We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Papers
61,005 resultsShowing papers similar to Exploring the Biological Effects of Polystyrene Nanoplastics on Spermatogenesis: Insights From Transcriptomic Analysis in Mouse Spermatocytes
ClearIntegrated transcriptomic and metabolomic analysis reveals the underlying mechanisms for male reproductive toxicity of polystyrene nanoplastics in mouse spermatocyte-derived GC-2spd(ts) cells
Researchers used integrated transcriptomic and metabolomic analysis to investigate how polystyrene nanoplastics affect mouse spermatocyte cells. They found that nanoplastic exposure disrupted lipid metabolism, triggered oxidative stress, and activated cell death pathways in the reproductive cells. The study suggests that nanoplastic exposure may pose risks to male reproductive health by interfering with critical metabolic and gene expression processes in developing sperm cells.
Transcriptome and proteome analyses reveal the mechanisms involved in polystyrene nanoplastics disrupt spermatogenesis in mice
Using advanced genetic and protein analysis, researchers found that polystyrene nanoplastics disrupted sperm production in male mice after 28 days of exposure. The nanoplastics reduced sperm count and movement, damaged the structure of sperm-producing tubes, triggered cell death, and lowered hormone levels needed for male fertility. This study provides detailed molecular evidence for how nanoplastic exposure could contribute to male reproductive problems.
Toxicity to the Male Reproductive System after Exposure to Polystyrene Nanoplastics: A Macrogenomic and Metabolomic Analysis
Researchers exposed male mice to polystyrene nanoplastics of different sizes through their drinking water for four months and found significant harm to reproductive function. The nanoplastics disrupted gene activity and metabolic pathways in the gut, which was linked to reduced sperm quality and testicular damage. The study suggests that long-term nanoplastic exposure through drinking water may pose risks to male reproductive health.
The mouse model of induced sperm DNA damage caused by polystyrene microplastics exhibited distinct transcriptomic and proteomic features
Researchers established a mouse model of polystyrene microplastic-induced sperm DNA damage by administering 1 mg/kg/day for 60 days, which significantly elevated the sperm DNA fragmentation index, and characterized the transcriptomic and proteomic profiles associated with this reproductive toxicity.
Whole transcriptome characterization of polystyrene microplastic-induced sperm DNA damage mouse spermatocytes model
Researchers used whole transcriptome sequencing to investigate how polystyrene microplastics cause DNA damage in mouse sperm cells. They found that microplastic exposure significantly increased DNA fragmentation and altered the expression of numerous genes involved in immune response and cellular defense pathways. The study suggests that microplastics may harm sperm DNA integrity primarily by disrupting immune-related and oxidative stress pathways.
Multi-omics analysis of testis after long-term exposure to polystyrene nanoplastics reveals premature testicular aging and age-dependent damage in mice
Researchers used multi-omics analysis to study the effects of long-term polystyrene nanoplastic exposure on mouse testes and found signs of premature testicular aging. The damage was dependent on both the age of the mice and the duration of exposure, with younger animals showing particular vulnerability. The study suggests that protecting mRNA metabolism and testosterone production could help preserve reproductive function in males exposed to nanoplastics.
Exposure to polystyrene nanoplastics impairs sperm metabolism and pre-implantation embryo development in mice
This study found that male mice given polystyrene nanoplastics by mouth showed significant harm to sperm function and early embryo development, with changes in gene expression that could affect offspring. The findings raise concerns that nanoplastic exposure could impair male fertility and potentially pass harmful effects to the next generation.
Impact of Polystyrene Microplastics on Human Sperm Functionality: An In Vitro Study of Cytotoxicity, Genotoxicity and Fertility-Related Genes Expression
Researchers exposed human sperm samples to polystyrene microplastics in the lab and observed decreased sperm vitality and motility in a time-dependent manner. The microplastics also caused DNA damage, increased harmful reactive oxygen species, and reduced the expression of genes essential for fertilization. The study suggests that microplastic exposure could impair male fertility through oxidative stress and interference with key reproductive functions.
Integrated fecal microbiome and metabolome analysis explore the link between polystyrene nanoplastics exposure and male reproductive toxicity in mice
Researchers exposed mice to polystyrene nanoplastics of different sizes and doses, then analyzed fecal microbiome and metabolome changes alongside reproductive outcomes. The study found that nanoplastic exposure disrupted gut microbiota balance and metabolic pathways, which correlated with reduced sperm count, viability, and testosterone levels. The findings suggest that gut microbiota-metabolite disruption may play an important role in nanoplastic-induced male reproductive toxicity.
