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Papers
61,005 resultsShowing papers similar to Issue Information‐ToC
ClearPolystyrene nanoplastics aggravates lipopolysaccharide‐induced apoptosis in mouse kidney cells by regulating IRE1/XBP1 endoplasmic reticulum stress pathway via oxidative stress
Researchers investigated whether polystyrene nanoplastics could worsen kidney cell damage caused by bacterial toxins in mice. They found that nanoplastics aggravated cell death by triggering oxidative stress, which activated a specific endoplasmic reticulum stress pathway involving the IRE1/XBP1 signaling cascade. The study suggests that combined exposure to nanoplastics and bacterial compounds may pose greater risks to kidney health than either stressor alone.
Polystyrene nanoplastics exacerbate gentamicin-induced nephrotoxicity in adult rat by activating oxidative stress, inflammation and apoptosis pathways
Researchers co-exposed rats to polystyrene nanoplastics and the antibiotic gentamicin and found that the combination caused significantly greater kidney damage than either substance alone, amplifying oxidative stress, inflammation, and mitochondrial apoptosis in a synergistic manner.
Polystyrene nanoplastics induce apoptosis of human kidney proximal tubular epithelial cells via oxidative stress and MAPK signaling pathways
Researchers found that polystyrene nanoplastics cause programmed cell death in human kidney tubular cells through oxidative stress and activation of the MAPK signaling pathway. The toxic effects were dependent on both the size and dose of the nanoplastics, with smaller particles causing more damage. The study identifies specific molecular mechanisms by which nanoplastics may contribute to kidney cell injury.
Nanoplastic toxicity and uptake in kidney cells: differential effects of concentration, particle size, and polymer type
Human proximal tubule kidney cells were exposed to carboxylated polystyrene and PMMA nanoplastics of different sizes for 24 hours, revealing that cytotoxicity, cellular uptake, and oxidative stress were strongly dependent on particle concentration, size, and polymer type.
Toxicological effects and mechanisms of renal injury induced by inhalation exposure to airborne nanoplastics
Researchers studied what happens to mouse kidneys after breathing in airborne polystyrene nanoplastics and found the particles accumulated in kidney tissue after entering through the lungs. The nanoplastics activated stress and inflammation pathways that led to kidney cell damage and death. Testing on lab-grown human kidney organoids showed they were even more sensitive to nanoplastic exposure than standard cell lines, suggesting developing kidneys in embryos could be particularly vulnerable.
Nanoplastic toxicity and uptake in kidney cells: differential effects of concentration, particle size, and polymer type
Researchers exposed human kidney proximal tubule cells to nanoplastics of different polymer types, sizes, and concentrations to assess short-term toxic effects. They found that polystyrene and PMMA nanoparticles were readily internalized by kidney cells and caused concentration-dependent reductions in cell viability and changes in cell cycle distribution. The study suggests that nanoplastics can directly affect kidney cell function, with toxicity varying by polymer type and particle size.
Toxicity of polystyrene nanoplastics to human embryonic kidney cells and human normal liver cells: Effect of particle size and Pb2+ enrichment
Researchers tested polystyrene nanoplastics on human kidney and liver cells and found that particles smaller than 100 nanometers caused significant cell death, with kidney cells being more vulnerable. When nanoplastics carried lead contamination from water, their toxicity increased further. The study suggests that while nanoplastics alone in drinking water may pose limited risk, their ability to concentrate heavy metals is a serious concern.
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.
Nanoplastics trigger the aging and inflammation of porcine kidney cells
Researchers exposed pig kidney cells to nanoplastics in the laboratory and found that the particles were absorbed into cells in a time- and dose-dependent manner. The nanoplastics triggered oxidative stress, leading to a buildup of reactive oxygen species in mitochondria, which in turn caused inflammatory responses and premature cell aging. The findings provide new evidence that nanoplastic exposure may contribute to kidney cell damage through oxidative stress pathways.
The nephrotoxic potential of polystyrene microplastics at realistic environmental concentrations
Researchers tested polystyrene microplastics on human kidney cells at concentrations reflecting real-world environmental levels. They found that the particles attached to and were engulfed by the cells, triggering oxidative stress and inflammatory responses that reduced cell survival. The findings suggest that even realistic low-level microplastic exposure may pose risks to kidney health.
Effects of nano- and microplastics on kidney: Physicochemical properties, bioaccumulation, oxidative stress and immunoreaction
Researchers exposed mice to polystyrene nano- and microplastics of varying sizes and tracked their accumulation and effects in the kidneys. They found that the particles changed their physical properties during digestion, accumulated in kidney tissue, and caused oxidative stress and immune responses. The study suggests that plastic particle size plays an important role in determining the extent of kidney-related harm.
Combined exposure to polystyrene nanoplastics and bisphenol A results in mitochondrial damage and ferroptosis via the PI3K-AKT signaling pathway in mice kidneys
Researchers exposed mice to polystyrene nanoplastics combined with bisphenol A for six weeks and found that co-exposure caused significant kidney damage through mitochondrial dysfunction and a form of cell death called ferroptosis. The combined exposure was more harmful than either contaminant alone, operating through the PI3K-AKT signaling pathway. The findings suggest that nanoplastics acting as carriers for co-pollutants like BPA may amplify toxic effects on kidney tissue.
