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61,005 resultsShowing papers similar to Impact of leachate from boiled-water-treated plastic products on male reproductive health: insights from transcriptomic and metabolomic profiling
ClearAssessing 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.
Multi-mechanistic effects of bisphenol A on testicular dysfunction and endocrine disruption in adult male Labeo bata: oxidative stress, inflammation, and dysregulated energy sensors
Researchers studied how bisphenol A (BPA), a chemical that leaches from microplastics in water, affects reproductive function in male fish. They found that chronic BPA exposure at environmentally relevant concentrations caused significant testicular damage, including reduced sperm production, increased inflammation, and disrupted hormone signaling. The study reveals multiple mechanisms by which this common microplastic-associated chemical can impair male reproductive health in aquatic species.
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.
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.
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.
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.
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.
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.
Quantitative analysis and toxicological mechanisms of various male infertility inducers: A network meta-analysis and pharmacological approach.
This network meta-analysis of 201 rodent studies compared nine common male infertility inducers, finding that microplastics caused among the most severe impairments to sperm count and motility — on par with the chemotherapy drug cyclophosphamide. Oxidative stress emerged as a shared mechanistic pathway across all inducers, pointing to it as a key target for understanding and potentially mitigating reproductive harm from environmental exposures.
Exploring the Biological Effects of Polystyrene Nanoplastics on Spermatogenesis: Insights From Transcriptomic Analysis in Mouse Spermatocytes
Researchers exposed mouse spermatocytes to polystyrene nanoplastics and observed membrane disruption, mitochondrial damage, increased oxidative stress, and DNA damage within 24 hours. Transcriptomic analysis revealed 134 genes with altered expression, many linked to critical reproductive processes like sperm development and mitochondrial organization. The study suggests that nanoplastic exposure may interfere with male reproductive health at the cellular and genetic level.
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.
The effects of exposure to microplastics in drinking water on sperm parameters and TNP1 and TNP2 sperm nuclear protein genes
Researchers compared sperm quality between men who primarily drank water from plastic bottles and carboys versus those who drank tap water. They found that men exposed to plastic-bottled water showed altered expression of sperm nuclear protein genes TNP1 and TNP2, along with differences in certain sperm parameters. The study suggests that microplastic exposure through drinking water containers may have measurable effects on male reproductive markers.
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.
Analyzing the toxicological effects of PET-MPs on male infertility: Insights from network toxicology, mendelian randomization, and transcriptomics
Using network toxicology, Mendelian randomisation, and transcriptomic analysis, researchers identified mechanisms by which PET microplastics may impair male fertility, linking shared gene targets to testicular oxidative stress, hormonal disruption, and spermatogenesis interference. The multi-evidence approach strengthens the case for a causal role of PET-MP exposure in male infertility.
Integrated 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.
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.
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.
Research Progress in Reproductive Toxicity of Micro- and Nanoplastics on Males and Its Mechanisms
This review summarized research on the reproductive toxicity of micro- and nanoplastics (MNPs) in males, finding that MNPs accumulate in reproductive organs and cause toxicity through oxidative stress, hormonal disruption, and DNA damage, with implications for both animal and human reproductive health.
Reproductive toxicity and related mechanisms of micro(nano)plastics in terrestrial mammals: Review of current evidence.
This review of terrestrial mammal studies found that micro- and nanoplastics induce reproductive toxicity through oxidative stress, inflammation, endocrine disruption, and DNA damage, affecting both male and female fertility. In males, effects include blood-testis barrier disruption and impaired spermatogenesis, while females show compromised oocyte maturation, ovarian fibrosis, and diminished ovarian reserve, with particles also capable of crossing the maternal-fetal interface.
The Threat of Micro-/Nanoplastics to Male Fertility: A Review of the Data and the Importance of Future Research
This review synthesizes findings from 21 studies examining how micro- and nanoplastics and their associated endocrine-disrupting chemicals affect male reproductive health at the cellular level. Researchers found evidence of multiple toxicity mechanisms including damage to the blood-testis barrier, disruption of hormone signaling, oxidative stress, and structural damage to testicular tissues. The study notes that while these findings from cell and animal studies are concerning, translating the results to human health requires further research with realistic exposure conditions.
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.
Microplastics and impaired male reproductive health—exploring biological pathways of harm: a narrative review
This narrative review summarizes the evidence that microplastics may harm male reproductive health through oxidative stress, hormone disruption, inflammation, and direct damage to reproductive cells. While animal studies show concerning effects on sperm quality, testicular function, and fertility, human studies are still lacking. The review calls for urgent research on microplastic impacts on human male fertility and for policies to reduce microplastic exposure.
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.
Therapeutic Repair of Sperm Quality Decline Caused by Polytetrafluoroethylene
Researchers found that PTFE (Teflon), a type of microplastic commonly used in non-stick cookware, was detected in nearly half of human male reproductive tissue samples and accumulated in the urogenital system. In mice, PTFE exposure damaged sperm development, disrupted DNA repair, and reduced fertility. The study also identified a potential treatment target, offering hope that some of this reproductive damage could be reversed.