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61,005 resultsShowing papers similar to Nrf2-dependent redox regulation protects myoblasts from polystyrene nanoplastic-induced premature senescence
ClearExposure to polystyrene nanoplastics promotes premature cellular senescence through mitochondrial ROS production and dysfunction in pre-differentiated skeletal myoblasts
This lab study found that polystyrene nanoplastics caused premature aging in muscle precursor cells by damaging their mitochondria and triggering excessive production of harmful molecules called reactive oxygen species. The nanoplastics were absorbed into cells, accumulated there, and caused the cells to stop dividing and show signs of aging. This suggests that nanoplastic exposure could contribute to muscle deterioration and aging-related conditions by damaging the cells responsible for muscle repair.
Polystyrene nanoplastics promote muscle cell senescence through microtubule hyper-stabilization-mediated mitophagy dysfunction and cGAS-Sting activation
Researchers found that polystyrene nanoplastics cause premature aging in human muscle cells by disrupting the internal skeleton of cells and impairing the cleanup of damaged mitochondria. The nanoplastics made the cell's structural framework too rigid, which blocked normal cell signaling and triggered an inflammatory aging response. This study suggests that nanoplastic exposure could contribute to muscle weakness and age-related muscle loss in humans.
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.
Oxidative stress-activated Nrf2 remitted polystyrene nanoplastic-induced mitochondrial damage and inflammatory response in HepG2 cells
Researchers discovered that polystyrene nanoplastics damage human liver cells by causing oxidative stress and mitochondrial damage, but the cells activate a protective pathway called Nrf2 to fight back. When the Nrf2 defense was blocked, the damage from nanoplastics became significantly worse, confirming its protective role. This study helps explain how the liver tries to defend itself against nanoplastic toxicity, and suggests that people with weaker antioxidant defenses may be more vulnerable to liver damage from plastic exposure.
Endogenous hydrogen sulfide counteracts polystyrene nanoplastics-induced mitochondrial apoptosis and excessive autophagy via regulating Nrf2 and PGC-1α signaling pathway in mouse spermatocyte-derived GC-2spd(ts) cells
Researchers investigated how polystyrene nanoplastics damage reproductive cells in mice and whether endogenous hydrogen sulfide can provide protection. The study found that nanoplastics induced mitochondrial damage, excessive autophagy, and cell death in spermatocyte-derived cells, while hydrogen sulfide counteracted these effects by regulating oxidative stress defense pathways.
Polystyrene nanoplastics exposure triggers spermatogenic cell senescence via the Sirt1/ROS axis
Male mice exposed to polystyrene nanoplastics for 60 days showed damaged sperm-producing cells that displayed signs of premature aging, linked to a specific molecular pathway involving the Sirt1 protein and oxidative stress. This study adds to growing evidence that nanoplastic exposure may harm male reproductive health by accelerating the aging of cells responsible for sperm production.
Stress Response of Mouse Embryonic Fibroblasts Exposed to Polystyrene Nanoplastics
Mouse embryonic fibroblasts exposed to polystyrene nanoplastics internalized particles via endocytosis without losing viability, but showed activation of antioxidant and autophagic stress pathways, suggesting subcellular dysfunction even in the absence of cell death.
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.
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.
Parthenolide Restores Testosterone Biosynthesis After Nanoplastic Exposure by Blocking ROS-Driven NF-κB Nuclear Translocation
Researchers found that polystyrene nanoplastics suppressed testosterone production in young male mice by activating NF-κB signaling, and that parthenolide — a natural compound — blocked this pathway and restored normal testosterone levels.
Evaluation of polyethylene microplastics toxicity using Nrf2/ARE and MAPK/Nrf2 signaling pathways
Researchers exposed male and female rats to varying doses of polyethylene microplastics and found dose-dependent increases in oxidative stress markers and disruptions to reproductive hormone levels. They identified specific cellular signaling pathways, including the Nrf2 antioxidant response system, that were affected by microplastic exposure. The study suggests that microplastic ingestion may trigger oxidative damage and reproductive effects through identifiable molecular mechanisms.
Potential toxicity of nanopolystyrene on lifespan and aging process of nematode Caenorhabditis elegans
Researchers chronically exposed C. elegans to nanopolystyrene across their aging lifespan and found that high concentrations shortened lifespan while lower concentrations still impaired locomotion and elevated intestinal reactive oxygen species in older animals, with nanoplastic exposure progressively suppressing immune genes, antioxidant defenses, and mitochondrial stress responses as worms aged.
