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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.
Abstract In today’s context, microplastics 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 was 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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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.
Micro- and Nanoplastics as Potential Chronic Abiotic Stressors: Cellular Senescence, Hallmarks of Ageing, and an Oxidative–Mitochondrial–Inflammatory Framework
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This review summarizes existing lab research on tiny plastic particles and cell ageing processes. Studies found effects on cell energy production, DNA, and inflammation signals, with strongest evidence for mitochondrial problems and cell senescence, but most used high doses and short exposures, so links to human ageing remain unconfirmed.
Assessing micro and nanoplastics toxicity using rodent models: Investigating potential mitochondrial implications
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This review examines recent rodent studies investigating how micro- and nanoplastics affect cellular health, with a focus on potential mitochondrial impacts. Researchers found that while no study has directly targeted mitochondrial effects, several reported molecular and biochemical changes consistent with disrupted mitochondrial function, including oxidative stress. The study suggests that mitochondria may be an important but understudied target of micro- and nanoplastic toxicity.
Microplastics/nanoplastics contribute to aging and age-related diseases: Mitochondrial dysfunction as a crucial role
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This review examines how microplastics and nanoplastics may contribute to aging and age-related conditions by damaging mitochondria, the energy-producing structures inside cells. Researchers describe how these tiny plastic particles enter the body through food, water, and air, and accumulate in various organs where they can disrupt normal mitochondrial function. The study suggests that microplastic-driven mitochondrial damage could be an underappreciated factor in the aging process and related health decline.
Environmental nanoplastics induce mitochondrial dysfunction: A review of cellular mechanisms and associated diseases
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This review summarizes how nanoplastics, which are small enough to enter individual cells, damage mitochondria (the energy-producing structures inside cells) by disrupting their shape, function, and ability to produce energy. This mitochondrial damage has been linked to a range of diseases including neurodegeneration, diabetes, cardiovascular disease, and reproductive problems. The findings help explain why nanoplastic exposure may contribute to multiple chronic health conditions through a common cellular mechanism.
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