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61,005 resultsShowing papers similar to Polystyrene micro- and nanoplastics induce gastric toxicity through ROS mediated oxidative stress and P62/Keap1/Nrf2 pathway
ClearSize-dependent toxicity of polystyrene microplastics on the gastrointestinal tract: Oxidative stress related-DNA damage and potential carcinogenicity
Researchers found that polystyrene microplastics accumulate mainly in stomach tissue, where smaller nanoscale particles cause more severe damage than larger ones. The nanoplastics reduced antioxidant enzyme activity, increased DNA damage markers, and activated signaling pathways associated with cancer development. These size-dependent effects on the gastrointestinal tract suggest that the smallest plastic particles may pose the greatest risk to digestive health.
Nano-plastics and gastric health: Decoding the cytotoxic mechanisms of polystyrene nano-plastics size
Researchers examined how different sizes of polystyrene nanoplastics affect human stomach cells in the laboratory. They found that smaller nanoplastics were more readily taken up by the cells and caused greater damage, including increased oxidative stress and reduced cell survival. The study suggests that nanoplastic particle size plays a critical role in determining their potential impact on gastrointestinal health.
Polystyrene nanoplastics deteriorate LPS-modulated duodenal permeability and inflammation in mice via ROS drived-NF-κB/NLRP3 pathway
Researchers found that polystyrene nanoplastics worsened intestinal inflammation and increased gut permeability in mice already exposed to bacterial endotoxin. The combined exposure triggered higher levels of oxidative stress and activated inflammatory pathways, leading to greater damage to the intestinal lining than either substance alone. The study suggests that nanoplastic exposure could make the gut more vulnerable to inflammation and barrier breakdown when other stressors are present.
Polystyrene nanoplastics exposure causes inflammation and death of esophageal cell
Researchers exposed human esophageal cells to polystyrene nanoplastics and found that the particles triggered significant inflammation and cell death. The nanoplastics activated inflammatory signaling pathways and caused oxidative damage to the cells at concentrations relevant to human dietary exposure. The findings raise concerns about the potential effects of nanoplastic contamination in food and drinking water on the upper digestive tract.
Polystyrene microplastic-induced oxidative stress triggers intestinal barrier dysfunction via the NF-κB/NLRP3/IL-1β/MCLK pathway
Mice that swallowed polystyrene microplastics for 28 days developed oxidative stress and inflammation in their colons, leading to a weakened intestinal barrier with reduced protective mucus and loosened cell connections. The largest microplastics (5 micrometers) caused the most severe gut damage through a specific inflammatory pathway (NF-kB/NLRP3/MLCK), and antioxidant treatment was able to partially reverse the effects.
Polystyrene Nanoplastics in Human Gastrointestinal Models—Cellular and Molecular Mechanisms of Toxicity
This review summarizes current knowledge on how polystyrene nanoplastics affect human gastrointestinal cells at the molecular level. Researchers found that once internalized, these particles can trigger oxidative stress, mitochondrial dysfunction, DNA damage, and disruptions to calcium signaling and metabolism. The evidence indicates that nanoplastics interact with biological systems in complex ways that may compromise cellular integrity in the digestive tract.
Additional file 2 of Underestimated health risks: polystyrene micro- and nanoplastics jointly induce intestinal barrier dysfunction by ROS-mediated epithelial cell apoptosis
This is a supplementary data file providing numerical values for a study on how polystyrene micro- and nanoplastics damage the intestinal barrier through oxidative stress-induced cell death. The underlying study is relevant to understanding how plastic particles ingested through food or water may harm the human gut lining.
Underestimated health risks: polystyrene micro- and nanoplastics jointly induce intestinal barrier dysfunction by ROS-mediated epithelial cell apoptosis
This mouse study found that when micro-sized and nano-sized polystyrene particles were present together, as they would be in the real world, they caused more intestinal damage than either size alone. The combined exposure increased gut permeability by killing intestinal lining cells through oxidative stress, weakening the barrier that keeps harmful substances out of the bloodstream. This is important because real-world microplastic exposure always involves a mix of particle sizes, meaning health risks may be greater than single-size lab studies suggest.
The detrimental effects of micro-and nano-plastics on digestive system: An overview of oxidative stress-related adverse outcome pathway
This review maps out how micro and nanoplastics damage the digestive system, identifying oxidative stress as the initial trigger that leads to inflammation, cell death, disrupted gut bacteria, and metabolic disorders. The authors use an adverse outcome pathway framework to connect molecular-level damage to broader health consequences. The findings suggest that ongoing microplastic exposure through food and water could contribute to digestive health problems.
PMMA nanoplastics induce gastric epithelial cellular senescence and cGAS-STING-mediated inflammation via ROS overproduction and NHEJ suppression
Researchers found that PMMA (acrylic) nanoplastics caused premature aging in stomach lining cells by generating excessive reactive oxygen species and blocking the cells' ability to repair DNA damage. The damaged cells released free DNA fragments that activated inflammatory immune pathways, and mice exposed to the nanoplastics showed behavioral changes associated with aging. This study is notable because most nanoplastic research focuses on polystyrene, and it shows that acrylic nanoplastics can also cause significant harm to the digestive system.
Polystyrene microplastics trigger colonic inflammation in rats via the TLR4/NF-κB/COX-2 pathway and modulation of intestinal microbiota
Rats exposed to polystyrene microplastics for 90 days developed significant colon inflammation, including damaged gut lining, increased inflammatory markers, and disrupted gut bacteria. The study identified a specific inflammatory pathway (TLR4/NF-kB/COX-2) through which microplastics trigger intestinal inflammation, providing important clues about how plastic particles in food and water could contribute to gut diseases in humans.
