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20 resultsShowing papers similar to Polystyrene nanoplastics induce haematotoxicity with cell oxeiptosis and senescence involved in C57BL / 6J mice
ClearNanoplastic impact on bone microenvironment: A snapshot from murine bone cells
This study found that nanoplastics are toxic to bone cells in mice, causing cell death, increased production of damaging reactive oxygen species, and disruption of the bone remodeling process. The nanoplastics impaired the ability of bone-building cells to migrate and promoted the formation of bone-destroying cells. These findings suggest that nanoplastic exposure could potentially contribute to bone diseases like osteoporosis, though more research in living animals and humans is needed.
Effects of polystyrene nanoplastics on endothelium senescence and its underlying mechanism
Researchers found that polystyrene nanoplastics can promote premature aging of endothelial cells that line blood vessel walls, using porcine coronary artery cells as a model. The study suggests that nanoplastic exposure may affect cardiovascular health by accelerating cellular senescence in the endothelium, a process linked to vascular dysfunction.
Preliminary study on impacts of polystyrene microplastics on the hematological system and gene expression in bone marrow cells of mice
Researchers studied the effects of polystyrene microplastics on the blood system and bone marrow gene expression in mice. They found that higher doses significantly decreased white blood cell counts and altered gene expression patterns in bone marrow cells, suggesting that microplastic exposure may affect the hematological system in mammals through changes in immune-related gene regulation.
Effect of polystyrene nanoplastics and their degraded forms on stem cell fate
Researchers studied how polystyrene nanoplastics and their degraded forms affect human bone marrow-derived stem cells. They found that both intact and degraded nanoplastics showed reactive oxygen species scavenging activity, enhanced mitochondrial fusion, and promoted cell proliferation and fat cell differentiation. However, the degraded nanoplastics showed higher long-term cytotoxicity, suggesting that as nanoplastics break down in the environment, their biological effects on human cells may change.
Polystyrene micro-/nanoplastics induced hematopoietic damages via the crosstalk of gut microbiota, metabolites, and cytokines
Researchers exposed mice to polystyrene micro- and nanoplastics and found that the particles caused damage to the blood-forming system through disruption of gut bacteria, metabolic changes, and inflammatory signaling. Smaller nanoplastics caused more severe effects than larger microplastics, altering gut microbial communities and triggering systemic inflammation. The study reveals a previously unknown pathway by which ingested plastic particles may harm the body's ability to produce healthy blood cells.
Polystyrene microplastics arrest skeletal growth in puberty through accelerating osteoblast senescence
Researchers found that polystyrene microplastics accumulated in the bones of mice during puberty, leading to reduced body and bone length and impaired bone structure. The microplastics accelerated premature aging (senescence) of bone-building cells called osteoblasts, suppressing their ability to form new bone. The study suggests that microplastic exposure during critical growth periods may pose a risk to skeletal development.
Nanoplastic-induced vascular endothelial injury and coagulation dysfunction in mice
Researchers exposed mice to polystyrene nanoplastics with different surface modifications and found that the particles caused structural damage to vascular endothelial cells and triggered inflammatory responses. The nanoplastics also disrupted blood coagulation function in the mice. The study suggests that nanoplastic exposure may pose risks to cardiovascular health due to the particles' ability to travel through the bloodstream and damage blood vessel linings.
Polystyrene microplastics induces senescence of osteocytes by activating the cyclooxygenase-2 signaling pathway
Researchers found that polystyrene microplastics can be taken up by osteocytes, the most abundant cells in bone tissue, and cause them to undergo premature aging through a process called senescence. The microplastics triggered oxidative stress and activated a specific inflammatory signaling pathway involving cyclooxygenase-2. The study suggests that microplastic exposure could potentially impair bone health by disrupting the normal function of the cells responsible for maintaining bone tissue.
Exposure to polystyrene nanoplastics promotes premature cellular senescence through mitochondrial ROS production and dysfunction in pre-differentiated skeletal myoblasts
This lab study found that polystyrene nanoplastics caused premature aging in muscle precursor cells by damaging their mitochondria and triggering excessive production of harmful molecules called reactive oxygen species. The nanoplastics were absorbed into cells, accumulated there, and caused the cells to stop dividing and show signs of aging. This suggests that nanoplastic exposure could contribute to muscle deterioration and aging-related conditions by damaging the cells responsible for muscle repair.
