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61,005 resultsShowing papers similar to Maternal Exposure to Polystyrene Nanoplastics Disrupts Spermatogenesis in Mouse Offspring by Inducing Prdm14 Overexpression in Undifferentiated Spermatogonia
ClearExposure 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.
Prenatal and postnatal exposure to polystyrene microplastics induces testis developmental disorder and affects male fertility in mice
Researchers exposed pregnant mice and their offspring to polystyrene microplastics from gestation through early life and found significant disruption to testicular development and male reproductive function. The exposed males showed reduced sperm quality, lower testosterone levels, and structural damage to testicular tissue. The study suggests that early-life microplastic exposure may have lasting effects on male fertility.
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.
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.
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.
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.
Oral exposure to polystyrene nanoplastics reduced male fertility and even caused male infertility by inducing testicular and sperm toxicities in mice
Researchers fed male mice polystyrene nanoplastics of different sizes (25, 50, and 100 nm) for 56 days and found that all sizes reduced fertility and some caused complete infertility. The nanoplastics accumulated in the testes, causing oxidative stress, cell death, and inflammation that damaged sperm and reproductive tissue. This study raises concerns that human exposure to nanoplastics through food and water could contribute to declining male fertility.
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.
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.
Maternal exposure to polystyrene nanoplastics during gestation and lactation induces hepatic and testicular toxicity in male mouse offspring
Researchers exposed pregnant and nursing mice to polystyrene nanoplastics and studied the effects on their male offspring. The offspring showed reduced body weight, liver damage with inflammation and disrupted sugar metabolism, and testicular harm including decreased sperm counts. The findings suggest that nanoplastic exposure during pregnancy and breastfeeding can cause significant organ damage in the next generation.
Maternal exposure to polystyrene nanoplastics during gestation and lactation caused fertility decline in female mouse offspring
When pregnant mice were exposed to nanoplastics during pregnancy and nursing, their female offspring had significantly reduced fertility as adults. The nanoplastics caused premature activation of egg cells in the ovaries and damaged crucial connections between eggs and their supporting cells. This raises concerns that a mother's exposure to nanoplastics could have lasting effects on her daughters' ability to have children.
Perinatal exposure to polystyrene microplastics induces multigenerational impairment of male reproduction via disrupted steroidogenesis and proteostasis
Scientists found that when pregnant and nursing rats were exposed to tiny plastic particles (microplastics), their male babies and grandbabies had damaged reproductive systems with lower sperm counts and reduced fertility hormones. While the grandbabies showed some ability to recover from this damage, the study suggests that microplastics in our environment could potentially harm male fertility across multiple generations. This research is concerning because humans are increasingly exposed to microplastics through food, water, and air.
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.
Low-dose polystyrene microplastics exposure impairs fertility in male mice with high-fat diet-induced obesity by affecting prostate function
Male mice exposed to low doses of microplastics had lower sperm quality and fewer offspring, and these effects were significantly worse when combined with a high-fat diet. The combination triggered inflammation and cell death in the prostate gland, reducing key nutrients in seminal fluid needed for sperm health. This suggests that microplastic exposure may be an overlooked factor in declining male fertility, especially for those with metabolic conditions like obesity.
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.
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.
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.
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.
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.
Polystyrene nanoplastics aggravated dibutyl phthalate-induced blood-testis barrier dysfunction via suppressing autophagy in male mice
In a mouse study, polystyrene nanoplastics combined with dibutyl phthalate (a common plasticizer chemical) caused significantly worse damage to the blood-testis barrier than either substance alone. The nanoplastics carried the phthalate into the reproductive system, where the combination reduced sperm quality, impaired sperm development, and damaged the protective barrier around the testes. This research shows how nanoplastics can make other common plastic chemicals more dangerous to male fertility.
MicroRNA and Gut Microbiota Alter Intergenerational Effects of Paternal Exposure to Polyethylene Nanoplastics
In a mouse study, when fathers were exposed to polyethylene nanoplastics, their male offspring suffered reproductive damage including lower sperm counts and testicular injury — even though the offspring were never directly exposed. The effects were passed down through changes in small RNA molecules and gut bacteria, suggesting that nanoplastic exposure could affect fertility across generations.
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.
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.