We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Dietary patterns reshape organ-specific biodistribution and toxicity upon exposure to polystyrene nanoplastics: role of ROS-mediated intestinal senescence
AI summary Read the abstract
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.
More Papers Like This
Oral Exposure to Polystyrene Microplastics of Mice on a Normal or High-Fat Diet and Intestinal and Metabolic Outcomes
AI summary Read the abstract
Researchers found that polystyrene microplastics caused metabolic problems like diabetes and fatty liver disease in mice, but only when combined with a high-fat diet. The high-fat diet appeared to damage the gut lining enough to allow microplastics to deposit in the intestinal wall, triggering inflammation that altered nutrient absorption. This suggests that people with poor diets may be more vulnerable to the harmful effects of microplastic exposure.
A Western-style diet shapes the gut and liver responses to low-dose, fit-for-purpose polystyrene nanoplastics in mice
AI summary Read the abstract
A subchronic mouse study found that low-dose polystyrene nanoplastics designed to mimic real-world particle characteristics impaired gut and liver health in a non-monotonic, diet-dependent manner, with Western-style diet amplifying the effects.
Polystyrene microplastics exposure increases the disruption of intestinal barrier integrity and gut microbiota homeostasis during obesity and aging
AI summary Read the abstract
Researchers found that polystyrene microplastic exposure worsened intestinal barrier dysfunction in mice on high-fat diets, with the combination of obesity and microplastic exposure producing greater gut permeability and inflammation than either factor alone, suggesting compounding risks in metabolically vulnerable individuals.
Exploring the Mechanism of Kidney Injury in Mice Induced by High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Through the Kidney-Gut Axis
AI summary Read the abstract
In a mouse study, the combination of a high-fat diet and polystyrene nanoplastics caused worse kidney damage than either exposure alone, working through the kidney-gut connection. The nanoplastics plus high-fat diet disrupted gut bacteria, increased inflammation, and triggered a harmful immune response that traveled from the gut to the kidneys. This suggests that people who eat high-fat diets may be more vulnerable to kidney damage from nanoplastic exposure.
High-fat diet primes vulnerability to polyethylene terephthalate nanoplastic toxicity via the gut microbiota-metabolism axis
AI summary Read the abstract
Mice on a high-fat diet suffered much more gut damage from plastic nanoparticles (the kind found in food packaging) than mice on a normal diet, including a leakier gut lining, more inflammation, and disrupted gut bacteria. This suggests that eating a high-fat diet may make your gut more vulnerable to the harmful effects of the tiny plastic particles we're increasingly exposed to through food and water, meaning diet and plastic exposure together could pose a bigger health risk than either one alone.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.