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Bisphenol-A disrupts mitochondrial functionality leading to senescence and apoptosis in human amniotic mesenchymal stromal cells
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Researchers studied how bisphenol-A, a chemical released during microplastic degradation, affects stem cells from the human placental membrane that normally protects the developing fetus. They found that BPA exposure damaged mitochondrial function, increased harmful reactive oxygen species, and triggered premature cell aging and death in these protective cells. The findings raise concerns about how microplastic-derived chemicals encountered during pregnancy could potentially compromise the placental barrier.
In today's context, microplastic pollution has become an increasingly pressing issue not only for the environmental fallout but also for the assumed negative effects on human health. It is now well-established that microplastics (>1 mm in size) can enter the human body through ingestion, inhalation, dermal contact and also maternal-fetal transmission. Alarming were the recent findings of microplastics within the human term placenta. Among the degradation by-products of microplastics, Bisphenol-A (BPA) has emerged as a hazardous chemical, with potential toxicity at multisystemic level, particularly on the earliest stages of human development. Based on these findings, our study focuses on assessing the impact of BPA on properties and functions of mesenchymal stromal cells isolated from the amniotic membrane (hAMSC) of the human term placenta. The amniotic membrane surrounds the fetus, playing a fundamental protective role toward toxic chemicals and pollutants that the mother may encounter. Our research revealed how exposure to increasing concentrations of BPA compromise mitochondrial functionality in hAMSC, resulting in enhanced production of reactive oxygen species at mitochondrial level (mtROS). This, in turn, leads to the stabilization of p53, which triggers an increased expression of p21 and p27 encoding genes and an imbalance in the genetic expression of Bax and Bcl-2. Additionally, we observed upregulated expression of cytokines and chemokines associated with the senescence-associated secretory phenotype (SASP). The increased oxidative stress, which plays a central role in BPA-mediated toxicity, can trigger the activation of the senescence pathways, or culminate in cell death, due to the overwhelming stress conditions. Therefore, our results provide novel insights into the mechanism of action of BPA and elucidates its impact on the functionality of hAMSC. This underscores the pressing need to reconsider the use of BPA as a plastic additive, mitigating the potential adverse effects on babies.
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Bisphenol A Disrupts Mitochondrial Functionality Leading to Senescence and Apoptosis in Human Amniotic Mesenchymal Stromal Cells
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This study investigated how bisphenol A disrupts mitochondrial function in cells, finding that BPA exposure induces mitochondrial stress, promotes cellular senescence, and triggers apoptosis at environmentally relevant concentrations.
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.
Intracellular fate of micro- and nanoplastics in human placenta: Organelle-specific toxicity and mechanistic convergence
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Scientists have found tiny plastic particles (microplastics and nanoplastics) inside the placenta, and this review pulls together existing research to explain what might be happening at a cellular level: these particles seem to overwhelm cells' waste-disposal systems, damage their energy-producing mitochondria, and trigger stress responses that don't fully shut off. This matters because the placenta is what nourishes and protects a developing baby, so if plastics are disrupting its cells this way, it could have implications for fetal development, though this is a proposed theoretical model based on current evidence, not a confirmed cause-and-effect finding, and more
Polystyrene microplastics induce biochemical and metabolism changes in human placental explants
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Researchers investigated the effects of polystyrene microplastics on human placental cells, finding that exposure altered biochemical pathways and metabolic activity. The results suggest that microplastics reaching the placenta can disrupt cellular functions important for fetal development.
Adverse effects of a realistic concentration of human exposure to microplastics on markers of placental barrier permeability in pregnant rats
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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.
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