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20 resultsShowing papers similar to Palliative effect of taurine against hepatic injury induced by polystyrene microplastics through antioxidant and metabolic pathway modulation in mice
ClearTable 1_Palliative effect of taurine against hepatic injury induced by polystyrene microplastics through antioxidant and metabolic pathway modulation in mice.docx
This study investigated the molecular mechanisms underlying liver toxicity caused by polystyrene microplastics, finding that PS-MPs accumulated in hepatic tissues and disrupted lipid metabolism through oxidative stress and inflammatory signaling. The results mapped specific molecular pathways through which microplastics impair liver function.
Polystyrene microplastics impact on cardiac and pulmonary physiology and microenvironment in a mouse model: Role of taurine supplementation and molecular docking insights
Researchers investigated the effects of polystyrene microplastics on heart and lung tissues in mice and found that exposure disrupted antioxidant defenses, increased lipid peroxidation, and elevated cardiac injury markers and pro-inflammatory cytokines. Microplastic exposure also upregulated inflammatory and pyroptotic gene expression in both tissues. Co-administration of taurine significantly ameliorated these alterations, suggesting it may offer protective effects against microplastic-induced cardiopulmonary damage.
Taurine improves bovine oocyte maturation through recovering mitochondrial dysfunction and oxidative stress-induced apoptosis after microplastics exposure
This study found that taurine supplementation protected bovine oocytes from microplastic-induced toxicity by recovering mitochondrial dysfunction during oocyte maturation, suggesting a potential dietary intervention strategy to mitigate reproductive damage from plastic exposure.
Hepatic and metabolic outcomes induced by sub-chronic exposure to polystyrene microplastics in mice
Researchers studied the effects of sub-chronic polystyrene microplastic exposure on mouse livers using multiple analytical approaches. They found that microplastics accumulated in liver tissue and caused inflammation, oxidative stress, and disruption of normal metabolic processes including lipid and amino acid metabolism. The study suggests that prolonged microplastic ingestion may pose significant risks to liver health.
Impact of the Oral Administration of Polystyrene Microplastics on Hepatic Lipid, Glucose, and Amino Acid Metabolism in C57BL/6Korl and C57BL/6-Lepem1hwl/Korl Mice
Researchers investigated the effects of orally administered polystyrene microplastics on liver metabolism in normal and obese mice over eight weeks. They found that microplastic exposure altered lipid, glucose, and amino acid metabolism pathways in the liver and adipose tissues. The study suggests that microplastic ingestion may disrupt hepatic metabolic functions, with potentially different impacts depending on baseline metabolic health status.
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.
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.
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.
Subchronic oral exposure to polystyrene microplastics affects hepatic lipid metabolism, inflammation, and oxidative balance in gilthead seabream (Sparus aurata)
Gilthead seabream fed polystyrene microplastics for 21 days developed signs of liver damage including fat buildup, inflammation, and oxidative stress -- changes similar to early-stage fatty liver disease. Since fish liver responds to microplastics in ways comparable to mammalian livers, these findings raise concerns about what chronic microplastic exposure might do to liver health in humans and other animals.
Polystyrene microplastics induce hepatotoxicity and disrupt lipid metabolism in the liver organoids
Using lab-grown human liver organoids, researchers showed that polystyrene microplastics caused liver cell damage even at concentrations found in the environment. The microplastics disrupted fat metabolism, increased harmful reactive oxygen species, and triggered inflammation in the liver tissue. This study provides early evidence that microplastic exposure could contribute to liver problems like fatty liver disease in humans.
Integrated transcriptomics and proteomics analyses reveal the ameliorative effect of hepatic damage in tilapia caused by polystyrene microplastics with chlorella addition
Tilapia fish were exposed to polystyrene microplastics of different sizes, and researchers found that the particles caused liver damage including fat metabolism disruption, oxidative stress, and inflammation. Interestingly, adding the green algae Chlorella to the exposure partially helped reduce the harmful effects, suggesting that natural microorganisms may offer some protective benefit against microplastic toxicity in fish.
Polystyrene microplastic particles induced hepatotoxic injury via pyroptosis, oxidative stress, and fibrotic changes in adult male albino rats; the therapeutic role of silymarin
Researchers examined the liver toxicity of polystyrene microplastic particles in adult male rats and evaluated whether silymarin, a liver-protective compound, could mitigate the damage. The study found that exposure to 1 and 5 micrometer microplastics induced liver injury through pyroptosis, oxidative stress, and fibrotic changes, and that silymarin treatment showed potential therapeutic effects against these microplastic-induced injuries.
Proinflammatory properties and lipid disturbance of polystyrene microplastics in the livers of mice with acute colitis
Researchers studied the effects of polystyrene microplastics on the livers of mice fed a high-fat diet and found that the particles triggered significant inflammatory responses and disrupted lipid metabolism. The microplastics worsened fat accumulation in the liver and activated inflammatory signaling pathways. The findings suggest that microplastic exposure combined with a high-fat diet may amplify liver damage and metabolic disturbances.
Long-term exposure to polystyrene microplastics induces hepatotoxicity by altering lipid signatures in C57BL/6J mice
Researchers exposed mice to tiny polystyrene particles for 16 weeks and found the plastics accumulated in their livers, disrupting fat metabolism and energy production. The microplastics altered lipid profiles and interfered with key enzymes involved in cellular energy cycles. The study suggests that long-term microplastic exposure may contribute to liver damage through metabolic disruption.
Untargeted lipidomics uncover hepatic lipid signatures induced by long-term exposure to polystyrene microplastics in vivo
Researchers exposed rats to polystyrene microplastics over 6 and 12 months and used advanced lipid profiling to assess liver damage. They found that long-term exposure caused liver inflammation, fatty liver changes, and significant alterations in eight key lipid metabolites involved in fat processing. The study provides evidence that chronic microplastic exposure can disrupt liver lipid metabolism, raising concerns about long-term health effects.
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.
Probiotics ameliorate polyethylene microplastics-induced liver injury by inhibition of oxidative stress in Nile tilapia (Oreochromis niloticus)
Researchers investigated whether probiotics could protect Nile tilapia from liver damage caused by polystyrene microplastics. The study found that fish pre-fed with probiotics showed significantly reduced oxidative stress markers in the liver compared to those exposed to microplastics alone, suggesting that probiotics may help mitigate microplastic-induced hepatic oxidative damage in fish.
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.
Disruption of hepatic metabolism in Lep KO mice.
Researchers found that polystyrene microplastics administered orally for nine weeks accumulated in liver tissue of leptin-knockout obese mice and induced histopathological liver alterations, including disruption of hepatic lipid, glucose, and amino acid metabolism.
Potential toxicity of microplastics on vertebrate liver: A systematic review and meta–analysis
This meta-analysis of 118 studies found that microplastics damage vertebrate livers by inducing oxidative stress and intracellular toxicity, altering biotransformation processes, and disrupting lipid metabolism. Organisms at earlier life stages, exposed to smaller particles, and for longer durations showed the greatest liver damage, with catalase, GST, reactive oxygen species, and alkaline phosphatase levels progressively increasing with microplastic concentration.