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61,005 resultsShowing papers similar to Canidin-3-glucoside prevents nano-plastics induced toxicity via activating autophagy and promoting discharge
ClearFood-derived cyanidin-3-O-glucoside reverses microplastic toxicity via promoting discharge and modulating the gut microbiota in mice
Researchers found that cyanidin-3-O-glucoside (C3G), a naturally occurring anthocyanin compound found in many fruits and vegetables, helped reduce the harmful effects of polystyrene microplastics in mice. C3G supplementation promoted the excretion of microplastics, reduced tissue accumulation, and alleviated oxidative stress and inflammation caused by the particles. The study also showed that C3G helped restore healthy gut microbiota that had been disrupted by microplastic exposure.
Cyanidin-3-O-glucoside reduces nanopolystyrene-induced toxicity and accumulation: roles of mitochondrial energy metabolism and cellular efflux
Cyanidin-3-O-glucoside, a plant pigment, reduced the toxicity and cellular accumulation of polystyrene nanoplastics in model organisms by enhancing mitochondrial energy metabolism and boosting the activity of ABC transporter proteins that export nanoplastics from cells.
Cyanidin-3-O-glucoside promotes stress tolerance and lifespan extension of Caenorhabditis elegans exposed to polystyrene via DAF-16 pathway
The flavonoid cyanidin-3-O-glucoside (C3G) was found to reduce oxidative stress and partially reverse the lifespan reduction caused by polystyrene microplastic exposure in the nematode Caenorhabditis elegans, acting through the DAF-16 transcription factor pathway. The results suggest dietary antioxidants may offer some protection against microplastic-induced toxicity.
Assessment of the cytotoxicity micro- and nano-plastic on human intestinal Caco-2 cells and the protective effects of catechin.
Researchers used a human intestinal cell line (Caco-2) to test cytotoxicity of polystyrene micro- and nano-plastics, finding dose-dependent cell damage and disruption of intestinal barrier function. The study supports growing concerns that ingested microplastics could contribute to gut inflammation and compromise the protective lining of the human intestine.
Nobiletin‐mediated autophagy mitigates nanoplastic‐induced toxicity in human intestinal Caco‐2 cells
Researchers found that nobiletin, a natural compound from citrus peel, can protect human intestinal cells from damage caused by nanoplastics. The compound worked by activating autophagy, a cellular cleanup process that helps cells remove harmful materials. The study suggests that certain plant-derived compounds may offer a protective effect against the intestinal damage associated with nanoplastic exposure.
Modulation of Gut Microbial Metabolism by Cyanidin-3-O-Glucoside in Mitigating Polystyrene-Induced Colonic Inflammation: Insights from 16S rRNA Sequencing and Metabolomics
A natural plant compound called cyanidin-3-O-glucoside (C3G), found in red bayberry and other berries, reduced colon inflammation caused by polystyrene microplastic exposure in mice. C3G worked by reshaping the gut bacteria community and restoring healthy levels of anti-inflammatory signaling molecules. This suggests that certain dietary antioxidants may help protect the gut from damage caused by microplastic exposure.
Cyanidin-3-O-glucoside impacts fecal discharge of polystyrene microplastics in mice: Potential role of microbiota-derived metabolites
Researchers found that the dietary compound cyanidin-3-O-glucoside accelerated the fecal discharge of polystyrene microplastics in mice by remodeling gut microbiota composition and altering microbiota-derived metabolites, suggesting a potential dietary strategy for reducing microplastic accumulation.
Toxicity of microplastics polystyrene to freshwater planarians and the alleviative effects of anthocyanins
Researchers determined the lethal concentration of polystyrene microplastics for freshwater planarians for the first time and found that exposure disrupted their internal balance, caused oxidative damage, and triggered nerve cell changes and cell death. Notably, long-term exposure to low, environmentally relevant concentrations was more harmful than short-term exposure to high doses. The study also found that anthocyanins, natural plant pigments, could effectively reduce the toxic effects of polystyrene on these organisms.
Compromised Autophagic Effect of Polystyrene Nanoplastics Mediated by Protein Corona Was Recovered after Lysosomal Degradation of Corona
Researchers discovered that when polystyrene nanoplastics enter biological environments, proteins coat their surface forming a protective corona that initially reduces their toxic effects on cells. However, once cells internalize the particles and break down the protein layer in lysosomes, the original toxicity returns, including blocked autophagy and lysosomal damage. The study reveals that protein coronas temporarily mask nanoplastic toxicity rather than permanently neutralizing it.
Autophagic response of intestinal epithelial cells exposed to polystyrene nanoplastics
Researchers found that polystyrene nanoplastics accumulate in the cytoplasm of intestinal epithelial cells, impairing autophagic flux and triggering an autophagic stress response confirmed in both cell and animal models.
The impact of nanomaterials on autophagy across health and disease conditions
Researchers examined how nanomaterials — including nanoplastics — interact with autophagy, the cell's internal recycling and cleanup system. Depending on the type and dose, nanoplastics can either trigger helpful cellular defense responses or push cells toward self-destruction, a dual nature that has important implications for both environmental health and the design of nanomaterial-based medicines.
Lipophagy suppression: a novel mechanism for developmental disruption by nanoplastics/MC-LR in zebrafish
Researchers co-exposed zebrafish embryos to polystyrene nanoplastics and microcystin-LR (a cyanobacterial toxin) and found that combined exposure suppressed lipophagy—a cellular process that breaks down lipid droplets—more severely than either substance alone. Disruption of lipophagy impaired early development, identifying this autophagy pathway as a novel target for nanoplastic developmental toxicity.
