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61,005 resultsShowing papers similar to Oxidative stress-activated Nrf2 remitted polystyrene nanoplastic-induced mitochondrial damage and inflammatory response in HepG2 cells
ClearExposure to polystyrene nanoplastics induces hepatotoxicity involving NRF2-NLRP3 signaling pathway in mice
Mice and liver cells exposed to 20-nanometer polystyrene nanoplastics developed liver damage through a specific molecular pathway involving oxidative stress and inflammation. The study showed that activating the body's natural antioxidant defense system (called NRF2) could protect against this liver injury, offering a potential avenue for reducing nanoplastic-related harm to human liver health.
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.
Didymin protects against polystyrene nanoplastic-induced hepatic damage in male albino rats by modulation of Nrf-2/Keap-1 pathway
Researchers tested whether didymin, a natural compound found in citrus fruits, could protect rat livers from damage caused by polystyrene nanoplastics. They found that didymin significantly reduced oxidative stress and inflammation by activating a key protective cellular pathway. The study suggests that certain dietary compounds may help counteract some of the harmful effects of nanoplastic exposure on the liver.
Polystyrene nanoplastics exacerbated Pb-induced liver toxicity in mice
Researchers found that polystyrene nanoplastics exacerbated lead-induced liver toxicity in mice, with co-exposure causing higher lead accumulation, more severe inflammation, increased oxidative stress, and greater disruption of protective Nrf2 signaling pathways compared to lead alone.
Rhamnetin abrogates polystyrene microplastics prompted hepatic damage by regulating Nrf-2/Keap-1 pathway
Researchers investigated whether rhamnetin, a natural flavonoid, could protect against liver damage induced by polystyrene microplastics in rats administered 0.01 mg/kg PS-MPs for the experimental period. They found that PS-MPs suppressed the Nrf-2/Keap-1 antioxidant pathway, reduced activities of SOD, CAT, GPx, GST, and HO-1 enzymes, elevated ALT, AST, and ALP liver injury markers, and increased apoptotic signaling, while co-administration of 50 mg/kg rhamnetin mitigated all these effects through hepatoprotective, anti-inflammatory, and antioxidant mechanisms.
Keap1-Nrf2 pathway up-regulation via hydrogen sulfide mitigates polystyrene microplastics induced-hepatotoxic effects
Researchers investigated whether hydrogen sulfide could protect against liver damage caused by polystyrene microplastics in mice. They found that hydrogen sulfide activated the Keap1-Nrf2 antioxidant defense pathway, which reduced oxidative stress and inflammation in liver tissues exposed to microplastics. The study suggests that the Keap1-Nrf2 pathway plays a protective role against microplastic-induced hepatotoxicity and that hydrogen sulfide could be a potential therapeutic agent.
ROS and DRP1 interactions accelerate the mitochondrial injury induced by polystyrene nanoplastics in human liver HepG2 cells
This study found that polystyrene nanoplastics damage human liver cells by triggering harmful interactions between reactive oxygen species (ROS) and a protein called DRP1 that controls mitochondria. The nanoplastics caused mitochondria to break apart, leading to cell injury and death. This research helps explain how microplastic exposure could contribute to liver damage in humans at the cellular level.
Acute exposure to polystyrene nanoparticles promotes liver injury by inducing mitochondrial ROS-dependent necroptosis and augmenting macrophage-hepatocyte crosstalk
Researchers discovered that very small polystyrene nanoparticles (20 nanometers) cause liver damage in mice by accumulating inside immune cells called macrophages, disrupting their energy-producing structures (mitochondria), and triggering a form of cell death that then spreads damage to liver cells. This study reveals a specific mechanism by which nanoplastic exposure could harm the liver, an organ critical for filtering toxins from the body.
