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61,005 resultsShowing papers similar to Polystyrene microplastics induce apoptosis in chicken testis via crosstalk between NF-κB and Nrf2 pathways
ClearPolystyrene microplastics induce blood–testis barrier disruption regulated by the MAPK-Nrf2 signaling pathway in rats
Researchers fed rats polystyrene microplastics for 90 days and found significant damage to male reproductive health, including reduced sperm quality, damaged sperm-producing tissue, and increased cell death. The study identified a specific molecular pathway where microplastics triggered oxidative stress that disrupted the blood-testis barrier, a critical protective structure in the testes. These findings provide new evidence that microplastic exposure may pose risks to male reproductive function.
Polystyrene microplastics mediate inflammatory responses in the chicken thymus by Nrf2/NF-κB pathway and trigger autophagy and apoptosis
Researchers exposed chickens to polystyrene microplastics and found significant damage to the thymus, a key immune organ. The microplastics triggered oxidative stress, inflammation, and cell death through specific molecular pathways. The study suggests that microplastic exposure could compromise immune function in animals by damaging organs responsible for immune cell development.
Polystyrene microplastics induce blood-testis barrier disruption regulated by MAPK-Nrf2 signaling pathway in rats
Researchers found that polystyrene microplastics (PS-MPs) disrupted the blood-testis barrier in male rats after 90 days of exposure, with higher doses (0.15 and 1.5 mg/d) causing significant spermatogenic cell apoptosis and reduced sperm motility through activation of the MAPK-Nrf2 signaling pathway.
Polystyrene microplastics induced oxidative stress, inflammation and necroptosis via NF-κB and RIP1/RIP3/MLKL pathway in chicken kidney
Researchers exposed chickens to different doses of polystyrene microplastics for six weeks to study kidney damage. The study found that microplastic exposure triggered oxidative stress, inflammation, and a form of cell death called necroptosis in kidney tissue through the NF-kappaB and RIP1/RIP3/MLKL signaling pathways.
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.
The crosstalk between M1 macrophage polarization and energy metabolism disorder contributes to polystyrene nanoplastics-triggered testicular inflammation
Researchers investigated how polystyrene nanoplastics cause testicular inflammation in mice by studying the interplay between immune cell behavior and energy metabolism. They found that nanoplastics triggered a pro-inflammatory immune response involving M1 macrophage activation, disrupted cellular energy processes, and caused testicular tissue damage. The study reveals a specific biological mechanism by which nanoplastic exposure may impair male reproductive health.
Chronic exposure to polystyrene microplastics induced LHR reduction and decreased testosterone levels through NF-κB pathway
Mice given drinking water containing polystyrene microplastics for 180 days showed significant drops in testosterone levels through a newly identified mechanism. The microplastics triggered immune cells in the testes to release inflammatory signals that suppressed a key hormone receptor (LHR), disrupting the entire hormonal pathway needed for testosterone production. This finding adds to growing evidence that microplastic exposure may impair male reproductive health.
Polystyrene nanoplastics aggravate reproductive system damage in obese male mice by perturbation of the testis redox homeostasis
Researchers found that polystyrene nanoplastics worsened reproductive damage in male mice already fed a high-fat diet, reducing sperm quality and testosterone production beyond what obesity alone caused. The nanoplastics disrupted the protective blood-testis barrier and increased oxidative stress in reproductive tissues. The study suggests that nanoplastic exposure combined with obesity may create compounding risks to male fertility.
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.
Polystyrene microplastics disrupt the blood-testis barrier integrity through ROS-Mediated imbalance of mTORC1 and mTORC2
Researchers found that polystyrene microplastics can disrupt the blood-testis barrier in mice by triggering oxidative stress and disrupting cellular signaling pathways. The damage was linked to an imbalance between two protein complexes that regulate cell structure and barrier integrity in reproductive tissues. The study suggests that microplastic exposure may impair male reproductive health by compromising the protective barrier that shields developing sperm cells.
Comparative analysis of reproductive toxicity of polystyrene‐nanoplastics and polystyrene‐microplastics in rat Sertoli cells
This comparative study found that polystyrene nanoplastics cause greater toxicity to Sertoli cells than microplastics due to cellular internalization, disrupting blood-testis barrier integrity via oxidative stress and apoptosis, while microplastics primarily triggered extracellular inflammation.
Polystyrene Microplastics Disrupt Spermatogenesis through Oxidative Stress in Rat Testicular Tissue
Male Wistar rats orally administered polystyrene microplastics showed excessive oxidative stress in testicular tissue across all exposure groups, with spermatogenesis impairment and reduced fertility correlating with dose, demonstrating reproductive toxicity in a mammalian model.
Polystyrene microplastic exposure in mice: oxidative stress-induced testicular damage, AR gene suppression, and histopathological alterations
Researchers exposed mice to polystyrene microplastics at two different concentrations and observed significant impacts on reproductive health, including increased oxidative stress in testicular tissue. The study found elevated reactive oxygen species, reduced sperm count and motility, and suppression of androgen receptor gene expression. Evidence indicates that microplastic exposure may pose reproductive health risks by disrupting antioxidant defenses and damaging testicular cells.
