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Impact of Environmental Microplastic Exposure on Caco-2 Cells: Unraveling Proliferation, Apoptosis, and Autophagy Activation
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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.
Microplastics (MPs) are pervasive environmental pollutants that have raised concerns due to their potential toxic impacts on human health. This study investigates the impact of polyethylene (PE) and polyethylene terephthalate (PET) microplastics on Caco-2 cells, a commonly used in vitro model for the intestinal barrier. Caco-2 cells were exposed to MPs of different sizes (1 µm and 2.6 µm) for 72 h. The results demonstrated a significant decrease in cell viability, accompanied by increased reactive oxygen species (ROS) production, suggesting oxidative-stress-induced cytotoxicity. Flow cytometry and Western blot analyses revealed that the MPs induced apoptosis, as evidenced by an increased Bax/Bcl-2 ratio and caspase-3 activation. Additionally, MPs triggered autophagy, indicated by elevated LC3-II levels and decreased p62 expression. The use of bafilomycin A1 further confirmed the enhancement of autophagic flux. These findings highlight the potential cytotoxic effects of MPs on intestinal epithelial cells, raising concerns about their impact on human health.
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Researchers tested the effects of micro-sized polyethylene particles on two types of human colon cancer cells commonly used in gut research. The microplastics reduced cell survival and triggered oxidative stress, which is a type of cellular damage caused by an imbalance of harmful molecules. This study provides evidence that microplastics reaching the human gut through food and water could damage intestinal cells, though more research is needed at real-world exposure levels.
Autophagic response of intestinal epithelial cells exposed to polystyrene nanoplastics
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Researchers found that polystyrene nanoplastics accumulate in the cytoplasm of intestinal epithelial cells, impairing autophagic flux and triggering an autophagic stress response confirmed in both cell and animal models.
Effect of microplastics and nanoplastics in gastrointestinal tract on gut health: A systematic review.
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This systematic review of 30 in vitro studies found that microplastics and nanoplastics cause size- and concentration-dependent damage to human gastrointestinal cells, including increased oxidative stress, mitochondrial dysfunction, inflammation, and apoptosis. Smaller particles consistently showed greater cellular uptake and biological effects, though chronic low-dose exposure generally produced minimal impacts.
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.
Nanoplastics induce more severe apoptosis through mitochondrial damage in Caco-2 cells compared to sub-micron plastics
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Researchers found that 20 nm polystyrene nanoplastics cause more severe apoptosis in intestinal Caco-2 cells than 200 nm sub-micron plastics, disrupting cell membrane integrity at 80 ug/mL, localizing in lysosomes and mitochondria, and triggering mitochondria-mediated cell death pathways more intensively than larger particles. The study suggests nanoplastic size is a critical determinant of cytotoxicity in the gastrointestinal tract.
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