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Size-dependent toxicity of polystyrene microplastics on the gastrointestinal tract: Oxidative stress related-DNA damage and potential carcinogenicity
Summary
Researchers found that polystyrene microplastics accumulate mainly in stomach tissue, where smaller nanoscale particles cause more severe damage than larger ones. The nanoplastics reduced antioxidant enzyme activity, increased DNA damage markers, and activated signaling pathways associated with cancer development. These size-dependent effects on the gastrointestinal tract suggest that the smallest plastic particles may pose the greatest risk to digestive health.
Microplastics (MPs) and nanoplastics (NPs) have been generally regarded as emerging pollutants and received worldwide attention in recent years. Water and food consumption are the primary pathways for human exposure to MPs/NPs, thus gastrointestinal tracts may be susceptible to their toxicity. Although the recent report has indicated the presence of MPs/NPs in multiple human organs, little is known about their gastric effects. Therefore, this study focused on the adverse effects of polystyrene microplastics (PS-MPs) on gastric epithelium in vivo and in vitro. Surface-enhanced Raman spectroscopy (SERS) revealed the distribution of PS-MPs was associated with their particle sizes, and predominantly concentrated in gastric tissues. Gastric barrier injury and mitochondrial damage were observed in rats after exposure to PS-MPs. Compared with the larger ones, polystyrene nanoplastics (PS-NPs) more significantly reduced the activity of antioxidant enzymes while enhancing the level of MDA, 8-OhdG and γ-H2AX. Meanwhile, PS-MPs caused upregulation of β-catenin/YAP through redox-dependent regulation of nucleoredoxin (NXN) and dishevelled (Dvl). These findings supported the size-dependent effects of PS-MPs on oxidative stress and DNA damage. Moreover, the redox-dependent activation of the β-catenin/YAP cascade suggested a novel toxic mechanism for PS-MPs and implied the potential carcinogenic effects.
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