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Impact of Environmental Microplastic Exposure on Caco-2 Cells: Unraveling Proliferation, Apoptosis, and Autophagy Activation
Summary
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.