Polystyrene nanoplastics mediate oxidative stress, senescence, and apoptosis in a human alveolar epithelial cell line
A cell study found that polystyrene nanoplastics cause dose-dependent damage to human lung cells, triggering oxidative stress, premature cell aging, and cell death. These findings suggest that breathing in nanoplastics could harm lung tissue over time and potentially contribute to cancer risk from air pollution.
Polystyrene Nanoplastics Induce Lung Injury via Activating Oxidative Stress: Molecular Insights from Bioinformatics Analysis
Researchers found that polystyrene nanoplastics induce lung cell injury through oxidative stress pathways, identifying key transcription factors and the molecule TNFRSF12A as crucial mediators of nanoplastic-triggered redox imbalance and respiratory damage.
Polystyrene microplastics induces senescence of osteocytes by activating the cyclooxygenase-2 signaling pathway
Researchers found that polystyrene microplastics can be taken up by osteocytes, the most abundant cells in bone tissue, and cause them to undergo premature aging through a process called senescence. The microplastics triggered oxidative stress and activated a specific inflammatory signaling pathway involving cyclooxygenase-2. The study suggests that microplastic exposure could potentially impair bone health by disrupting the normal function of the cells responsible for maintaining bone tissue.
Exposure 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.
Effects of polystyrene nanoplastics on endothelium senescence and its underlying mechanism
Researchers found that polystyrene nanoplastics can promote premature aging of endothelial cells that line blood vessel walls, using porcine coronary artery cells as a model. The study suggests that nanoplastic exposure may affect cardiovascular health by accelerating cellular senescence in the endothelium, a process linked to vascular dysfunction.
Polystyrene microplastics induce apoptosis in chicken testis via crosstalk between NF-κB and Nrf2 pathways
Researchers found that polystyrene microplastics caused testicular damage in chickens through crosstalk between inflammatory and antioxidant defense pathways. Exposure to microplastics through drinking water disrupted the blood-testis barrier, triggered oxidative stress by inhibiting the Nrf2 pathway, activated inflammatory signaling through NF-kB, and ultimately induced cell death in testicular tissue.
Microplastics exposure causes the senescence of human lung epithelial cells and mouse lungs by inducing ROS signaling
Researchers found that four common types of microplastics all caused premature aging (senescence) in human lung cells by increasing harmful reactive oxygen species, and that an antioxidant treatment could partially reverse this effect. When PVC microplastics were introduced into mouse lungs, the animals showed reduced physical function, increased body-wide inflammation, and accumulation of aged cells, suggesting that inhaling microplastics could accelerate lung aging.
Polystyrene nanoplastics induce ovarian granulosa cell senescence via autophagy suppression
Researchers found that polystyrene nanoplastics induce premature cellular aging (senescence) in human ovarian granulosa cells by suppressing autophagy, triggering inflammatory signaling and mitochondrial dysfunction, and that restoring autophagy with rapamycin reversed these effects — pointing to a potential mechanism linking nanoplastic exposure to accelerated ovarian aging.
Epigallocatechin-gallate ameliorates polystyrene microplastics-induced oxido-inflammation and mitochondria-mediated apoptosis in testicular cells via modulation of Nrf2/HO-1, /mTOR/Atg-7, and Cx-43/NOX-1 levels
Researchers found that polystyrene microplastics caused oxidative stress, inflammation, and reduced sperm quality in rats, but that treatment with EGCG — a compound found in green tea — reversed most of these harmful effects by restoring antioxidant defenses and reducing cell death pathways in testicular tissue.
Nano-sized microplastics exposure induces skin cell senescence via triggering the mitochondrial localization of GSDMD
Researchers found that nano-sized microplastics enter skin cells and trigger premature aging (senescence) by damaging the energy-producing structures inside cells (mitochondria) and activating inflammatory pathways. This study suggests that microplastic exposure could accelerate skin aging and inflammation, adding to concerns about the health effects of plastic pollution on organs exposed to the environment.
Impact of polystyrene nanoplastics on apoptosis and inflammation in zebrafish larvae: Insights from reactive oxygen species perspective
Researchers showed that polystyrene nanoplastics accumulate in zebrafish larvae and trigger excessive reactive oxygen species production via NADPH oxidase upregulation, causing mitochondrial dysfunction, apoptosis, and NF-κB-driven inflammation — with inhibiting ROS generation effectively blocking downstream cell death and inflammatory responses.
Cellular Distribution of Polystyrene Nanoplastics from Food Chain and Their Effects on Mitochondrial Quality in H9C2 Cells
Researchers investigated the cellular distribution of polystyrene nanoplastics entering via the food chain and examined their effects on mitochondrial quality in H9C2 cardiac cells, assessing how nanoplastic accumulation disrupts mitochondrial function.