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61,005 resultsShowing papers similar to N6-methyladenosine RNA methylation regulates microplastics-induced cell senescence in the rainbow trout liver
ClearHepatotoxic effects of environmentally relevant concentrations of polystyrene microplastics on senescent Zebrafish (Danio rerio): Patterns of stress response and metabolomic alterations
Researchers exposed aging zebrafish to environmentally realistic levels of polystyrene microplastics and found significant liver damage, including disrupted stress responses and altered metabolism. This study is notable because it focused on older organisms, suggesting that elderly populations may be more vulnerable to the toxic effects of microplastic exposure.
Toxicity assessment of pollutants sorbed on environmental sample microplastics collected on beaches: Part I-adverse effects on fish cell line
Environmental microplastics from Pacific island beaches were tested on rainbow trout liver cells (RTLW-1), with MPs from all three island locations causing cytotoxicity and inducing metabolic enzyme activity, while virgin MPs showed no significant effects. The study demonstrates that contaminant loading on beach-collected microplastics drives cell-level toxicity beyond the physical plastic particle effects alone.
N6-methyladenosine methylation mediates non-coding RNAs modification in microplastic-induced cardiac injury
Researchers found that microplastic exposure in mice led to accumulation in organs and triggered cell death, particularly affecting heart tissue. Using advanced sequencing techniques, they discovered that microplastics altered chemical modifications (m6A methylation) on non-coding RNA molecules in heart cells, which may disrupt important gene regulatory networks. The study suggests a potential molecular mechanism through which microplastic exposure could contribute to heart damage, though more research is needed to understand the full implications.
Genotoxicity and metabolic changes induced via ingestion of virgin and UV-aged polyethylene microplastics by the freshwater fish Perca fluviatilis
Freshwater perch fed UV-aged polyethylene microplastics showed greater DNA damage and more severe metabolic disruption in liver and muscle tissue than fish fed virgin (new) microplastics. The aged plastics disrupted energy metabolism, amino acid processing, and neurotransmitter levels. Since most microplastics in the environment have been weathered by sunlight, these findings suggest the real-world health risks to fish — and potentially to the humans who eat them — may be greater than lab studies using fresh plastics indicate.
Microplastic exposure linked to accelerated aging and impaired adipogenesis in fat cells
Researchers found that microplastic exposure accelerates aging in fat tissue by triggering cellular senescence (a state where cells stop dividing and release inflammatory signals) in both mice and cell cultures. The microplastics accumulated in fat tissue, increased markers of aging and inflammation, and disrupted the normal development of new fat cells. These findings suggest that chronic microplastic exposure could contribute to age-related metabolic problems and obesity-related diseases in humans.
Microplastic exposure is associated with epigenomic effects in the model organism Pimephales promelas (fathead minnow)
Researchers exposed fathead minnows to microplastics and found changes in DNA methylation -- a chemical modification that controls which genes are turned on or off -- across multiple organs including the brain, liver, and gonads. These epigenetic changes are heritable, meaning microplastic exposure could affect not just the exposed fish but also future generations, raising concerns about long-term ecological and evolutionary impacts.
Dietary intake of microplastics impairs digestive performance, induces hepatic dysfunction, and shortens lifespan in the annual fish Nothobranchius guentheri
Researchers fed microplastics to the annual fish Nothobranchius guentheri and tracked the effects over their lifespan. The study found that dietary microplastic intake impaired digestion, caused liver dysfunction, and notably shortened the fish's lifespan while accelerating age-related changes. This represents some of the first evidence in vertebrates that chronic microplastic exposure may affect aging and longevity.
Unravelling the Potential Role of Nanoplastics and Microplastics‐Induced Toxicity in Freshwater Fish: Emerging Role of Programmed Cell Death Mechanisms
This review examines how micro- and nanoplastics trigger various forms of programmed cell death in freshwater fish, including apoptosis, autophagy, ferroptosis, and pyroptosis. The study highlights that exposure to these plastic particles generates oxidative stress, inflammation, and DNA damage, with the resulting cell death mechanisms potentially compromising fish health and raising concerns about contamination reaching humans through seafood consumption.
