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Cellular uptake of micro and nano plastics Induces Mitochondrial Dysfunction
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Scientists found that tiny plastic particles from our environment can travel through the bloodstream and get absorbed into placenta cells, where they damage the cell's energy-producing "batteries" (mitochondria) and cause inflammation. In mouse and lab-based human cell studies, this damage weakened the cells' ability to function properly, raising concerns that microplastic exposure during pregnancy could potentially harm placental health and fetal development. More research is needed to confirm these effects in humans, but the findings suggest another reason to minimize plastic exposure during pregnancy.
Abstract Micro and nano plastics (MNPs) have become ubiquitous contaminants in the environment with their occurrence being detected in air, water and food. They can cross biological barriers and slowly build up in different organs, including the placenta, raising concerns about possible impacts on maternal and fetal health. Placenta, a highly metabolically active organ composed primarily of trophoblast cells, requires substantial energy for proper development and function. However, the effects of MNPs exposure on trophoblast biology and mitochondrial health remain poorly understood. This study investigated the in vivo systemic accumulation of MNP in different organs of pregnant mice and their localization within various organelles in vitro. These effects influenced trophoblast energy metabolism and led to reduced migration. Mice received fluorescent polystyrene MNPs via their drinking water. Biodistribution was evaluated in vivo using IVIS whole-body imaging, while ex vivo fluorescence imaging confirmed accumulation of these particles in multiple organs and cells. In parallel, human HTR-8/SVneo trophoblast cells were exposed to MNPs, demonstrating rapid cellular uptake and mitochondrial and nuclear localization via fluorescence microscopy. TEM analysis uncovered mitochondrial structural alterations and the localization of MNPs. Seahorse analysis revealed impaired mitochondrial respiration and oxygen consumption rates, indicating compromised cellular bioenergetics in MNPs-treated cells, which led to inflammation, altered mtDNA copy number, and impaired trophoblast migration. Overall, these findings indicate that pregnant mice exposed to MNPs undergo systemic transfer, with trophoblast uptake marked by mitochondrial dysfunction, inflammation, and reduced migration. Our study identifies mitochondrial dysfunction as a central mechanism underlying MNP-mediated placental toxicity and underscores the potential role of environmental microplastic exposure in adverse pregnancy outcomes. Highlights Cellular uptake of MNPs and their localization across various organelles. Uptake of MNPs disrupts mitochondrial function and promotes inflammation. Cellular uptake of MNPs impairs cell migration.
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