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Transfer toxicity of polystyrene microplastics in vivo: Multi-organ crosstalk

Environment International 2025 11 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 68 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Zhanhang Wang, Zhanhang Wang, Zhanhang Wang, Zhanhang Wang, Zhanhang Wang, Zhanhang Wang, Shujuan Liu, He Yang, Muhua Luo, Shujuan Liu, Muhua Luo, Shujuan Liu, Shujuan Liu, Jinxing Hou, Binyun Cao, Binyun Cao, Xiaopeng An Xiaopeng An Xiaopeng An

Summary

In a mouse study, polystyrene microplastics fed to nursing mothers spread to their gut, liver, and mammary glands, and were passed to offspring through breast milk by breaking down gut and blood-milk barriers. The microplastics disrupted the gut microbiome and liver bile acid metabolism, causing inflammation across multiple organs and demonstrating how microplastic toxicity can transfer between a mother and her young.

Polymers
Models
Study Type In vivo

The accumulation of microplastics (MPs) within the environment caused serious ecological and health problems. Nevertheless, its systemic toxicity to organisms and its mechanisms lack effective evidence. This study established a model of MP exposure through the gavage of polystyrene (PS)-MPs particles to maternal mice on days 1 to 21 of lactation. The results demonstrated that PS-MPs were distributed widely in maternal mice, occurring mainly in the feces, colon, liver and mammary glands. Further experiments revealed that the gut and blood-milk barriers were disrupted, and pathological injury and inflammatory reactions were observed in the liver, gut, and mammary glands. Metabolomic and metagenome analysis indicated abnormalities in hepatic bile acid metabolism and significant alterations in the gut microbiota after exposure to PS-MPs. These alterations led to increased disruption of the intestine-liver axis. Notably, with fecal microbiota transplantation and antibiotic experiments, we observed that elimination of the intestinal microbiota reduced tissue inflammation and improved gut and blood-milk barrier leakage. These findings demonstrated that PS-MPs exaggerated intestine-liver axis disorders by inducing colonic injury, intestinal ecological dysregulation and abnormal hepatic bile acid metabolism. Furthermore, PS-MPs translocated via the intestine-liver axis and exerted broader toxic effects on mammary tissue. Overall, our study uncovered the transfer toxicity of PS-MPs in mice, proposing the possibility of a gut-liver-mammary axis.

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