Airborne polystyrene nanoplastic exposure leads to splenic cell senescence and immune imbalance
Researchers investigated the effects of inhaled polystyrene nanoplastics on spleen immune function in mice. They found that airborne nanoplastic exposure led to splenic cell senescence and disrupted the balance of immune cell populations in this critical immune organ. The study provides early evidence that nanoplastic inhalation may compromise immune system regulation, highlighting a potential health concern for occupational and environmental exposure scenarios.
Polystyrene nanoplastics exposure triggers spermatogenic cell senescence via the Sirt1/ROS axis
Male mice exposed to polystyrene nanoplastics for 60 days showed damaged sperm-producing cells that displayed signs of premature aging, linked to a specific molecular pathway involving the Sirt1 protein and oxidative stress. This study adds to growing evidence that nanoplastic exposure may harm male reproductive health by accelerating the aging of cells responsible for sperm production.
Polystyrene nanoplastics mediate oxidative stress, senescence, and apoptosis in a human alveolar epithelial cell line
A cell study found that polystyrene nanoplastics cause dose-dependent damage to human lung cells, triggering oxidative stress, premature cell aging, and cell death. These findings suggest that breathing in nanoplastics could harm lung tissue over time and potentially contribute to cancer risk from air pollution.
Long-term polystyrene nanoparticles exposure reduces electroretinal responses and exacerbates retinal degeneration induced by light exposure
Researchers found that three months of polystyrene nanoplastic exposure in mice caused particles to penetrate the blood-retinal barrier, accumulate in retinal tissue, generate oxidative stress, and reduce light-sensitivity responses — and that prior nanoplastic exposure significantly worsened light-induced photoreceptor degeneration, with a transcriptomic profile resembling age-related macular degeneration.
Hazard assessment of different-sized polystyrene nanoplastics in hematopoietic human cell lines
Researchers tested how different sizes of polystyrene nanoplastics (50, 200, and 500 nm) affect human blood cell lines. While none of the sizes caused direct cell death, all three were taken up by cells and disrupted mitochondrial function in immune-related cell types. The study suggests that even without killing cells outright, nanoplastics may interfere with important cellular energy processes, with effects varying by particle size and cell type.
Metabolomic characteristics in human CD34+ hematopoietic stem/progenitor cells exposed to polystyrene nanoplastics
Researchers examined metabolomic changes in human CD34+ hematopoietic stem/progenitor cells exposed to polystyrene nanoplastics, finding significant metabolic disruptions that suggest nanoplastics may impair human blood cell development.
Enhancement of biological effects of oxidised nano- and microplastics in human professional phagocytes
Researchers studied how virgin and environmentally aged polystyrene nano- and microplastics affect human immune cells (monocytes and macrophages). The study found that oxidized particles, which simulate environmental aging, caused significantly greater DNA damage and oxidative stress than virgin particles, suggesting that weathered plastics in the environment may pose higher health risks.
Stress Response of Mouse Embryonic Fibroblasts Exposed to Polystyrene Nanoplastics
Mouse embryonic fibroblasts exposed to polystyrene nanoplastics internalized particles via endocytosis without losing viability, but showed activation of antioxidant and autophagic stress pathways, suggesting subcellular dysfunction even in the absence of cell death.
Polystyrene nanoplastics exacerbated lipopolysaccharide‐induced necroptosis and inflammation via the ROS/MAPK pathway in mice spleen
Researchers found that polystyrene nanoplastics worsened the inflammatory damage caused by bacterial toxins in the spleens of mice. The nanoplastics triggered oxidative stress that activated inflammatory signaling pathways, leading to cell death, and these effects were significantly amplified when nanoplastics were combined with bacterial endotoxin. The study suggests that nanoplastic exposure may compromise the immune system's ability to handle infections and inflammation.
Cytotoxic effect of polystyrene nanoplastics in human umbilical vein endothelial cells (HUVECs) and normal rat kidney cells (NRK52E)
Researchers tested how polystyrene nanoplastics affect human blood vessel cells and rat kidney cells in the lab. They found that nanoplastic exposure caused oxidative stress and reduced cell survival in both cell types, with effects increasing at higher concentrations. The study adds to growing evidence that nanoplastics can damage mammalian cells, though the implications for whole-body health require further investigation.
Polystyrene nanoplastics exposure induces cognitive impairment in mice via induction of oxidative stress and ERK/MAPK-mediated neuronal cuproptosis
This mouse study found that polystyrene nanoplastics caused cognitive impairment by triggering oxidative stress and activating a cell-death process called cuproptosis in brain neurons. The findings suggest that copper buildup and specific signaling pathways may be therapeutic targets for reducing brain damage from nanoplastic exposure, though these results still need to be confirmed in human-relevant models.