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61,005 resultsShowing papers similar to Microplastics induced inflammation in the spleen of developmental Japanese quail (Coturnix japonica) via ROS-mediated p38 MAPK and TNF signaling pathway activation1
ClearToxicity induced via ingestion of naturally-aged polystyrene microplastics by a small-sized terrestrial bird and its potential role as vectors for the dispersion of these pollutants
Researchers exposed Japanese quail to naturally aged polystyrene microplastics to evaluate health effects from ingestion. The study found significant body weight reduction, increased oxidative damage in the liver, brain, intestine, and gizzard, and evidence that birds can transport microplastics to new environments through excretion. These findings suggest that even small terrestrial birds may serve as vectors for microplastic dispersal.
The effects of microplastics exposure on quail's hypothalamus: Neurotransmission disturbance, cytokine imbalance and ROS/TGF-β/Akt/FoxO3a signaling disruption
Japanese quail exposed to polystyrene microplastics for five weeks showed significant brain damage in the hypothalamus, including structural changes to neurons, disrupted chemical signaling, and inflammation. The microplastics caused oxidative stress and interfered with important cell-survival pathways in the brain. While studied in birds, these neurotoxic effects are relevant because similar brain pathways exist in humans, and they suggest microplastic exposure could affect neurological function.
Polystyrene microplastics mediate inflammatory responses in the chicken thymus by Nrf2/NF-κB pathway and trigger autophagy and apoptosis
Researchers exposed chickens to polystyrene microplastics and found significant damage to the thymus, a key immune organ. The microplastics triggered oxidative stress, inflammation, and cell death through specific molecular pathways. The study suggests that microplastic exposure could compromise immune function in animals by damaging organs responsible for immune cell development.
Transcriptomic and metabolomic analysis reveals hepatic lipid metabolism disruption in Japanese quail under polystyrene microplastics exposure
Researchers fed Japanese quail polystyrene microplastics at environmentally relevant concentrations for 35 days and analyzed liver effects using transcriptomics and metabolomics. Low doses caused increased food intake and weight gain with liver lipid accumulation, while high doses led to decreased intake and weight loss, suggesting a hormetic dose-response pattern. The study found that microplastic exposure disrupted hepatic lipid metabolism pathways and caused liver oxidative stress in birds.
New insights into the spleen injury by mitochondrial dysfunction of chicken under polystyrene microplastics stress
Chickens exposed to polystyrene microplastics in their drinking water developed significant spleen damage, with higher doses causing worse effects. The microplastics disrupted mitochondrial function in spleen cells, triggering both apoptosis (programmed cell death) and ferroptosis (iron-dependent cell death), along with harmful oxidative stress. These findings are relevant to human health because the spleen plays an important role in immune function, and similar damage pathways could potentially occur in people exposed to microplastics.
Polystyrene microplastics disrupted physical barriers, microbiota composition and immune responses in the cecum of developmental Japanese quails
Researchers fed Japanese quails environmentally relevant concentrations of polystyrene microplastics for five weeks and examined their gut health. They found that microplastics damaged the physical barriers of the cecum, disrupted the gut microbial community, and impaired immune responses. The study suggests that even low-level microplastic contamination in the environment could compromise gut health and immune function in birds.
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.
Immune 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-induced cardiotoxicity in chickens via the ROS-driven NF-κB-NLRP3-GSDMD and AMPK-PGC-1α axes
Researchers found that polystyrene microplastics caused serious heart damage in chickens by triggering oxidative stress, inflammation, and disruption of the cells' energy production systems. The microplastics activated inflammatory pathways that led to a type of cell death called pyroptosis and damaged the mitochondria that power heart cells. These findings suggest that microplastic exposure could pose risks to cardiovascular health in animals, with potential implications for understanding heart-related effects in humans.
Polystyrene microplastics induced inflammation with activating the TLR2 signal by excessive accumulation of ROS in hepatopancreas of carp (Cyprinus carpio)
Researchers exposed carp to polystyrene microplastics and found that the particles induced inflammation in the hepatopancreas by triggering excessive accumulation of reactive oxygen species and activating the TLR2 immune signaling pathway. Both tissue-level and cellular experiments confirmed increased expression of inflammatory molecules including TNF-alpha and IL-1beta. The study reveals a specific molecular mechanism by which microplastics cause inflammatory damage in freshwater fish organs.
Micro- and nano-plastics activation of oxidative and inflammatory adverse outcome pathways
This review maps the biological harm caused by micro- and nanoplastics to formal toxicity pathways, finding that oxidative stress is a common starting point for damage at every level from cells to whole organisms. Researchers found that in ecological settings, this oxidative damage cascades into growth inhibition and behavioral changes, while in human health contexts it may trigger inflammatory responses. The study highlights that more mammalian research is needed to fully define the health risks of plastic particle exposure.
