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Adverse effects of a realistic concentration of human exposure to microplastics on markers of placental barrier permeability in pregnant rats

Environmental Science and Pollution Research 2025 4 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count. Score: 58 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Asma Haddadi, Massimo Venditti, Kaouthar Kessabi, Imed Messaoudi

Summary

Researchers exposed pregnant rats to polystyrene microplastics at concentrations realistic for human exposure and examined effects on the placenta. They found that the microplastics accumulated in placental tissue, caused oxidative stress, triggered cell death, and reduced the expression of proteins that maintain the placental barrier. The study provides the first evidence that realistic levels of microplastic exposure can compromise the protective barrier between mother and developing offspring.

Polymers
Body Systems

Although the presence of microplastics (MPs) in the placenta of mammals and their toxicity are currently well proven, the mechanism of their translocation across the maternal-fetal barrier has not been completely uncovered. We hypothesize that the translocation of MPs and their toxic effects partly involve the alteration of the placental barrier permeability. For this purpose, the effects of realistic concentration of human exposure (0.1 mg/kg) of spherical polystyrene microplastics (PS-MPs) with a diameter of 5 µm were assessed in female rat during pregnancy, focusing on tissue expression changes of ion channels and junction proteins as markers of placental barrier permeability. The toxicity of PS-MPs, accumulated mainly in the labyrinth zone (LZ), was manifested by some histological alterations of the placental tissue, notably the reduction of the LZ thickness, the disturbance of the oxidative status, and by the apoptosis induction. In addition, exposure to PS-MPs affected placental barrier permeability by reducing gap junction (CX43) and tight junction (ZO1, Claudin 3, and Claudin 4) protein expression as well as by changes in the expression pattern of placental ion transporters with a significant decrease of Na/K-ATPase expression versus an increase in that of Na-K-Cl cotransporter. Overall, these findings confirmed the direct toxic effects of PS-MPs on placental tissue and demonstrated, for the first time, that realistic concentrations of human exposure to MPs adversely affected placental barrier permeability in pregnant rats.

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