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61,005 resultsShowing papers similar to Polystyrene microplastics induce blood–testis barrier disruption regulated by the MAPK-Nrf2 signaling pathway in rats
ClearPolystyrene 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.
Exposure to polystyrene microplastics causes reproductive toxicity through oxidative stress and activation of the p38 MAPK signaling pathway
Researchers exposed male mice to polystyrene microplastics for six weeks and observed significant reproductive harm, including decreased sperm count, reduced motility, and increased deformity rates. The damage was linked to oxidative stress and activation of a specific cellular signaling pathway called p38 MAPK. The findings suggest that microplastic exposure may pose risks to male reproductive health in mammals through oxidative stress mechanisms.
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.
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.
Adverse effects and potential mechanisms of polystyrene microplastics (PS-MPs) on the blood-testis barrier
This review examines how polystyrene microplastics damage the blood-testis barrier, a critical structure that protects developing sperm cells from harmful substances. Microplastics can break down this barrier through oxidative stress, inflammation, and disruption of gut bacteria, allowing pollutants and immune cells to enter the reproductive system. These findings suggest that microplastic exposure may contribute to declining male fertility, a trend observed globally in recent decades.
Polyethylene microplastics disrupt focal adhesion kinase (FAK) signaling and sertoli cell metabolism, compromising blood-testis barrier function and spermatogenesis
Researchers exposed rats to polyethylene microplastics orally for 56 days and found dose-dependent damage to the blood-testis barrier, a structure critical for protecting developing sperm. The microplastics disrupted key signaling pathways in Sertoli cells, which support sperm development, leading to reduced sperm quality and altered testicular metabolism. The study suggests that polyethylene microplastic exposure may compromise male reproductive function by destabilizing the protective environment around developing sperm cells.
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 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.
Impact of polystyrene microplastic exposure at low doses on male fertility: an experimental study in rats
Researchers exposed adult male rats to varying doses of polystyrene microplastics and found dose-dependent declines in semen quality along with disrupted reproductive hormone levels. Higher doses caused increased oxidative stress, mitochondrial damage, and inflammatory responses in testicular tissue. The study suggests that even relatively low doses of microplastic exposure may have adverse effects on male reproductive health in animal models.
Polystyrene microplastics cause reproductive toxicity in male mice
Male mice exposed to polystyrene microplastics for six weeks showed significant reproductive damage, including reduced sperm count and motility, lower testosterone levels, and visible tissue damage in the testes. The microplastics caused oxidative stress and triggered cell death pathways in the reproductive tissue. These findings add to growing evidence that microplastic exposure could contribute to declining male fertility.
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 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.
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.
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.
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.
Assessment of microplastic toxicity on blood-testis barrier using 3D cell spheroids
Researchers used 3D cell spheroids to model the blood-testis barrier and tested how polystyrene microplastics affect male reproductive tissue. They found that microplastic exposure triggered endoplasmic reticulum stress in Sertoli cells, with effects varying by particle size and concentration. The study suggests that microplastics may pose risks to reproductive health by disrupting the cellular stress response in testicular barrier tissues.
Effects of polystyrene microparticles exposures on spermatogenic cell differentiation and reproductive endpoints in male mice
Researchers found that very small polystyrene microplastics (0.1 micrometers) accumulated in mouse testicular tissue and sperm-producing cells, leading to reduced sperm quality and impaired reproductive function. The particles triggered oxidative stress and disrupted the normal process of sperm cell development. This study adds to growing evidence that microplastic exposure could contribute to male fertility problems in humans, particularly from the smallest particles that can penetrate reproductive tissues.
Polystyrene microplastics induced male reproductive toxicity in mice
Researchers exposed male mice to polystyrene microplastics of different sizes and found that the particles accumulated in testicular tissue and entered reproductive cells. After 28 days of exposure, sperm quality and testosterone levels declined, and tissue examination revealed disorganized sperm-producing cells and inflammation. The study suggests that microplastic exposure may pose risks to male reproductive health in mammals.
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.
Oral exposure to polystyrene nanoplastics altered the hypothalamic–pituitary–testicular axis role in hormonal regulation, inducing reproductive toxicity in albino rats
This study found that oral exposure to polystyrene nanoplastics disrupted the hormone signaling pathway between the brain and testes in male rats, leading to reproductive damage. The nanoplastics interfered with the hormones that regulate sperm production and testicular function. These findings add to growing evidence that nanoplastic exposure through food and water could be a contributing factor to declining male fertility.
Polystyrene microplastics induce male reproductive toxicity in mice by activating spermatogonium mitochondrial oxidative stress and apoptosis
A mouse study found that polystyrene microplastics significantly reduced sperm count and motility while increasing sperm deformities. The damage was caused by oxidative stress in the energy-producing mitochondria of sperm-forming cells, which triggered cell death -- raising concerns about microplastics' potential impact on male fertility.
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.
Chronic toxic effects of polystyrene microplastics on reproductive parameters of male rats
Researchers studied the chronic toxic effects of polystyrene microplastics on the reproductive system of male rats over 90 days. The study found significant reductions in sperm volume, motility, epididymal count, and serum testosterone levels, along with disrupted testicular architecture and decreased antioxidant capacity. The findings suggest that chronic microplastic exposure may adversely affect male reproductive parameters in mammals.
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.