Impact of micro- and nanoplastics on gastrointestinal diseases: Recent advances.
Micro- and nanoplastics (MNPs) are ubiquitous contaminants increasingly recognized for their potential to adversely affect gastrointestinal (GI) health.
APA
Zhao H, Lin G, et al. (2025). Impact of micro- and nanoplastics on gastrointestinal diseases: Recent advances.. European journal of internal medicine, 139, 106419. https://doi.org/10.1016/j.ejim.2025.07.015
MLA
Zhao H, et al.. "Impact of micro- and nanoplastics on gastrointestinal diseases: Recent advances.." European journal of internal medicine, vol. 139, 2025, pp. 106419.
PMID
40701881
Abstract
Micro- and nanoplastics (MNPs) are ubiquitous contaminants increasingly recognized for their potential to adversely affect gastrointestinal (GI) health. This review provides a comprehensive overview regarding the impact of MNPs exposure on GI diseases, especially their toxicological mechanisms, such as oxidative stress, inflammation, apoptosis, gut microbiota dysbiosis, and intestinal barrier dysfunction. Excessive reactive oxygen species production and persistent GI inflammation triggered by MNPs exposure drive epithelial cell apoptosis and compromise the intestinal barrier. Meanwhile, MNPs-induced gut microbiota dysbiosis further exacerbate intestinal inflammation and barrier dysfunction. Through these interconnected pathways, chronic MNPs exposure may be associated with the occurrence and progression of GI diseases, including gastritis, gastric cancer, inflammatory bowel disease, and colorectal cancer. However, there are very limited human evidence, and the long-term impacts of low-dose, chronic MNPs exposure have not been sufficiently explored. Future research should address these uncertainties through longitudinal epidemiological studies, advanced experimental models, and standardized MNPs detection methods, to refine risk assessment and guide evidence-based policies that safeguard human health.
MeSH Terms
Humans; Gastrointestinal Diseases; Microplastics; Gastrointestinal Microbiome; Oxidative Stress; Dysbiosis; Apoptosis; Inflammation
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