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Impact of environmental microplastic exposure on HepG2 cells: unraveling proliferation, mitochondrial dynamics and autophagy activation
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Lab experiments on human liver cells found that exposure to common microplastics (polyethylene and PET) increased cell growth but also triggered oxidative stress, damaged mitochondria (the cell's energy centers), and activated autophagy -- a process where cells try to clean up internal damage. These findings suggest that microplastics may disrupt normal liver cell function in ways that could have long-term health consequences.
The rise of microplastic (MPs) pollution presents a pressing environmental issue, raising concerns about its potential health impacts on human populations. Given the critical role of the liver in detoxification and metabolism, understanding the effects of MPs on the human hepatoma cell line HepG2 cells is essential for comprehensively assessing the dangers associated with MPs pollution to human health. Until now, the assessment of the harmful impact of polyethylene (PE) and polyethylene terephthalate (PET) on HepG2 has been incomplete and lacks certain essential data points. In this particular setting, we examined parameters such as cell viability, oxidative stress, mtDNA integrity, mitochondrial membrane potential, and autophagy in HepG2 cells exposed for 72 h to PET and PE at a concentration of 10 µg/mL. Our data revealed that exposure of HepG2 to MPs causes an increase in cell viability accompanied by a heightened ROS and altered mitochondrial function, as revealed by decreased mtDNA integrity and membrane potential. In addition, results demonstrated that exposure to PET and PE activated autophagic events, as suggested by the increased levels of the specific markers LC3 and p62. This last point was further confirmed using bafilomycin, a specific blocker that hinders the merging of autophagosomes and lysosomes, thereby blocking autophagic degradation processes. Given the increasing evidence of food chain MPs contamination and its possible harmful effects, our data should be carefully considered.
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Researchers exposed human intestinal cells to polyethylene and PET microplastics of different sizes and observed significant decreases in cell survival along with increased oxidative stress. The microplastics triggered both programmed cell death (apoptosis) and the cell's self-recycling process (autophagy), with effects varying by particle size. The study suggests that microplastic exposure may compromise the intestinal barrier through multiple pathways of cellular damage.
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This review summarizes existing research on how tiny nanoplastic particles may affect liver cells. Studies found links between nanoplastic exposure and problems like cell stress, damaged energy-producing structures, and triggered cell death pathways, though results varied depending on the plastic type and test conditions used. The authors note gaps in understanding how these findings relate to real-world health risks.
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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.
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This study found that polystyrene nanoplastics damage human liver cells by triggering harmful interactions between reactive oxygen species (ROS) and a protein called DRP1 that controls mitochondria. The nanoplastics caused mitochondria to break apart, leading to cell injury and death. This research helps explain how microplastic exposure could contribute to liver damage in humans at the cellular level.
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