We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Chronic exposure to polyvinyl chloride microplastics induces liver injury and gut microbiota dysbiosis based on the integration of liver transcriptome profiles and full-length 16S rRNA sequencing data
Summary
Researchers exposed mice to polyvinyl chloride microplastics for 60 days and found significant liver damage accompanied by changes in gut bacteria composition. Gene expression analysis revealed that the liver injury involved inflammatory and metabolic pathways, while the gut microbiome shifted toward disease-associated bacterial profiles. The study suggests a connection between chronic microplastic exposure, gut health disruption, and liver toxicity.
Microplastics (MPs) have become harmful environmental pollutants, and their potential toxicity to organisms has attracted extensive attention. However, the effects of polyvinyl chloride MPs (PVC-MPs) on the liver and their associated mechanism in mice remain obscure. Here, male mice were exposed to 2-μm PVC-MPs (0.5 mg/day) for 60 days and then sacrificed, and their liver, blood and gut feces were subsequently collected for testing. The liver tissue and fecal samples were subjected to RNA sequencing and full-length 16S rRNA sequencing analysis, respectively. Our results showed that the levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the mice exposed to PVC-MPs were markedly higher than those in the control group, implying hepatic injury, as evidenced by hepatic histopathological changes. Moreover, the serum and hepatic triglyceride (TG) and total bile acid (TBA) levels were decreased after exposure to PVC-MPs. The RNA sequencing of mouse liver tissue identified a total of 1540 differentially expressed genes (DEGs) associated with 47 pathways, including the lipid metabolic pathway, oxidative stress, and the phosphoinositide 3 kinase (PI3K)/protein kinase B (Akt) signaling pathway, and these DEGs were enriched in the mouse livers. The full-length 16S rRNA sequencing analysis of the gut microbiota in mouse fecal samples revealed that PVC-MPs exposure decreased the relative abundance of probiotics and increased the abundance of conditionally pathogenic bacteria. In conclusion, chronic PVC-MPs exposure causes hepatotoxicity and gut microbiota dysbiosis in mice, and these findings provide new insight into the potential risks of PVC-MPs to human health.
Sign in to start a discussion.
More Papers Like This
Polyethylene microplastics induced gut microbiota dysbiosis leading to liver injury via the TLR2/NF-κB/NLRP3 pathway in mice
Mice exposed to polyethylene microplastics developed liver damage that was traced back to disrupted gut bacteria -- the microplastics increased harmful bacteria while decreasing beneficial ones, triggering inflammation through the TLR2/NF-kB/NLRP3 immune pathway. This study provides new evidence that microplastics may harm the liver not just through direct contact, but indirectly by first throwing off the balance of gut bacteria.
Combined exposure to polyvinyl chloride and polystyrene microplastics induces liver injury and perturbs gut microbial and serum metabolic homeostasis in mice
Mice exposed to a combination of PVC and polystyrene microplastics for 60 days developed liver damage, gut barrier breakdown, and disrupted gut bacteria. The co-exposure also raised cholesterol and triglyceride levels in both blood and liver, and altered hundreds of metabolites related to fat metabolism. Since people are typically exposed to multiple types of microplastics simultaneously, this study suggests the combined effects may be worse than exposure to a single type alone.
Gut dysbiosis exacerbates inflammatory liver injury induced by environmentally relevant concentrations of nanoplastics via the gut-liver axis
This mouse study found that swallowing nanoplastics at levels found in the environment disrupted gut bacteria and damaged the intestinal barrier, allowing toxins to leak into the bloodstream and cause liver inflammation. When researchers transplanted gut bacteria from nanoplastic-exposed mice into healthy mice, those mice also developed liver damage. This demonstrates that nanoplastics may harm the liver indirectly by first disrupting the gut, a finding relevant to understanding how everyday plastic exposure could affect human health.
Oral exposure to polyethylene microplastics of adult male mice fed a normal or western-style diet: impact on gut and gut-liver axis homeostasis
Researchers exposed adult male mice to polyethylene microplastics on normal or Western diet for 90 days, examining synergistic effects between plastic and dietary stress on gut and liver health. Microplastic exposure disrupted gut barrier integrity, altered the microbiome, and affected liver homeostasis, with some effects differing between normal and Western diet groups.
Chronic exposure to polyethylene terephthalate microplastics induces gut microbiota dysbiosis and disordered hepatic lipid metabolism in mice
Researchers found that mice exposed to PET microplastics (the type commonly found in plastic bottles) over 17 weeks developed liver damage, including fat buildup, oxidative stress, and cell death. The study revealed that the damage was driven by changes in gut bacteria that altered lipid metabolism, and when researchers depleted the gut bacteria, the liver damage was reduced. This suggests the gut microbiome plays a key role in how microplastics cause harm to internal organs.