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Exposure to Polypropylene Microplastics via Oral Ingestion Induces Colonic Apoptosis and Intestinal Barrier Damage through Oxidative Stress and Inflammation in Mice
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Researchers gave mice polypropylene microplastics (smaller than 10 micrometers) by mouth for 28 days and found significant damage to the colon, including inflammation, destruction of the gut barrier, and increased cell death. The smaller particles caused more severe damage than larger ones, triggering an inflammatory pathway that broke down the protective lining of the intestine. This is one of the first studies on polypropylene, the most common plastic found in human tissue, showing it can damage the gut at sizes small enough to be absorbed by the body.
Extensive environmental pollution by microplastics has increased the risk of human exposure to plastics. However, the biosafety of polypropylene microplastics (PP-MPs), especially of PP particles < 10 μm, in mammals has not been studied. Thus, here, we explored the mechanism of action and effect of exposure to small and large PP-MPs, via oral ingestion, on the mouse intestinal tract. Male C57BL/6 mice were administered PP suspensions (8 and 70 μm; 0.1, 1.0, and 10 mg/mL) for 28 days. PP-MP treatment resulted in inflammatory pathological damage, ultrastructural changes in intestinal epithelial cells, imbalance of the redox system, and inflammatory reactions in the colon. Additionally, we observed damage to the tight junctions of the colon and decreased intestinal mucus secretion and ion transporter expression. Further, the apoptotic rate of colonic cells significantly increased after PP-MP treatment. The expression of pro-inflammatory and pro-apoptosis proteins significantly increased in colon tissue, while the expression of anti-inflammatory and anti-apoptosis proteins significantly decreased. In summary, this study demonstrates that PP-MPs induce colonic apoptosis and intestinal barrier damage through oxidative stress and activation of the TLR4/NF-κB inflammatory signal pathway in mice, which provides new insights into the toxicity of MPs in mammals.
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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.
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Researchers fed mice polyethylene microplastics of two sizes commonly found in human stool for six weeks and examined the effects on gut health. The study found that microplastic exposure altered gut structure, disrupted immune cell function, changed gene expression related to inflammation and gut barrier integrity, and shifted the composition of gut bacteria. Mice exposed to both sizes simultaneously showed the most severe effects, suggesting that real-world exposure to mixed microplastic sizes may compound the damage.
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Researchers fed mice polyethylene microplastics for 30 days and found that even low doses reduced protective mucus in the colon, altered inflammation markers, and shifted the composition of gut bacteria. The microplastics increased the ratio of Bacteroides to Firmicutes bacteria and affected metabolic pathways in the gut microbiome. The study suggests that oral microplastic exposure may disrupt intestinal health by modifying the gut microbial community and its metabolism.
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Researchers fed mice micro- and nanoplastics at environmentally relevant levels and found significant gut damage, including disrupted gut bacteria, weakened intestinal barriers, and reduced immune function. The ratio of beneficial to harmful gut bacteria shifted, and immune cells in the gut decreased. Importantly, the duration of exposure and the size of plastic particles mattered more than the amount consumed, suggesting even low-level long-term exposure could harm gut health.
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