Short-term polystyrene nanoplastic exposure alters zebrafish male and female germline and reproductive outcomes, unveiling pollutant-impacted molecular pathways
A short 96-hour exposure to polystyrene nanoplastics harmed both male and female reproductive cells in zebrafish. In males, nanoplastics crossed the testicular barrier, entered reproductive cells directly, and caused abnormal sperm with reduced movement. In females, the exposure disrupted egg development, suggesting that even brief nanoplastic contact could impair fertility in aquatic species and raising questions about similar risks for human reproductive health.
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.
Determination of Biological and Molecular Attributes Related to Polystyrene Microplastic-Induced Reproductive Toxicity and Its Reversibility in Male Mice
Researchers exposed male mice to polystyrene microplastics through drinking water and found that the particles caused mitochondrial damage in testicular tissue, including reduced membrane potential and disrupted energy production. This mitochondrial dysfunction led to decreased sperm quality, likely driven by oxidative stress. Importantly, the study found that sperm quality recovered after one to two spermatogenic cycles without further exposure, suggesting that reproductive toxicity from microplastics may be reversible.
Gut microbiota combined with metabolome dissects long-term nanoplastics exposure-induced disturbed spermatogenesis
Researchers studied how long-term exposure to nanoplastics affects sperm production in mice by analyzing changes in gut bacteria and metabolic pathways. They found that nanoplastic exposure disrupted spermatogenesis, with amino-modified nanoplastics causing more severe effects than standard polystyrene particles. The study suggests that nanoplastics may harm male reproductive health by altering gut microbiota and lipid metabolism.
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.
Long‐term nanoplastics exposure contributes to impaired steroidogenesis by disrupting the hypothalamic‐testis axis: Evidence from integrated transcriptome and metabolome analysis
Researchers exposed male mice to nanoplastics for 12 weeks and found that long-term exposure disrupted the hormonal signaling pathway between the brain and testes, leading to reduced sperm quality and lower testosterone levels. Evidence indicates that the disruption involved changes in key enzymes and metabolic pathways responsible for producing reproductive hormones.
Polystyrene nanoplastics disrupt epididymal initial segment by perturbing NK cell differentiation and epithelial homeostasis
Using single-cell transcriptomics and multi-omics analysis, researchers found that polystyrene nanoplastics disrupt the epididymal initial segment in mice by perturbing natural killer cell differentiation and epithelial homeostasis. The work reveals a previously unknown mechanism by which nanoplastics may impair sperm maturation and male fertility.
The emerging risk of exposure to nano(micro)plastics on endocrine disturbance and reproductive toxicity: From a hypothetical scenario to a global public health challenge
Researchers administered polystyrene nanoplastics orally to male rats for five weeks and found significant reductions in testosterone, LH, and FSH levels, sperm DNA damage, altered testicular gene expression, and dose-dependent histological lesions, indicating that nanoplastic exposure disrupts the hormonal axis governing male reproductive function.
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 Affect the Reproductive Performance of Male Mice and Lipid Homeostasis in Their Offspring
Researchers found that long-term exposure to environmentally relevant doses of polystyrene microplastics over 21 weeks significantly impaired reproductive function in male mice, including decreased testicle weight and sperm quality. The study also revealed transgenerational effects, with offspring showing disrupted lipid homeostasis.
Maternal Exposure to Polystyrene Nanoplastics Disrupts Spermatogenesis in Mouse Offspring by Inducing Prdm14 Overexpression in Undifferentiated Spermatogonia
When pregnant mice were exposed to nanoplastics (extremely small plastic particles), their male offspring had lower testosterone, fewer sperm, and damaged sperm-producing cells. The nanoplastics caused inflammation in the cells responsible for sperm production, disrupting a key gene (Prdm14) that controls sperm development. This suggests that a mother's plastic exposure during pregnancy could affect her sons' fertility later in life.
In Vitro Nano-Polystyrene Toxicity: Metabolic Dysfunctions and Cytoprotective Responses of Human Spermatozoa
Researchers investigated the effects of polystyrene nanoplastics (50 and 100 nm) on mature human sperm cell metabolism in vitro. The study found that smaller 50 nm particles showed higher toxicity, causing acrosomal damage, oxidative stress, DNA fragmentation, and decreased mitochondrial activity, while 100 nm particles primarily affected the acrosome, suggesting size-dependent impacts of nanoplastics on reproductive cell function.
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.
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.