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61,005 resultsShowing papers similar to Polyethylene terephthalate (PET) microplastics induced male reproductive toxicity in mice by activating the p38-MAPK pathway
ClearPolyethylene Terephthalate Microplastic Exposure Induced Reproductive Toxicity Through Oxidative Stress and p38 Signaling Pathway Activation in Male Mice
Male mice exposed to PET microplastics (the type found in plastic bottles and clothing) for 42 days showed significant reproductive damage, including lower sperm quality and testicular tissue injury. The damage was caused by oxidative stress activating a specific cell-death pathway called p38 signaling, and was reversed when researchers blocked these pathways. This study identifies a clear mechanism by which a very common type of microplastic could harm male fertility.
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.
Assessing the impact of sub-chronic polyethylene terephthalate nanoplastic exposure on male reproductive health in mice
Researchers exposed male mice to nanoplastics made from PET (the same plastic used in water bottles and food containers) and found significant damage to their reproductive health. The nanoplastics reduced sperm quality, damaged testicular tissue, and disrupted hormone levels, raising concerns about how everyday plastic packaging may affect male fertility.
Exploring the impact of polyethylene terephthalate nanoplastics on male reproductive health: Insights from a mouse model study
Researchers investigated the impact of polyethylene terephthalate nanoplastics on male reproductive health, examining whether nanoplastic exposure contributes to infertility by affecting sperm function, hormone levels, or testicular tissue. Results showed PET nanoplastics impaired reproductive endpoints in the male reproductive system, adding to growing concern about plastic particle effects on 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.
Microplastics cause reproductive toxicity in male mice through inducing apoptosis of spermatogenic cells via p53 signaling
In a mouse study, polystyrene micro and nanoplastics taken orally for 60 days caused damage to sperm-producing cells in the testes by triggering a cell-death pathway called p53. Both larger microplastics and smaller nanoplastics led to tissue damage and increased cell death in reproductive organs. This research suggests that microplastic exposure could be a meaningful risk factor for male reproductive health.
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.
Exploring the impact of polyethylene terephthalate nanoplastics on male reproductive health: Insights from a mouse model study
Researchers investigated the effects of PET nanoplastics on male reproductive function, examining sperm quality, hormone levels, and testicular tissue in animal models. PET nanoplastic exposure reduced sperm motility and caused histological changes in testicular tissue, suggesting a potential role in male infertility.
Polystyrene 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 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.
A meta-analysis-based adverse outcome pathway for the male reproductive toxicity induced by microplastics and nanoplastics in mammals
This meta-analysis of 39 studies mapped the adverse outcome pathway for microplastic and nanoplastic-induced male reproductive toxicity in mammals. Increased reactive oxygen species triggers a cascade of cellular damage including mitochondrial dysfunction, sperm DNA damage, and disrupted hormone signaling, ultimately leading to reduced sperm quality, impaired spermatogenesis, and decreased testosterone levels.
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 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.
Unseen Threats: The Long‐term Impact of PET‐Microplastics on Development of Male Reproductive Over a Lifetime
Mice that ingested tiny PET plastic particles (the same plastic used in water bottles) over 29 weeks showed serious damage to their reproductive systems. Males had 69% fewer sperm, 24% less testosterone, and significantly smaller reproductive organs. These findings raise concerns that long-term exposure to microplastics from everyday plastics could harm male fertility in humans.
The male reproductive toxicity after nanoplastics and microplastics exposure: Sperm quality and changes of different cells in testis
A mouse study compared the reproductive toxicity of nanoplastics versus microplastics and found that both damaged the testes after 12 weeks of exposure, but microplastics caused more severe harm in some measures. The plastics disrupted sperm production, caused inflammation and oxidative stress, and damaged the cells that support sperm development. These findings suggest that plastic particle exposure could contribute to male fertility problems, with different particle sizes affecting reproductive health through different biological pathways.
Testicular mitochondrial redox imbalance and impaired oxidative phosphorylation underlie microplastic-induced testicular dysfunction in Wistar rats
Researchers investigated how polyethylene microplastics affect male reproductive function in rats by examining testicular mitochondrial health. The study found that microplastic exposure disrupted mitochondrial redox balance and impaired oxidative phosphorylation in testicular tissue, providing mechanistic evidence for how microplastics may contribute to male reproductive toxicity.
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 spermatogenesis disorder via disrupting mitochondrial function through the regulation of the Sirt1-Pgc1α signaling pathway in male mice
Researchers investigated how polystyrene microplastics of different sizes affect sperm development in male mice and found that exposure decreased sperm motility and caused structural abnormalities. The microplastics disrupted mitochondrial function in reproductive cells by interfering with a key energy regulation pathway. The study provides evidence that microplastic exposure may contribute to male reproductive health problems through mitochondrial damage.
Microplastics and male reproductive system: A comprehensive review based on cellular and molecular effects
This comprehensive review examines how microplastics affect the male reproductive system at cellular and molecular levels, drawing on studies from multiple scientific databases. Researchers found that microplastics can damage testicular structure and function, impair spermatogenesis, and disrupt sperm parameters through mechanisms including oxidative stress, inflammation, and activation of cell death pathways. The review highlights that microplastics reduce ATP production and trigger signaling cascades that may contribute to male fertility problems.
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.
Enhanced reproductive toxicities induced by phthalates contaminated microplastics in male mice (Mus musculus)
Researchers investigated the combined reproductive toxicity of phthalate-contaminated microplastics in male mice over a 30-day exposure period. They found that microplastics enhanced the accumulation of phthalates in the liver and gut, and the combination significantly worsened reproductive damage including reduced sperm quality and testicular tissue changes. The study suggests that microplastics may amplify the harmful effects of chemical contaminants they carry by increasing their bioavailability in the body.
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.
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.
Reproductive toxicity of polystyrene microplastics: In vivo experimental study on testicular toxicity in mice
Researchers exposed mice to polystyrene microplastics and examined the effects on male reproductive function. They found that microplastic exposure significantly reduced viable sperm count, increased sperm abnormalities, and caused structural damage to testicular tissue, suggesting that microplastics may pose risks to male fertility.