The effects of exposure to microplastics on grass carp (Ctenopharyngodon idella) at the physiological, biochemical, and transcriptomic levels
Researchers exposed grass carp to microplastics at two concentrations for 21 days and observed liver damage, inhibited growth, and increased oxidative stress. Transcriptome analysis revealed over 1,500 differentially expressed genes related to immune response, metabolism, and cellular stress pathways. The study suggests that microplastic exposure can trigger broad physiological and molecular disruptions in freshwater fish.
The involvement of oxidative stress mediated endoplasmic reticulum pathway in apoptosis of Golden Pompano (Trachinotus blochii) liver under PS-MPs stress
Researchers exposed golden pompano, a commercially important marine fish in China, to polystyrene microplastics at three concentrations for 14 days and observed slowed growth and significant liver damage. The microplastics induced oxidative stress and triggered endoplasmic reticulum-mediated apoptosis in liver cells. The study provides evidence that coastal aquaculture species face real toxicological risks from microplastic pollution in their farming environments.
Oxidative and inflammatory responses to virgin and beached microplastics in marine fish liver
This study compared oxidative stress and inflammation responses in marine organisms exposed to virgin microplastics versus weathered, beach-collected microplastics. Beached particles, which have undergone environmental aging, triggered different and in some cases stronger toxic responses than their pristine counterparts.
Investigating the Epigenetic Effects of Polystyrene Nanoplastic Exposure in Bluegill (Lepomis macrochirus) Epithelial Cells Using Methylation-Sensitive AFLPs
Researchers exposed bluegill fish cells to polystyrene nanoplastics and examined whether the exposure caused changes in DNA methylation, a type of genetic modification that can alter how genes function. They found that nanoplastic exposure did cause methylation changes across the genome, but the effect was not dependent on dose or exposure time -- simply being exposed to nanoplastics was enough to trigger the changes. The findings suggest that even low-level nanoplastic exposure could have epigenetic effects on aquatic organisms.
The regulation of circRNA_kif26b on alveolar epithelial cell senescence via miR-346-3p is involved in microplastics-induced lung injuries
Researchers found that inhaled polystyrene microplastics caused lung damage in rats by accelerating the aging of cells lining the air sacs, through a specific molecular pathway involving circular RNA. The microplastics triggered inflammation, fibrosis, and premature cell aging in lung tissue over a 35-day exposure period. The study reveals a new mechanism by which inhaled microplastics may contribute to lung injury.
Genome-wide identification of socs gene in rainbow trout (Oncorhynchus mykiss) and response to microplastic exposure
Researchers identified 27 members of the SOCS gene family in rainbow trout and studied how their expression changed after microplastic exposure. They found that several of these immune-regulating genes were significantly up- or down-regulated in the liver, intestine, and brain following exposure. The study provides new insights into the molecular mechanisms by which microplastics may disrupt immune signaling in freshwater fish.
Polyethylene microplastics cause apoptosis via the MiR-132/CAPN axis and inflammation in carp ovarian
Researchers exposed carp to polyethylene microplastics in water and found that the particles caused significant damage to the fish's ovarian tissue through both cell death and inflammation. They identified a specific molecular pathway involving a microRNA and a protein-cutting enzyme that mediated the harmful effects on reproductive cells. The study provides evidence that microplastic contamination in waterways could impair the reproductive health of commonly consumed fish species.
Oxidative and inflammatory responses to virgin and beached microplastics in marine fish liver
This study compared oxidative stress and inflammatory responses in marine fish exposed to virgin versus beached, weathered microplastics, finding that aging changes particle toxicity. Beached microplastics triggered stronger or qualitatively different inflammatory responses than their pristine counterparts, underscoring the importance of using environmentally realistic particles in toxicity studies.
