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Interaction of Polystyrene Nanoplastics with Biomolecules and Environmental Pollutants: Effects on Human Hepatocytes
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This lab study tested how polystyrene nanoplastics interact with cadmium and fatty acids in human liver cells. While the nanoplastics alone showed minimal toxicity at realistic concentrations, they actually reduced cadmium's toxic effects by binding to the metal. However, the nanoplastics also grabbed onto fatty acids in the cell environment, reducing their availability to cells, which suggests nanoplastics could interfere with normal nutrient absorption in the body.
The inevitable exposure of humans to micro/nanoplastics has become a pressing global environmental issue, with growing concerns regarding their impact on health. While the direct effects of micro/nanoplastics on human health remain largely unknown, increasing attention is being given to their potential role as carriers of environmental pollutants and organic substances. This study investigates the direct toxicity of 500 nm polystyrene nanoplastics (NPs) on human hepatocytes (HepG2) in vitro, both alone and in combination with cadmium (Cd), a hazardous heavy metal and a prevalent environmental pollutant. One-hour exposure to 100 µg/mL of NPs causes a significant increase in ROS production (+25% compared to control) but cell viability remains unaffected even at concentrations much higher than environmental levels. Interestingly, NPs significantly reduce Cd cytotoxicity at LC50 concentrations (cell viability compared to control: 55.4% for 50 µM Cd, 66.9% for 50 µM Cd + 10 µg/mL NPs, 68.4% for 50 µM Cd + 100 µg/mL NPs). Additionally, NPs do not alter the cellular lipid content after short-term exposure (24 h). However, when Cd and fatty acids are added to the medium, NPs appear to sequester fatty acids, reducing their availability and impairing their uptake by cells in a dose-dependent manner. We confirmed by Dynamic Light Scattering and Scanning Electron Microscopy the interaction between NPs, Cd and free fatty acids. Although polystyrene NPs exhibited minimal cytotoxicity in our experimental model, collectively our findings suggest that predicting the effects of cell exposure to NPs is extremely challenging, due to the potential interaction between NPs, environmental pollutants and specific components of the biological matrix.
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Polystyrene Nanoplastics as Carriers of Metals. Interactions of Polystyrene Nanoparticles with Silver Nanoparticles and Silver Nitrate, and Their Effects on Human Intestinal Caco-2 Cells
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Researchers investigated whether polystyrene nanoplastics can act as carriers of silver contaminants, testing their interactions with silver nanoparticles and silver nitrate and their combined effects on human intestinal Caco-2 cells. The study found that nanoplastics can adsorb silver compounds and that the combined exposure increased toxicity compared to either contaminant alone, suggesting nanoplastics may enhance metal uptake in the human gut.
Polystyrene nanoplastics potentiate cadmium-induced pyroptosis and apoptosis in primary duck hepatocytes: differential responses to N-acetylcysteine
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In lab-grown duck liver cells, combining nanoplastics with cadmium (a toxic metal) caused more cell death than cadmium alone, through two pathways called pyroptosis and apoptosis. An antioxidant, N-acetylcysteine, reduced the apoptosis-related damage but not the pyroptosis-related damage.
Polystyrene Nanoplastics Exacerbate HFD-induced MASLD by Reducing Cathepsin Activity and Triggering Large Vacuole Formation via Impaired Lysosomal Acidification
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Researchers found that polystyrene nanoplastics, when combined with a high-fat diet in mice, significantly worsened fatty liver disease symptoms compared to either factor alone. The nanoplastics impaired the function of lysosomes, the cell's recycling centers, by preventing proper acidification and reducing enzyme activity. The study suggests that nanoplastic exposure could amplify diet-related liver problems by interfering with how cells process and break down fats.
Polystyrene microplastics induce hepatotoxicity and disrupt lipid metabolism in the liver organoids
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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.
Hydrogen bonding-mediated interaction underlies the enhanced membrane toxicity of chemically transformed polystyrene microplastics by cadmium
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This study found that cadmium, a toxic heavy metal, makes polystyrene microplastics more damaging to cell membranes by changing the plastic's surface properties. Cadmium-treated microplastics formed stronger hydrogen bonds with cell membrane fats, disrupting cells more effectively than untreated microplastics. Since both cadmium and microplastics are common environmental pollutants, their combined effect could be more harmful to human health than either one alone.
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