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61,005 resultsShowing papers similar to Impact of polystyrene nanoplastics on apoptosis and inflammation in zebrafish larvae: Insights from reactive oxygen species perspective
ClearImmune response to polystyrene microplastics: Regulation of inflammatory response via the ROS-driven NF-κB pathway in zebrafish (Danio rerio)
Researchers found that polystyrene microplastics triggered immune system inflammation in zebrafish by generating reactive oxygen species (ROS) that activated the NF-kB signaling pathway. The microplastics accumulated mainly in the intestines, causing tissue damage and behavioral changes in the fish. This study identifies a specific molecular mechanism by which microplastics cause immune dysfunction, which could be relevant to understanding inflammation in humans exposed to microplastics.
Polystyrene microplastics induce apoptosis via ROS-mediated p53 signaling pathway in zebrafish
Researchers discovered that polystyrene microplastics trigger programmed cell death in zebrafish gills through a molecular pathway involving reactive oxygen species and the p53 gene. The microplastics caused dose- and time-dependent oxidative damage, inflammation, and physical injury to gill tissue at concentrations as low as 10 micrograms per liter. The study provides molecular-level evidence explaining how microplastic exposure can harm aquatic organisms.
Polystyrene nanoplastics induced cardiomyocyte apoptosis and myocardial inflammation in carp by promoting ROS production
Researchers exposed carp to polystyrene nanoplastics of different sizes and found that the particles caused heart muscle cell death and cardiac inflammation. Smaller nanoplastics penetrated deeper into heart tissue and caused more severe damage by promoting the production of reactive oxygen species. The study provides evidence that nanoplastic pollution in aquatic environments can directly harm fish cardiovascular health.
Toxicological impacts of nanopolystyrene on zebrafish oocyte with insight into the mechanism of action: An expression-based analysis
Researchers investigated the mechanism by which nanopolystyrene causes toxicity in zebrafish oocytes, finding it triggers oxidative stress, immune disruption, and mitochondrial dysfunction through changes in key gene expression pathways.
Evaluation of nanoplastics-induced redox imbalance in cells, larval zebrafish, and daphnia magna with a superoxide anion radical fluorescent probe
Researchers developed a fluorescent probe to detect oxidative damage caused by nanoplastics in living cells, zebrafish larvae, and water fleas. The study suggests that nanoplastic exposure triggers the production of harmful superoxide radicals through specific inflammatory signaling pathways, providing new insight into how these tiny plastic particles may cause biological harm.
Polystyrene nanoplastics cause developmental abnormalities, oxidative damage and immune toxicity in early zebrafish development
Zebrafish embryos exposed to polystyrene nanoplastics showed dose-dependent developmental problems including delayed hatching, reduced survival, smaller body size, and the nanoplastics accumulated in critical organs like the eyes, heart, liver, and brain. The particles triggered oxidative stress that damaged cells and activated inflammatory immune responses, demonstrating how nanoplastic contamination in water can cause widespread harm to developing organisms.
The mechanism of polystyrene nanoplastics hepatotoxicity in zebrafish (Danio rerio)
This study investigated the hepatotoxic mechanisms of polystyrene nanoplastics in zebrafish (Danio rerio), finding that nanoplastics accumulating in the liver triggered oxidative stress and cellular injury pathways. The results highlight nanoplastics as a significant liver toxicant in aquatic vertebrates.
Aged polystyrene microplastics exposure affects apoptosis via inducing mitochondrial dysfunction and oxidative stress in early life of zebrafish
Zebrafish embryos exposed to UV-aged polystyrene microplastics at environmental concentrations showed more severe developmental problems than those exposed to fresh microplastics. The aged particles caused greater oxidative stress and mitochondrial damage, triggering increased cell death during early development -- suggesting that weathered microplastics in the real environment may be more harmful than the pristine particles typically used in lab studies.
Developmental toxicity of carboxylated microplastics in zebrafish mediated by mitochondrial dysfunction and inflammatory activation
Researchers exposed zebrafish larvae to carboxylated polystyrene microplastics at environmentally relevant concentrations (0.1–100 μg/L) and found dose-dependent developmental defects including reduced tail coiling and slowed heart rate, linked to mitochondrial dysfunction and inflammatory activation.
Polystyrene Nanoplastic Exposure Induces Developmental Toxicity by Activating the Oxidative Stress Response and Base Excision Repair Pathway in Zebrafish (Danio rerio)
Researchers exposed zebrafish embryos to polystyrene nanoplastics at various concentrations and found significant developmental abnormalities including reduced hatching rates and increased malformations. The nanoplastics activated oxidative stress responses and DNA repair pathways, indicating cellular damage during critical early development stages. The study provides mechanistic evidence for how nanoplastic exposure can disrupt normal embryonic development in aquatic organisms.
Current Aspects on the Plastic Nano- and Microparticles Toxicity in Zebrafish—Focus on the Correlation between Oxidative Stress Responses and Neurodevelopment
This review examines how nano- and micro-sized plastic particles cause toxic effects in zebrafish, focusing on the link between oxidative stress and neurodevelopmental damage. Researchers found that plastic particle exposure disrupts the balance of reactive oxygen species in cells, which can impair brain development and nervous system function. The study suggests these oxidative stress responses may serve as early warning signals of plastic particle toxicity in aquatic organisms.
Polystyrene nanoplastic induces ROS production and affects the MAPK-HIF-1/NFkB-mediated antioxidant system in Daphnia pulex
Researchers exposed the freshwater crustacean Daphnia pulex to polystyrene nanoplastics and found dose-dependent overproduction of reactive oxygen species (ROS) alongside activation of the MAPK-HIF-1/NFkB stress-signaling cascade, revealing that epigenetic and oxidative pathways mediate nanoplastic toxicity in zooplankton.