Attenuative effects of tamarixetin against polystyrene microplastics‐induced hepatotoxicity in rats by regulation of Nrf‐2/Keap‐1 pathway
Researchers investigated whether tamarixetin, a naturally occurring flavonoid, could reduce liver damage caused by polystyrene microplastic exposure in rats. The study found that tamarixetin helped protect against microplastic-induced liver toxicity by activating antioxidant defense pathways, suggesting potential protective effects of certain plant-derived compounds against microplastic-related oxidative stress.
Hepatoprotective effects of astragalin against polystyrene microplastics induced hepatic damage in male albino rats by modulating Nrf-2/Keap-1 pathway
Researchers investigated whether astragalin, a natural plant compound, could protect against liver damage caused by polystyrene microplastics in rats. They found that microplastic exposure triggered oxidative stress and inflammation in the liver, but astragalin treatment restored antioxidant enzyme activity and reduced damage. The study suggests that natural compounds may help counteract some of the harmful effects microplastics have on liver health.
Polystyrene nanoplastics potentiate the development of hepatic fibrosis in high fat diet fed mice
Researchers found that polystyrene nanoplastics worsened liver damage in mice fed a high-fat diet by increasing oxidative stress, inflammation, and the infiltration of immune cells in liver tissue. The nanoplastic exposure accelerated the progression from fatty liver to hepatic fibrosis in the diet-induced model. The study suggests that nanoplastic exposure may compound the health risks associated with metabolic conditions affecting the liver.
Ginkgetin alleviates polystyrene microplastics-instigated liver injury in rats through Nrf-2/Keap-1 pathway activation
The biflavonoid ginkgetin protected rat livers from polystyrene microplastic-induced hepatotoxicity by activating the Nrf2/Keap1 antioxidant signaling pathway, restoring antioxidant enzyme activities and liver function markers at a dose of 25 mg/kg.
Polystyrene nanoplastics trigger ferroptosis in Nrf2-deficient gut via ether phospholipid accumulation
Researchers discovered that polystyrene nanoplastics trigger a specific type of cell death called ferroptosis in gut lining cells by disrupting fat metabolism, and that mice lacking a key protective protein (Nrf2) in their intestines were especially vulnerable. A high-fat diet made the damage worse, suggesting that people with poor diets or reduced antioxidant defenses may be at greater risk of intestinal harm from nanoplastic exposure.
Polystyrene microplastics induce hepatic lipid metabolism and energy disorder by upregulating the NR4A1-AMPK signaling pathway
Researchers found that polystyrene microplastics accumulate in the liver and disrupt fat and energy metabolism by activating a specific molecular pathway called NR4A1-AMPK. This activation triggers a self-cleaning process called autophagy that reduces fat production in liver cells, while also increasing harmful reactive oxygen species. The findings suggest that long-term microplastic exposure could lead to ongoing liver damage through this metabolic disruption.
Sinensetin mitigates polystyrene nanoplastics induced hepatotoxicity in albino rats: A biochemical and histopathological study
Exposure to polystyrene nanoplastics caused significant liver damage in rats, including oxidative stress, inflammation, and cell death, along with elevated liver enzymes that are markers of liver injury in clinical settings. Treatment with sinensetin — a natural plant flavonoid — substantially reversed these effects, restoring antioxidant enzyme activity and reducing inflammatory markers. The findings establish a potential protective role for natural compounds against nanoplastic-induced organ toxicity and illuminate the mechanisms by which nanoplastics harm the liver.
Polystyrene Nanoplastic Exposure Causes Reprogramming of Anti-Oxidative Genes Hmox1 and Sod3 by Inhibiting Nuclear Receptor RORγ in the Mouse Liver
Researchers examined how polystyrene nanoplastics affect liver function in mice and found that exposure led to reduced body weight, increased oxidative stress markers, and liver enzyme changes. The study suggests that nanoplastics suppress antioxidant gene expression in the liver by inhibiting the nuclear receptor RORgamma and altering epigenetic modifications at key gene locations.