Environmental microplastics exposure decreases antioxidant ability, perturbs gut microbial homeostasis and metabolism in chicken
Researchers studied the effects of microplastic exposure on chickens and found that it decreased growth performance and antioxidant capacity while causing damage to the intestine, liver, kidney, and spleen. The study also revealed significant changes in gut microbiota composition, including decreased diversity and shifts in taxonomic makeup, suggesting microplastics disrupt gut microbial homeostasis in poultry.
Immunomodulatory and biochemical alterations in chick embryos exposed to polystyrene microplastics
Chick embryos were exposed to polystyrene microplastics at 150 and 300 ug/ml to assess effects on immune system function and key biochemical markers over an incubation period. The study documented immunomodulatory changes and biochemical alterations, raising concerns about developmental effects of microplastic exposure in avian models.
Microplastic Ingestion Induces Size-Specific Effects in Japanese Quail
Researchers found that Japanese quail ingesting environmentally collected microplastics showed size-specific effects, with small particles under 125 micrometers causing different physiological responses than larger 3mm particles, demonstrating that particle size matters for avian microplastic toxicity.
Effect of polystyrene microplastics on the antioxidant system and immune response in GIFT (Oreochromis niloticus)
Farmed tilapia exposed to polystyrene microplastics of different sizes showed elevated oxidative stress and immune inflammation markers, particularly in the brain, compared to unexposed fish. The findings suggest chronic microplastic exposure can impair immune defenses in commercially important freshwater fish, raising concerns for both aquaculture and wild fisheries.
Toxic effects of microplastics on freshwater fish (Channa argus): mechanisms of inflammation, apoptosis, and autophagy
Freshwater snakehead fish exposed to polystyrene microplastics for four weeks developed inflammation, cell death, and tissue damage in their liver, intestines, kidneys, and gills. The damage worsened with higher microplastic concentrations and involved disruption of the fish's antioxidant defenses and immune system. Since snakehead is a commonly consumed fish in Asia, these findings raise questions about whether microplastics in aquaculture environments could affect the safety of fish as human food.
The impact of polystyrene nanoplastics on the chicken gut and liver: Based on transcriptomics and microbiomics
Researchers fed polystyrene nanoplastics to chickens for 21 days and found that the particles triggered inflammation and oxidative stress in the gut and liver, damaged the intestinal lining, and disrupted the gut microbiome — with some effects persisting even after exposure stopped. Because poultry is a major protein source for humans globally, these findings raise concerns about nanoplastic contamination in the food supply.
The impact of polyethylene microplastics exposure on the, growth performance, reproductive performance, antioxidant capacity, and intestinal microbiota of quails
Researchers fed quails different levels of polyethylene microplastics and found that exposure harmed their growth, reproduction, and gut health. The microplastics reduced antioxidant defenses and disrupted the balance of beneficial bacteria in the birds' intestines. Since poultry is a major food source for people, microplastic contamination in farm animals raises concerns about indirect human exposure through the food chain.
The ingestion of microplastics affects the diversity of the gut microbiome and testicular development in Japanese quail
This study examined how microplastic ingestion affects gut microbiome diversity and composition in an animal model, finding that microplastic exposure alters microbial community structure in ways that may impair digestive and immune function.
Cellular and Systemic Effects of Micro- and Nanoplastics in Mammals—What We Know So Far
This review summarized known cellular and systemic effects of micro- and nanoplastics in mammals, finding that while ingestion is common, knowledge of health impacts remains limited, with oxidative stress and inflammation as the most reported biological responses.
Exposure to microplastics affects fatty acid composition in the Japanese quail depending on sex and particle size
Researchers exposed Japanese quail to microplastics and found that the effects on fatty acid composition varied depending on both the sex of the bird and the size of the plastic particles. The study suggests that microplastic ingestion may disrupt lipid metabolism in birds, with potential implications for their health and reproductive fitness.
Polystyrene microplastics induce an immunometabolic active state in macrophages
Researchers found that polystyrene microplastics taken up by macrophages — immune cells lining the gut and lungs — triggered a metabolic shift toward an inflammatory state. This finding suggests microplastics reaching human tissues may alter immune function in ways that could contribute to inflammation-related diseases.
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.
Inhalation of Microplastics Induces Inflammatory Injuries in Multiple Murine Organs via the Toll-like Receptor Pathway
After mice inhaled polystyrene microplastics, the particles spread to the brain, liver, kidneys, spleen, and other organs within days, triggering widespread inflammation through a specific immune signaling pathway called TLR/NF-kB. These findings suggest that breathing in microplastics could cause inflammatory damage across multiple organ systems in the body.