Effects of polystyrene nanoplastic size on zebrafish embryo development
Researchers exposed zebrafish embryos to polystyrene nanoplastics of four sizes and found only the smallest (30 nm) caused mortality and altered oxidative stress and apoptosis gene expression, while larger particles (100–450 nm) were ingested and accumulated in the digestive system without causing developmental malformations.
Effects of nanoplastics on zebrafish embryo-larval stages: A case study with polystyrene (PS) and polymethylmethacrylate (PMMA) particles
Researchers assessed the effects of polystyrene and polymethylmethacrylate nanoparticles on zebrafish embryos and larvae over 96 hours. The study found that these nanoplastics affected biochemical endpoints related to neurotransmission, antioxidant status, oxidative damage, and energy metabolism, with effects varying by plastic type. Evidence suggests that smaller plastic particles may have increased bioavailability and reactivity compared to larger fragments.
Nanoplastic contamination: Impact on zebrafish liver metabolism and implications for aquatic environmental health
Zebrafish exposed to polystyrene nanoparticles for 28 days showed significant disruptions in liver metabolism, including altered fat processing, signs of inflammation, oxidative stress, and DNA damage. Notably, at lower doses the liver's detox enzymes appeared to break down the nanoplastics themselves, while higher doses overwhelmed these defenses and caused more severe injury.
Mechanisms underlying mitochondrial dysfunction and intestinal damage induced by ingestion of microplastics in Leuciscus waleckii: The role of the NF-κB/Nrf2 signaling pathway
This study found that polystyrene microplastics harmed juvenile fish by triggering immune dysfunction, oxidative stress, and mitochondrial damage in their intestines. The microplastics activated inflammatory pathways, damaged the intestinal barrier, and shifted the gut microbiome toward harmful bacteria. These findings suggest that microplastic ingestion could have cascading effects on fish health through multiple biological pathways.
Molecular effects of polystyrene nanoplastics toxicity in zebrafish embryos (Danio rerio)
Researchers exposed zebrafish embryos to polystyrene nanoplastics at various concentrations and measured gene expression changes related to stress, inflammation, and DNA repair. They found dose-dependent activation of oxidative stress and apoptotic pathways at the highest concentration, along with inhibition of the neurotransmitter-related gene acetylcholinesterase and DNA repair genes. The study suggests that nanoplastic exposure at the molecular level may compromise cellular defense mechanisms and neurological function in developing fish.
From mothers to offspring: Polystyrene nanoplastics create a hidden toxic legacy via mitochondrial dysfunction
Researchers exposed female zebrafish to polystyrene nanoplastics before mating with unexposed males and found that maternal exposure at 100 μg/L reduced offspring hatching success and caused developmental defects in the F1 generation raised in clean water, demonstrating transgenerational toxicity via mitochondrial dysfunction.
Nanoplastics Cause Neurobehavioral Impairments, Reproductive and Oxidative Damages, and Biomarker Responses in Zebrafish: Throwing up Alarms of Wide Spread Health Risk of Exposure
Researchers exposed adult zebrafish to polystyrene nanoplastics and found that the particles accumulated in the brain, liver, intestine, and gonads, causing significant behavioral and physiological changes. The fish showed disrupted energy metabolism, oxidative stress, and altered locomotion, aggression, and predator avoidance behaviors. The findings raise concerns about the widespread health risks of nanoplastic exposure, as these particles are small enough to cross biological membranes.
Reactive gliosis in adult zebrafish telencephalon following daily nanoplastic consumption
Adult zebrafish fed polystyrene nanoplastics daily for an extended period developed reactive gliosis in the brain, indicating that nanoplastics crossing the blood-brain barrier triggered an immune response in neural tissue.
Immunotoxicity responses to polystyrene nanoplastics and their related mechanisms in the liver of zebrafish (Danio rerio) larvae
Researchers studied how polystyrene nanoplastics affect the immune system of zebrafish larvae by examining inflammatory responses in the liver. They found that smaller nanoparticles caused more severe immune reactions, including increased neutrophil and macrophage activity and activation of inflammatory signaling pathways. The study provides evidence that nanoplastics can trigger significant immune system disruption in fish even at early life stages.
Exposure to Polystyrene Nanoplastics Led to Learning and Memory Deficits in Zebrafish by Inducing Oxidative Damage and Aggravating Brain Aging
Zebrafish exposed to polystyrene nanoplastics developed significant learning and memory problems, taking longer to navigate mazes and showing signs of accelerated brain aging. The nanoplastics caused oxidative damage, energy shortages, and disrupted the cell cycle in brain tissue. This study adds to growing evidence that nanoplastics small enough to cross the blood-brain barrier could impair cognitive function, raising concerns about long-term brain health effects from environmental nanoplastic exposure.
Maternal polystyrene nanoplastics suppress zebrafish offspring development and locomotion through mitochondrial dysfunction
Researchers found that zebrafish mothers exposed to nanoplastics at environmentally relevant concentrations passed developmental harm to offspring, with transcriptomic analysis pointing to suppressed oxidative phosphorylation genes as the mechanism — showing nanoplastics can impair embryo energy metabolism across generations even when offspring are not directly exposed.
Superoxide Dismutase 3 Deficiency Disrupts the Regulation of Oxidative Stress Caused by Polystyrene Nanoplastics
Researchers used superoxide dismutase 3 (SOD3) knockout zebrafish to investigate the role of extracellular antioxidant defenses in polystyrene nanoplastic toxicity, finding that SOD3 deficiency worsened nanoplastic-induced oxidative stress, demonstrating that extracellular antioxidant capacity is an important determinant of nanoplastic harm.