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Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Food & Water Gut & Microbiome Human Health Effects Nanoplastics Remediation Sign in to save

Synergistic Toxicity of Combined Exposure to Acrylamide and Polystyrene Nanoplastics on the Gut–Liver Axis in Mice

Biology 2025 3 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 58 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Yongchuang Liu, Rong Luo, Zhongke Sun, Yidan Zhang, Yuqi Guo, Yanjuan Chen, Lili Li, Zonghao Yue

Summary

Researchers exposed mice to a combination of acrylamide, a common food processing byproduct, and polystyrene nanoplastics through drinking water and found that the combined exposure caused more severe gut and liver damage than either substance alone. The co-exposure disrupted gut barrier integrity, altered gut bacteria composition, and caused widespread metabolic changes. The study suggests that the interaction between nanoplastics and other food contaminants may amplify health risks beyond what each poses individually.

Polymers
Models
Study Type Environmental

Acrylamide (AA) and nanoplastics (NPs) are common food toxicants. However, their combined toxicity and health risks call for further studies. This study aimed to investigate the combined toxicity of AA and polystyrene NPs (PS-NPs) in mice through drinking water exposure. Co-exposure to AA and PS-NPs aggravated colon and liver damage, including more severe inflammatory infiltration, higher levels of colonic and hepatic pro-inflammatory cytokines, and elevated serum content of lipopolysaccharide and activities of diamine oxidase, alanine aminotransferase, and aspartate aminotransferase compared to single exposures. Co-exposure also significantly downregulated the expression of colonic tight-junction genes ZO-1 and Claudin-5. Metabolomics revealed that co-exposure induced more profound metabolic disorders in the liver, particularly affecting amino acid and carbohydrate metabolism. 16S amplicon sequencing showed that co-exposure caused more drastic gut microbiota dysbiosis, characterized by a decrease in beneficial bacteria (unclassified_f__Oscillospiraceae, Roseburia, UCG-005, Ruminiclostridium, unclassified_o__Clostridia_UCG-014, Fournierella, and Acetatifactor) and an increase in pathogenic bacteria (Eubacterium_xylanophilum_group and Eubacterium_nodatum_group). Correlation analysis indicated a negative correlation between beneficial bacteria and intestinal-liver toxicity indicators and a positive correlation between pathogenic bacteria and these indicators. Overall, our findings showed that AA and PS-NPs exerted synergistic toxicity to the gut-liver axis in mammals, highlighting the higher health risks of their combined ingestion.

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