Benzo [a] pyrene-loaded aged polystyrene microplastics promote colonic barrier injury via oxidative stress-mediated notch signalling
Researchers found that aged polystyrene microplastics loaded with benzo[a]pyrene, a common environmental carcinogen, caused significantly more damage to the colon lining in mice than clean microplastics. The contaminated particles triggered oxidative stress, inflammation, and disrupted the protective barrier of the intestine through a specific cell signaling pathway. This suggests that real-world microplastics, which commonly carry absorbed toxic chemicals, may be more harmful to gut health than pristine lab particles.
Impacts of polystyrene microplastic on the gut barrier, microbiota and metabolism of mice
Researchers exposed mice to polystyrene microplastics for six weeks and found that the particles accumulated in the gut, reduced protective mucus secretion, and damaged the intestinal barrier. The microplastics also significantly altered the composition of gut bacteria, decreasing beneficial species and increasing harmful ones. The study suggests that microplastic ingestion could disrupt gut health in mammals by simultaneously impairing the physical barrier and reshaping the microbiome.
Intrinsic Peroxidase-like Activity of Polystyrene Nanoplastics Mediates Oxidative Stress
Scientists discovered that polystyrene nanoplastics have a built-in enzyme-like ability to generate harmful reactive oxygen species, similar to how the body's own peroxidase enzymes work. This activity increased with the nanoplastics' size and aromatic chemical structure. The finding provides a new explanation for why nanoplastics cause oxidative stress in living things, which is a key mechanism behind potential health damage from plastic particle exposure.
Pro-Inflammatory and Cytotoxic Effects of Polystyrene Microplastics on Human and Murine Intestinal Cell Lines
Researchers tested the effects of polystyrene microplastics on human and mouse intestinal cell lines. They found that microplastic exposure increased cell death and triggered inflammatory responses, including the release of inflammatory signaling molecules. The study suggests that microplastics may promote inflammation in the gut lining, which could have implications for digestive health.
Tissue distribution of polystyrene nanoplastics in mice and their entry, transport, and cytotoxicity to GES-1 cells
Scientists tracked polystyrene nanoplastics in mice after oral exposure and found the particles accumulated in the stomach, intestines, and liver tissues. In human gastric cells, the nanoplastics entered through multiple pathways and were transported through the cell's internal trafficking system, ultimately reducing cell growth and increasing cell death. The study provides detailed evidence of how nanoplastics can cross biological barriers and cause cellular damage in mammalian systems.
Role of Nanoplastics in Decreasing the Intestinal Microbiome Ratio: A Review of the Scope of Polystyrene
This scoping review of 56 studies found consistent evidence that polystyrene nanoplastics (≤100 nm) disrupt gut homeostasis through a three-stage cascade: ROS generation and oxidative stress, intestinal barrier dysfunction, and gut microbiome dysbiosis, with downstream effects on immunity and multiple organs.
Polystyrene microplastics induce endoplasmic reticulum stress, apoptosis and inflammation by disrupting the gut microbiota in carp intestines
Researchers fed carp polystyrene microplastics and found that the particles disrupted their gut bacteria, killing off beneficial species and promoting those linked to diseases. The microplastics triggered a stress response in intestinal cells that led to inflammation, cell death, and tissue damage. Since carp is a widely eaten fish, these gut health effects raise questions about how microplastics in aquatic environments could affect the safety of fish that humans consume.
Polystyrene nanoparticles induced mammalian intestine damage caused by blockage of BNIP3/NIX-mediated mitophagy and gut microbiota alteration
Researchers found that polystyrene nanoparticles can damage the intestines of mammals by blocking a cellular cleanup process called mitophagy, which normally removes damaged mitochondria. In both cell cultures and animal models, exposure to these nanoparticles disrupted gut barrier function and altered gut microbiota composition. The study suggests that nanoplastic accumulation in food sources could pose a real risk to digestive health.
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.
Assessment of the Toxicity of Polystyrene Microplastic in the Colon and Liver of Adult NMRI Mice
Researchers orally administered polystyrene microplastics to adult male mice at four doses for four weeks and examined histological changes in the colon and liver. Both organs showed dose-dependent tissue damage including inflammation and oxidative stress markers, with the colon showing earlier onset injury due to direct contact with ingested particles.
Adverse effects of pristine and aged polystyrene microplastics in mice and their Nrf2-mediated defense mechanisms with tissue specificity
Researchers exposed mice to pristine and UV-aged polystyrene microplastics via intratracheal instillation and found structural damage to the gut, liver, spleen, and testis. Aged microplastics caused greater functional damage than pristine particles, including increased liver enzymes and cholesterol, reduced antioxidant capacity, and tissue-specific activation of the Nrf2 defense pathway.
Exposure to Polystyrene Microplastic Differentially Affects the Colon and Liver in Adult Male Mice
Researchers fed male mice polystyrene microplastics at varying doses for six weeks and examined the effects on their colon and liver. They found that the microplastics reduced antioxidant enzyme activity, damaged the intestinal barrier, disrupted mucus production, and caused tissue changes in both organs. The study provides further evidence that oral exposure to microplastics can cause oxidative stress and structural damage in the digestive system and liver.
Hepatotoxic of polystyrene microplastics in aged mice: Focus on the role of gastrointestinal transformation and AMPK/FoxO pathway
This study found that polystyrene microplastics caused liver damage in aged mice, with the particles undergoing chemical changes as they passed through the digestive system that may have made them more harmful. The microplastics disrupted key metabolic pathways in the liver, triggered inflammation, and caused DNA damage through oxidative stress. The findings are especially concerning because older individuals may be more vulnerable to the liver-damaging effects of microplastic exposure.