Biological Modulation of Autophagy by Nanoplastics: A Current Overview
This review examines how nanoplastics interfere with autophagy, the cell's natural recycling and cleanup process. While cells initially activate autophagy to deal with nanoplastic particles, prolonged exposure can overwhelm this system, leading to cell damage and death. Understanding this process is important because it may explain how long-term nanoplastic exposure contributes to tissue damage and disease in humans.
Cyanidin-3- O-glucoside alleviates trimethyltin chloride-induced neurodegeneration by maintaining glutamate homeostasis through modulation of the gut microbiota
Researchers found that cyanidin-3-O-glucoside, a common dietary anthocyanin found in berries and other foods, helped protect against chemically induced neurodegeneration in mice by restoring glutamate balance in the brain. The study suggests that this protective effect is mediated through modulation of gut microbiota, highlighting a potential gut-brain connection in neuroprotection.
The toxic differentiation of micro- and nanoplastics verified by gene-edited fluorescent Caenorhabditis elegans
Researchers used gene-edited fluorescent C. elegans to demonstrate that nanoplastic toxicity is size- and charge-dependent, with 100 nm positively charged polystyrene particles causing the greatest harm through intestinal accumulation and oxidative stress.
Neurodevelopmental Toxicity of Polystyrene Nanoplastics inCaenorhabditis elegansand the Regulating Effect of Presenilin
C. elegans exposed to 25, 50, and 100 nm polystyrene nanoplastics showed size-dependent neurodevelopmental toxicity — including reactive oxygen species generation, mitochondrial damage, and inhibited dopamine production — with smaller particles (25 nm) paradoxically showing weaker effects than the 50 nm size.
Fecal microbiota transplantation attenuates nano-plastics induced toxicity in Caenorhabditis elegans.
Nano-sized plastic particles ingested by the roundworm C. elegans penetrated the intestinal barrier, accumulated throughout the body, and were not excreted until the worms died — and transplanting human gut microbiota into the worms partially mitigated the toxicity. The study provides early evidence that a healthy gut microbiome may help protect against nanoplastic harm, and that these particles can persist indefinitely once inside an organism.
Toxicological Effects and Potential Therapeutics of Chronic Exposure to Polyurethane Nanoplastics in Caenorhabditis elegans
Researchers exposed the model organism C. elegans to polyurethane nanoplastics at environmentally relevant concentrations and found dose-dependent toxic effects including reduced reproduction, impaired movement, and shortened lifespan. The study also found that cinnamon essential oil showed potential as a therapeutic agent, enhancing antioxidant defenses and partially mitigating the harmful effects of nanoplastic exposure at lower concentrations.
Different Toxic Effects of Polystyrene Microplastics and Nanoplastics on Caenorhabditis elegans
Researchers compared the toxicity of 2-μm polystyrene microplastics and 0.1-μm nanoplastics in C. elegans, finding both impaired growth, locomotion, reproduction, and lifespan at 1 mg/L and above, with microplastics causing greater locomotion and reproductive toxicity and nanoplastics inducing stronger oxidative stress.
Micro-algal astaxanthin ameliorates polystyrene microplastics-triggered necroptosis and inflammation by mediating mitochondrial Ca2+ homeostasis in carp’s head kidney lymphocytes (Cyprinus carpio L.)
Researchers investigated whether astaxanthin, a natural pigment from microalgae, could protect carp immune cells from damage caused by polystyrene microplastics. They found that astaxanthin reduced inflammation and cell death triggered by microplastics by helping maintain calcium balance within the cells' mitochondria. The study suggests that natural antioxidant compounds may help mitigate some of the harmful immune effects of microplastic exposure in fish.
Polystyrene (nano)microplastics cause size-dependent neurotoxicity, oxidative damage and other adverse effects inCaenorhabditis elegans
Researchers found that polystyrene micro- and nanoplastics cause neurotoxicity and oxidative damage in the model organism C. elegans, with effects varying by particle size. Smaller nanoscale particles tended to cause more severe toxic responses than larger microplastic particles. The study highlights that the size of plastic particles is an important factor in determining how harmful they are to living organisms.
Neuronal damage induced by nanopolystyrene particles in nematodeCaenorhabditis elegans
C. elegans nematodes were chronically exposed to nanopolystyrene particles and found to develop neuronal damage affecting both development and function of the nervous system after long-term exposure at environmentally relevant concentrations. The study provides early evidence that nanoplastics can cause neurological harm in an animal model, raising questions about potential neurotoxicity in other species.
Uptake of nanopolystyrene particles induces distinct metabolic profiles and toxic effects in Caenorhabditis elegans
Researchers exposed the nematode C. elegans to 50 nm and 200 nm nanopolystyrene particles and used metabolomics to show that particles disrupt energy metabolism — reducing TCA cycle intermediates and altering glucose and lactate — while also decreasing locomotion, reproduction, and inducing oxidative stress.
Using acs-22 mutant Caenorhabditis elegans to detect the toxicity of nanopolystyrene particles
Researchers used C. elegans worms with a defective intestinal barrier to show that nanoplastics at environmentally predicted concentrations (1 µg/L) can translocate to internal organs and activate oxidative stress pathways when the gut barrier is compromised — suggesting susceptibility may increase under certain disease conditions.