl) phthalate and microplastics cause necroptosis and apoptosis in hepatocytes of mice by inducing oxidative stress
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Researchers investigated the combined toxic effects of the plasticizer DEHP and microplastics on liver cells in both mice and cell cultures. The study found that both substances individually caused oxidative stress, but their combined exposure significantly worsened the damage, leading to increased cell death through both apoptosis and necroptosis pathways. Evidence indicates that the antioxidant N-acetylcysteine could reverse these effects, confirming that oxidative stress is the key mechanism driving the liver damage.
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