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 Examining the Relationship Between Polystyrene Microplastics and Male Fertility: Insights From an In Vivo Study and In Vitro Sertoli Cell Culture
ClearPolystyrene 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.
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.
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.
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.
In This Issue on 07-October-2024
This journal issue summary highlights a study that exposed male mice to polystyrene microplastics through oral ingestion for 28 and 56 days. The researchers found significant decreases in sperm concentration, motility, and normal sperm proportion, along with increased inflammatory markers. When tested on cultured Sertoli cells (which support sperm development), the microplastics penetrated the cells and triggered inflammatory responses, providing evidence that microplastic ingestion can cause male reproductive dysfunction in mammals.
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 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.
Polystyrene microplastics impair the functions of cultured mouse Leydig (TM3) and Sertoli (TM4) cells by inducing mitochondrial-endoplasmic reticulum damage
Lab experiments showed that polystyrene microplastics damaged two key types of testicular cells in mice -- Leydig cells that produce testosterone and Sertoli cells that support sperm development -- by harming their mitochondria (the cell's energy centers) and stressing the endoplasmic reticulum. These findings suggest that microplastic exposure could contribute to male reproductive problems by disrupting hormone production and sperm development at the cellular level.
Comparing the effects of polystyrene microplastics exposure on reproduction and fertility in male and female mice
Researchers exposed both male and female mice to polystyrene microplastics for 30 to 44 days and found that the particles accumulated more in ovaries than testes, causing oxidative stress and reproductive damage in both sexes. Male mice had fewer viable sperm and more deformed sperm, while female mice had smaller ovaries with fewer eggs, and both sexes showed altered hormone levels and reduced fertility. This study suggests that microplastic exposure could contribute to declining fertility in both men and women.
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.
Impact of polystyrene microplastics (PS-MPs) on the entire female mouse reproductive cycle: Assessing reproductive toxicity of microplastics through in vitro follicle culture
Female mice exposed to polystyrene microplastics suffered significant damage to their reproductive systems, including ovarian cell death, abnormal egg development, and fewer offspring. The microplastics accumulated in the ovaries and triggered cell death pathways while disrupting survival signaling in the cells that support egg development, suggesting microplastic exposure could contribute to declining fertility.
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.
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.
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 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.
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.
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.
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.
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.
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.
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 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.
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 microplastics induce mitochondrial damage in mouse GC-2 cells
Researchers exposed mouse reproductive cells to polystyrene microplastics and found that the particles caused significant mitochondrial damage, reducing energy production and disrupting normal cellular function. The study observed decreased mitochondrial membrane potential, lower ATP levels, and increased oxidative stress in the exposed cells. These findings help explain how microplastic exposure may impair sperm development by damaging the energy-producing structures within reproductive cells.