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Dietary patterns reshape organ-specific biodistribution and toxicity upon exposure to polystyrene nanoplastics: role of ROS-mediated intestinal senescence
Summary
A new mouse study suggests that what you eat may change how nanoplastics (tiny plastic particles from food and packaging) affect your body. Mice on a high-fat diet showed more kidney damage from nanoplastic exposure, while mice on a high-sugar diet showed more liver damage, both linked to plastic-triggered stress that ages and weakens the gut lining. This suggests that poor diet may not just cause health problems on its own, but could also make the body more vulnerable to harm from the microplastics we're increasingly exposed to in daily life.
Polystyrene nanoplastics (PS-NPs) are emerging foodborne contaminants associated with multi-organ toxicity. Although dietary patterns can influence the biological effects of environmental contaminants, how they modify PS-NP biodistribution and organ injury remains unclear. Mice fed a normal diet (ND), high-fat diet (HFD), or high-fructose diet (HFrD) were orally exposed to PS-NPs (80 nm, 10 mg/kg) for 1, 4, or 8 weeks. Distinct organ-specific PS-NP distribution patterns were revealed by fluorescence imaging, characterized by greater intestinal and renal accumulation in the HFD-NP80 group and greater hepatic and renal accumulation in the HFrD-NP80 group compared with the ND-NP80 group. Moreover, these patterns were accompanied by distinct toxicological responses. HFD-NP80 showed stronger biochemical evidence of renal dysfunction, with serum creatinine 1.42 times that in ND-NP80. HFrD-NP80 exhibited stronger biochemical evidence of liver injury, with serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities 2.03 and 2.46 times those in ND-NP80, respectively. Mechanistically, PS-NP exposure under HFD or HFrD conditions was associated with reactive oxygen species (ROS)-mediated intestinal senescence and barrier impairment, which were alleviated by NAC intervention. Collectively, these findings suggest that dietary patterns reshape organ-specific PS-NP biodistribution and toxicological responses and that ROS-mediated intestinal senescence serves as a convergent mechanism during PS-NP exposure.