
TOTAL VIEWS: 428
Microplastics (particles < 5 µm in diameter) are pervasive environmental contaminants resulting from human activities. Common sources include polystyrene (PS) in disposable food containers, polyvinyl chloride in medical masks, and polyethylene terephthalate (PET) in synthetic textiles. Human exposure to micro-plastics frequently occurs through ingestion and inhalation, often without conscious awareness. This study investigated the effects of different sizes (80 nm and 200 nm) and concentrations of PS microplastics on the cell cycle and apop-tosis of HCT116 colorectal carcinoma cells. Additionally, the potential of chitosan to mitigate PS-induced cytotoxicity was evaluated in both intracellular and extracellular contexts. Assessments were conducted using MTT assays, cell cycle analysis, and apoptosis assays. MTT results indicated that higher concentrations of 80 nm PS microplastics significantly reduced HCT116 viability, whereas 200 nm particles had comparatively lesser effects. Cell cycle analysis revealed that exposure to 1 µg/mL PS significantly increased the proportion of cells in the G1 phase and decreased those in the S phase. These concentrations correspond to typical levels released from disposable plastic food containers when used with hot food (60–90°C). Apoptosis assays via flow cytometry confirmed that 80 nm PS microplastics induced more severe cytotoxic effects than their 200 nm counterparts. Notably, the addition of chitosan markedly reduced the toxicity of both PS variants. These findings suggest that chitosan may serve as a protective agent against microplastic-induced intestinal cell damage, offering a potential basis for future therapeutic strategies to safeguard human intestinal health.
Microplastics; intestines; cytotoxicity; HCT116
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The Cytotoxicity of Micro-plastics on Co-culture Models of Intestinal Cells and Investigation of Oxidative Stress Mechanisms
How to cite this paper: Xuan Wu. (2025) The Cytotoxicity of Micro-plastics on Co-culture Models of Intestinal Cells and Investigation of Oxidative Stress Mechanisms. Health and Prevention Journal, 2(1), 92-102.
DOI: http://dx.doi.org/10.26855/hpj.2025.12.008