An exploration into the transplacental transfer of microplastics through placental transporters.

Microplastic (MP) and nanoplastic (NP) exposure has been proven to cause placental damage and fetal dysplasia in mammals. The distribution and accumulation of MPs and NPs in human placental tissue were partly explored. However, the underlying mechanisms remain poorly understood. In this work, the adsorption processes of polystyrene (PS) and polyethylene (PE) NPs with six representative placental transporters, including breast cancer resistance protein (BCRP), ATP-binding cassette transporter B1 (MDR1), multi-drug resistance protein 1 (MRP1), human equilibrium nucleoside transporter 1 (hENT1), folate receptor α (FRα), and serotonin transporter (SERT) were simulated by molecular dynamics to explore the transplacental mechanism of NPs. The results suggested that the other five placental transporters could spontaneously adsorb on the surface of NPs except for the PE-BCRP system. In addition, by fitting the binding property parameters of NPs and placental proteins, including contact number, contact area, binding free energy, maximum adsorption number, surface water distribution, and secondary structure, a comprehensive binding capacity function was constructed for quantitative evaluation of nanoplastics-transporters adsorption ability. The values obtained based on the function directly reflected the strength of the binding ability between NPs and placental transporters. Based on the values, PS and PE NPs had similar abilities to promote placental transport by adsorbing the influx transporters. However, considering that three efflux transporters significantly inhibit the placental transport of PS NPs, the transplacental transport capacity of PE NPs was higher than that of PS NPs. The comprehensive binding capacity calculation system proposed in this research offers a new approach to quantitatively assess the risk of NPs placenta exposure and screen for potential toxic microplastics in the placenta.