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61,005 resultsShowing papers similar to Polystyrene nanoplastics induce apoptosis of human kidney proximal tubular epithelial cells via oxidative stress and MAPK signaling pathways
ClearNanoplastic 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.
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.
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.
Polystyrene microplastics disrupt kidney organoid development via oxidative stress and Bcl-2/Bax/caspase pathway
Researchers used lab-grown kidney organoids made from human stem cells to study how polystyrene microplastics affect kidney development. The microplastics triggered oxidative stress and activated cell death pathways, disrupting the formation of key kidney structures. This study provides direct evidence that microplastic exposure could interfere with human organ development, which is especially concerning for fetuses and young children.
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.
Issue Information‐ToC
This brief notice indicates a paper in the journal issue that examines how polystyrene nanoplastics worsen inflammation-triggered cell death (apoptosis) in mouse kidney cells exposed to bacterial toxins. The interaction between nanoplastics and inflammatory signals may amplify kidney damage beyond what either stressor alone would cause.
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.
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.
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.
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 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.
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.
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.
Nanoplastics-induced oxidative stress, antioxidant defense, and physiological response in exposed Wistar albino rats
Researchers orally exposed Wistar rats to polystyrene nanoplastics at multiple doses for five weeks and observed dose-dependent increases in oxidative stress. The study found significant alterations in liver and kidney function markers, disrupted energy metabolism, and changes in antioxidant enzyme activity, suggesting that nanoplastic exposure may affect multiple organ systems in mammals.
Polystyrene microplastics induced nephrotoxicity associated with oxidative stress, inflammation, and endoplasmic reticulum stress in juvenile rats
This study found that polystyrene microplastics caused kidney damage in young rats through a combination of oxidative stress, inflammation, and a cellular stress response called endoplasmic reticulum stress. The microplastics also reduced body weight growth and affected multiple organs including the heart and ovaries. These findings suggest that microplastic exposure during development could be particularly harmful to kidney health in young, growing organisms.
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.
Toxic effects of polystyrene nanoplastics on MDA-MB-231 breast cancer and HFF-2 normal fibroblast cells: viability, cell death, cell cycle and antioxidant enzyme activity
Researchers exposed human breast cancer cells and normal skin cells to polystyrene nanoplastics and found that smaller particles at higher concentrations caused significant cell death through apoptosis (programmed cell death) and reduced the cells' ability to defend against oxidative damage. The dose- and size-dependent toxicity suggests that nanoplastics small enough to enter cells are more biologically harmful than larger particles.
Assessment of cancer-related signaling pathways in responses to polystyrene nanoplastics via a kidney-testis microfluidic platform (KTP)
Researchers developed a kidney-testis microfluidic platform to assess cancer-related signaling pathway responses to polystyrene nanoplastics. The study found that nanoplastic exposure activated cancer-associated signaling pathways in both kidney and testis tissue models, providing new insights into the potential molecular mechanisms through which nanoplastics may affect organ health.
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 induce profound metabolic shift in human cells as revealed by integrated proteomic and metabolomic analysis
Researchers used integrated proteomic and metabolomic analysis to study how polystyrene nanoplastics affect human kidney and liver cell lines. The study quantified changes in thousands of proteins and hundreds of metabolites, revealing that nanoplastic exposure induced a profound metabolic shift in human cells. Evidence indicates that nanoplastics can be internalized by human cells and trigger significant biological changes at the molecular level.
Polystyrene micro(nano)plastics damage the organelles of RBL-2H3 cells and promote MOAP-1 to induce apoptosis
Researchers exposed immune cells to polystyrene particles of different sizes and found that the particles caused oxidative stress, damaged mitochondria and lysosomes, and triggered programmed cell death. The study identified a specific molecular mechanism involving the MOAP-1 protein that drives microplastic-induced cell death, with 50-nanometer particles causing the most severe effects.
Polystyrene microplastics exacerbate experimental chronic kidney disease via inflammatory and oxidative pathways involving NF-κB, ERK/p38 MAPK, and sirtuin-1
Researchers examined the effects of polystyrene microplastics on mice with chronic kidney disease and found that microplastic exposure worsened kidney dysfunction, inflammation, and tissue scarring. Even in healthy mice, microplastics reduced kidney filtration and increased markers of kidney damage. The study suggests that microplastic exposure may aggravate existing kidney conditions through inflammatory and oxidative stress pathways.
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.