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61,005 resultsShowing papers similar to Polystyrene nanoplastics exacerbate gentamicin-induced nephrotoxicity in adult rat by activating oxidative stress, inflammation and apoptosis pathways
ClearCombined 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.
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.
Aging amplifies the combined toxic effects of polystyrene nanoplastics and norfloxacin on human intestinal cells
Researchers investigated how environmental aging of polystyrene nanoplastics affects their combined toxicity with the antibiotic norfloxacin on human intestinal cells. They found that aged nanoplastics were taken up more readily by cells and significantly amplified the harmful effects of the antibiotic, including increased cell damage. The study suggests that weathered nanoplastics in the environment may pose greater health risks than fresh particles, especially when combined with other contaminants.
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.
Co-exposure to environmentally relevant concentrations of cadmium and polystyrene nanoplastics induced oxidative stress, ferroptosis and excessive mitophagy in mice kidney
A mouse study found that combined exposure to cadmium (a toxic metal) and polystyrene nanoplastics caused more kidney damage than either pollutant alone. The combination triggered a harmful chain reaction involving oxidative stress, iron buildup, and excessive breakdown of cellular energy factories called mitochondria. This is significant because people are often exposed to both nanoplastics and heavy metals simultaneously, and their combined effects may be worse than expected.
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.
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 Mechanism of Kidney Injury in Mice Induced by High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Through the Kidney-Gut Axis
In a mouse study, the combination of a high-fat diet and polystyrene nanoplastics caused worse kidney damage than either exposure alone, working through the kidney-gut connection. The nanoplastics plus high-fat diet disrupted gut bacteria, increased inflammation, and triggered a harmful immune response that traveled from the gut to the kidneys. This suggests that people who eat high-fat diets may be more vulnerable to kidney damage from nanoplastic exposure.
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.
Co-exposure of arsenic and polystyrene-nanoplastics induced kidney injury by disrupting mitochondrial homeostasis and mtROS-mediated ferritinophagy and ferroptosis
Researchers found that arsenic and polystyrene nanoplastics together — but not separately — cause kidney fibrosis in mice by disrupting mitochondrial function and triggering a form of iron-dependent cell death called ferroptosis, with mitochondria-targeted antioxidants significantly reducing the combined damage.
Amplified toxic effects of nanoplastic composite norfloxacin on liver cells in mice: Mechanistic insights and multiscale evaluation
Researchers examined the combined toxic effects of nanoplastics and the antibiotic norfloxacin on mouse liver cells and found that co-exposure was significantly more harmful than either contaminant alone. The nanoplastics acted as carriers that increased antibiotic accumulation inside cells, amplifying oxidative damage and disrupting key protective enzymes. The study highlights that nanoplastics in the environment can worsen the toxicity of co-occurring pollutants like antibiotics.
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.
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.
Combined effects of nanoplastics and 3-BHA at environmentally relevant concentrations significantly aggravated kidney injury via TGF-β/SMAD signaling pathway in mice
Researchers investigated combined exposure to nanoplastics and the synthetic antioxidant 3-BHA at environmentally relevant concentrations, finding that the combination caused greater disruption to renal function than either contaminant alone, suggesting synergistic kidney toxicity.
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.
Polystyrene nanoplastics exacerbated the ecotoxicological and potential carcinogenic effects of tetracycline in juvenile grass carp (Ctenopharyngodon idella)
Researchers found that polystyrene nanoplastics significantly worsened the toxic effects of the antibiotic tetracycline in juvenile grass carp. Combined exposure increased oxidative damage, upregulated genes associated with tissue remodeling and inflammation in the liver and intestine, and caused visible tissue lesions in the intestine and gills.
Polyethylene microplastics disrupt renal function, mitochondrial bioenergetics, redox homeostasis, and histoarchitecture in Wistar rats
Researchers gave rats polyethylene microplastics orally for 28 days and found dose-dependent kidney damage, including impaired filtration, electrolyte imbalances, and tissue inflammation. The microplastics depleted antioxidant defenses, increased oxidative stress markers, and disrupted mitochondrial energy production in kidney cells, identifying the kidneys as a critical target of microplastic toxicity.
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 effects of nanosized polystyrene and erythromycin on bacterial growth and resistance mutations in Escherichia coli
Researchers found that polystyrene nanoplastics — particularly amino-modified and 30 nm particles — increased antibiotic resistance mutations in Escherichia coli by inducing oxidative DNA damage and the bacterial SOS stress response, and that positively charged particles synergistically enhanced erythromycin toxicity by acting as antibiotic carriers.
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.
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 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.
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.