Nano-Selenium Modulates NF-κB/NLRP3 Pathway and Mitochondrial Dynamics to Attenuate Microplastic-Induced Liver Injury
Researchers found that nano-selenium particles could reduce liver inflammation caused by polystyrene microplastics in mice by regulating mitochondrial dynamics and modulating the NF-kB/NLRP3 inflammatory pathway. The study suggests that selenium nanoparticles may help counteract the inflammatory damage that microplastics cause in liver tissue, offering a potential avenue for mitigating microplastic-related organ injury.
Microplastic-induced NAFLD: Hepatoprotective effects of nanosized selenium
This study found that polystyrene microplastics caused nonalcoholic fatty liver disease in mice by disrupting fat metabolism and triggering oxidative stress, but selenium nanoparticles derived from a yak-sourced bacterium significantly prevented this damage. The microplastics suppressed two key protective pathways in the liver, while the selenium nanoparticles activated those same pathways to counteract the harm. These findings suggest that microplastic exposure may contribute to liver disease in humans and point to selenium-based supplements as a potential protective strategy.
Polystyrene microplastics exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis
Researchers found that long-term exposure to polystyrene microplastics worsened acute liver injury in mice by triggering a specific type of inflammatory cell death called pyroptosis in liver immune cells. When they blocked this cell death pathway either genetically or with a drug, the damaging effects of the microplastics were significantly reduced. The study suggests that microplastic exposure may make the liver more vulnerable to injury by amplifying inflammatory responses.
Nanoplastic propels diet-induced NAFL to NASH via ER-mitochondrial tether-controlled redox switch
Researchers investigated how nanoplastic exposure may accelerate the progression of diet-induced fatty liver conditions in animal models. The study found that nanoplastics disrupted the connections between the endoplasmic reticulum and mitochondria, triggering oxidative stress responses that worsened liver inflammation and damage.
Nrf2-mediated ferroptosis of spermatogenic cells involved in male reproductive toxicity induced by polystyrene nanoplastics in mice
When polystyrene nanoplastics were injected into the bloodstream of mice, they accumulated in the testes and caused significant damage to sperm-producing cells through a process called ferroptosis, a type of iron-dependent cell death. The nanoplastics disrupted a key protective pathway (Nrf2) that normally prevents this type of cell death. These findings suggest that nanoplastic exposure could harm male fertility by directly damaging the cells responsible for producing sperm.
Polyethylene microplastics induced gut microbiota dysbiosis leading to liver injury via the TLR2/NF-κB/NLRP3 pathway in mice
Mice exposed to polyethylene microplastics developed liver damage that was traced back to disrupted gut bacteria -- the microplastics increased harmful bacteria while decreasing beneficial ones, triggering inflammation through the TLR2/NF-kB/NLRP3 immune pathway. This study provides new evidence that microplastics may harm the liver not just through direct contact, but indirectly by first throwing off the balance of gut bacteria.
Dietary exposure to polystyrene microplastics exacerbates liver damage in fulminant hepatic failure via ROS production and neutrophil extracellular trap formation
In mice with acute liver failure, prior exposure to polystyrene microplastics made the liver damage significantly worse and increased mortality. The microplastics boosted harmful reactive oxygen species and triggered immune cells to form structures called neutrophil extracellular traps, which amplified inflammation in the liver. This study suggests that people with existing liver conditions could be especially vulnerable to the harmful effects of microplastic exposure.
Protective role of poncirin against polyethylene microplastics instigatedcardiac toxicity via regulating Nrf2/keap1 pathway
Researchers found that exposing rats to polyethylene microplastics caused significant heart damage — including oxidative stress, inflammation, and cell death — by disrupting the Nrf2 antioxidant defense pathway. Supplementing with poncirin, a natural plant flavonoid, substantially protected cardiac tissue by restoring antioxidant activity, suggesting a potential protective role against microplastic-induced heart toxicity.