Effects of Polystyrene Microplastic Exposure on Liver Cell Damage, Oxidative Stress, and Gene Expression in Juvenile Crucian Carp (Carassius auratus)
Researchers exposed young crucian carp to polystyrene microplastics at different concentrations and found dose-dependent liver damage, with higher concentrations causing more severe tissue injury and weaker antioxidant defenses. The microplastics disrupted genes involved in detoxification and stress response in liver cells. Since crucian carp is a commonly consumed freshwater fish, these findings raise questions about whether microplastic-contaminated fish could affect the health of people who eat them.
Molecular and Cellular Effects of Microplastics and Nanoplastics: Focus on Inflammation and Senescence
This review summarizes research showing that micro- and nanoplastics trigger oxidative stress, inflammation, and premature cell aging across many experimental models. These are the same biological processes linked to heart disease, brain disorders, and other age-related conditions. Particularly concerning, studies in animals show that plastic-related damage can be passed from parents to offspring, suggesting potential long-term generational health effects.
Investigating Polystyrene Nano-Plastic Effects on Largemouth Bass (Micropterus salmoides) Focusing on mRNA Expression: Endoplasmic Reticulum Stress and Lipid Metabolism Dynamics
Researchers investigated how polystyrene nanoplastics affect the liver of largemouth bass, focusing on endoplasmic reticulum stress and fat metabolism. They found that nanoplastic exposure disrupted normal lipid processing and triggered stress responses in liver cells, altering the expression of genes involved in fat storage and energy regulation. The study suggests that nanoplastic pollution in freshwater environments may impair metabolic health in fish.
Telomere length as a genomic biomarker for assessing microplastic-induced damage in farmed gilthead sea bream
Researchers used telomere length as a genomic biomarker to assess the biological impact of microplastic exposure in farmed gilthead sea bream. The study found that microplastic exposure was associated with changes in telomere length, suggesting that this measure of cellular aging and genomic integrity could serve as a useful indicator for monitoring the long-term health effects of microplastic contamination in aquaculture species.
Microplastics induced endoplasmic reticulum stress to format an inflammation and cell death in hepatocytes of carp (Cyprinus carpio)
Researchers fed carp water containing polystyrene microplastics and found significant liver damage, including inflammation, disrupted cell recycling processes, and cell death. The microplastics triggered a stress response in the cell's protein-folding machinery (endoplasmic reticulum), which set off a chain reaction of inflammation and tissue damage. These findings in freshwater fish suggest that microplastics can cause serious organ damage through specific cellular stress pathways.
Lipid Metabolism and Oxidative Stress Altered in Crucian Carp (Carassius auratus) Following Exposure to Microplastics Under Laboratory and Field Conditions
Researchers used high-throughput sequencing to assess the impact of microplastics on crucian carp under both field and laboratory conditions. After four weeks of in-situ exposure, intestinal microplastic levels slightly increased, and transcriptome analysis revealed over 3,000 differentially expressed genes in the liver, with notable enrichment in pathways related to lipid metabolism and oxidative stress.
Enrichment of polystyrene microplastics induces histological damage, oxidative stress, Keap1-Nrf2 signaling pathway-related gene expression in loach juveniles (Paramisgurnus dabryanus)
Researchers studied how polystyrene microplastics accumulate in loach juveniles raised in ponds lined with plastic film, finding dose-dependent enrichment in the fish. The study found that microplastic exposure caused liver tissue damage, disrupted antioxidant enzyme activity, and altered the expression of genes involved in oxidative stress defense pathways.
Hazards of microplastics exposure to liver function in fishes: A systematic review and meta-analysis
This meta-analysis found that microplastic exposure significantly impairs fish liver function, elevating key liver enzymes (AST, ALT, ALP, LDH) and triggering oxidative stress markers in liver tissue. The toxicological mechanisms include inflammation, apoptosis, and metabolic disruption, raising concerns about the health of fish populations in microplastic-contaminated waters and the safety of fish as a human food source.