Investigating polystyrene nanoplastics-induced reproductive toxicity in vitro: Focus on Nrf2-PKM2-autophagy signaling pathway
This lab study investigated how polystyrene nanoplastics damage male reproductive cells, finding they triggered autophagy (cellular self-digestion) and disrupted key proteins in a signaling pathway important for sperm cell survival. The findings suggest nanoplastics could impair male fertility by causing programmed cell death in testicular cells. This adds to growing evidence that plastic nanoparticles can harm reproductive health.
Reproductive Toxicity of Chronic Exposure To Polystyrene Microplastics And The Molecular Mechanism of Decrease In Testosterone Levels In Male Mice
Chronic exposure to polystyrene microplastics lowered testosterone levels in male mice and disrupted reproductive organ function. The study identified molecular pathways through which microplastics interfere with male hormone production, with implications for reproductive health in humans exposed through diet.
Polystyrene microplastics induce apoptosis and necroptosis in swine testis cells via ROS/MAPK/HIF1α pathway
Researchers exposed swine testis cells to polystyrene microplastics and found that the particles reduced cell viability and triggered both programmed cell death and necroptosis. The damage was driven by excessive production of reactive oxygen species that activated stress signaling pathways. Since pigs are physiologically similar to humans, the findings raise concerns about potential reproductive health effects of microplastic exposure in mammals.
Polystyrene microplastics exacerbate experimental chronic kidney disease via inflammatory and oxidative pathways involving NF-κB, ERK/p38 MAPK, and sirtuin-1
Researchers examined the effects of polystyrene microplastics on mice with chronic kidney disease and found that microplastic exposure worsened kidney dysfunction, inflammation, and tissue scarring. Even in healthy mice, microplastics reduced kidney filtration and increased markers of kidney damage. The study suggests that microplastic exposure may aggravate existing kidney conditions through inflammatory and oxidative stress pathways.
Polystyrene nanoplastics inhibit StAR expression by activating HIF-1α via ERK1/2 MAPK and AKT pathways in TM3 Leydig cells and testicular tissues of mice
Researchers discovered a molecular mechanism by which polystyrene nanoplastics reduce testosterone production in mice. The nanoplastics triggered a chain reaction in testicular cells: they produced harmful reactive oxygen species, which activated signaling pathways that increased a protein called HIF-1a, which in turn shut down the StAR protein needed to make testosterone. These findings help explain how nanoplastic exposure could contribute to declining male fertility and reproductive health.
Immune response to polystyrene microplastics: Regulation of inflammatory response via the ROS-driven NF-κB pathway in zebrafish (Danio rerio)
Researchers found that polystyrene microplastics triggered immune system inflammation in zebrafish by generating reactive oxygen species (ROS) that activated the NF-kB signaling pathway. The microplastics accumulated mainly in the intestines, causing tissue damage and behavioral changes in the fish. This study identifies a specific molecular mechanism by which microplastics cause immune dysfunction, which could be relevant to understanding inflammation in humans exposed to microplastics.
Male reproductive toxicity of polystyrene microplastics: Study on the endoplasmic reticulum stress signaling pathway
Researchers exposed mice to polystyrene microplastics for 35 days and found significant male reproductive toxicity, including decreased sperm counts and motility, increased sperm abnormalities, and reduced testosterone levels. The microplastics caused structural damage to the seminiferous tubules and triggered endoplasmic reticulum stress in testicular tissue. The study suggests that microplastic exposure may impair male reproductive health through stress-related signaling pathways in the testes.
Polystyrene microplastics-induced cardiotoxicity in chickens via the ROS-driven NF-κB-NLRP3-GSDMD and AMPK-PGC-1α axes
Researchers found that polystyrene microplastics caused serious heart damage in chickens by triggering oxidative stress, inflammation, and disruption of the cells' energy production systems. The microplastics activated inflammatory pathways that led to a type of cell death called pyroptosis and damaged the mitochondria that power heart cells. These findings suggest that microplastic exposure could pose risks to cardiovascular health in animals, with potential implications for understanding heart-related effects in humans.
Adolescent exposure to polystyrene nanoplastics induces male reproductive damage via the microbiome-gut-testis axis
Researchers exposed adolescent rats to polystyrene nanoplastics for five weeks and observed dose-dependent damage to testicular tissue, disrupted spermatogenesis, and compromised blood-testis barrier integrity. The study revealed a novel microbiome-gut-testis axis mechanism, where nanoplastics altered gut bacteria composition, which in turn contributed to reproductive toxicity in developing males.
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.
Dose-Dependent Effect of Polystyrene Microplastics on the Testicular Tissues of the Male Sprague Dawley Rats
Male rats exposed to increasing doses of polystyrene microplastics showed dose-dependent testicular damage including disrupted spermatogenesis and altered hormone levels, suggesting potential reproductive toxicity from microplastic accumulation.