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.
Screening for polystyrene nanoparticle toxicity on kidneys of adult male albino rats using histopathological, biochemical, and molecular examination results
Researchers found that oral exposure to polystyrene nanoparticles caused significant kidney damage in rats, including oxidative stress, impaired renal function, and tissue alterations that worsened with increasing dose, demonstrating their nephrotoxic potential.
Exploring the Mechanismof Kidney Injury in Mice Inducedby High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Throughthe Kidney-Gut Axis
This mouse study found that combining a high-fat diet with polystyrene nanoplastic exposure (100 nm, 25 mg/kg/day) worsened kidney toxicity beyond high-fat diet alone, with the combination disrupting lipid metabolism via tryptophan and glycerophospholipid pathways and exacerbating gut microbiota dysbiosis through the kidney-gut axis.
Neurotoxic potential of polystyrene nanoplastics in primary cells originating from mouse brain
Researchers exposed three types of primary mouse brain cells to 100 nm polystyrene nanoplastics and found that neurons underwent apoptosis while astrocytes survived but developed reactive astrocytosis with elevated inflammatory markers, suggesting that neuronal vulnerability to nanoplastic accumulation may be amplified by astrocyte-driven neuroinflammation.
Polystyrene microplastic-induced extracellular vesicles cause kidney-related effects in the crosstalk between tubular cells and fibroblasts
Researchers found that polystyrene microplastics cause kidney tubule cells to release tiny signaling packages (extracellular vesicles) that trigger stress responses and scarring in neighboring kidney cells. This cell-to-cell communication pathway spread the damage beyond the cells directly exposed to the microplastics. The findings suggest a mechanism by which microplastic exposure could contribute to kidney fibrosis and long-term kidney damage in humans.
Cytotoxicity and pro-inflammatory effect of polystyrene nano-plastic and micro-plastic on RAW264.7 cells.
Researchers found that polystyrene nano-plastics (80 nm) induced apoptosis and pro-inflammatory cytokine release in mouse macrophage RAW264.7 cells at lower concentrations than micro-plastics (3 μm), with nano-plastics also enhancing phagocytic activity and activating NF-kB signaling pathways more potently than their larger counterparts.
Reversibility of Renal Fibrosis Induced by Exposure to Polystyrene Nanoplastics: The Dual Role of Lysosomes
Researchers exposed mice to 100 nm and 500 nm polystyrene nanoplastics and examined renal fibrosis, lysosomal function, and autophagy pathways. PS100 induced more pronounced kidney fibrosis than PS500 by impairing lysosomal degradation and disrupting autophagic flux; notably, fibrosis partially reversed after cessation of exposure, suggesting some reversibility in nanoplastic-induced kidney injury.
Nanoplastics as a Potential Environmental Health Factor: From Molecular Interaction to Altered Cellular Function and Human Diseases
This review examined how nanoplastics — particularly polystyrene — interact with cells at the molecular level, potentially causing lasting changes that could contribute to developmental problems and degenerative disease. The study highlights growing concerns about nanoplastics as an emerging environmental health risk given their widespread presence in food, water, and air.
The Kidney-Related Effects of Polystyrene Microplastics on Human Kidney Proximal Tubular Epithelial Cells HK-2 and Male C57BL/6 Mice
This study found that polystyrene microplastics caused damage to human kidney cells in the lab and accumulated in the kidneys of mice. The microplastics triggered mitochondrial dysfunction, inflammation, and a cellular stress response called autophagy in kidney tissue. These results suggest that long-term microplastic exposure could be a risk factor for kidney disease.
Polystyrene microplastics induced oxidative stress, inflammation and necroptosis via NF-κB and RIP1/RIP3/MLKL pathway in chicken kidney
Researchers exposed chickens to different doses of polystyrene microplastics for six weeks to study kidney damage. The study found that microplastic exposure triggered oxidative stress, inflammation, and a form of cell death called necroptosis in kidney tissue through the NF-kappaB and RIP1/RIP3/MLKL signaling pathways.
PS-MPs promotes the progression of inflammation and fibrosis in diabetic nephropathy through NLRP3/Caspase-1 and TGF-β1/Smad2/3 signaling pathways.
In a mouse model of diabetic nephropathy, polystyrene microplastic exposure worsened kidney inflammation and fibrosis by activating the NLRP3/Caspase-1 and TGF-beta1/Smad2/3 signaling pathways, suggesting microplastics may accelerate progression of this common diabetic complication.
The combined effects of polystyrene of different sizes and cadmium in mouse kidney tissues
Researchers studied how polystyrene particles of different sizes combined with cadmium affect kidney health in mice. They found that smaller nanoplastic particles (100 nm) caused more severe kidney damage than larger ones (1 micrometer), and that exposure to both sizes together with cadmium produced the worst outcomes. The study suggests that in real-world conditions where plastics of various sizes coexist with heavy metals, the combined toxic effects on kidneys may be more complicated and harmful than exposure to any single contaminant.