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61,005 resultsShowing papers similar to Polystyrene microplastics cause reproductive toxicity in male mice
ClearReproductive 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.
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.
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.
Examining the Relationship Between Polystyrene Microplastics and Male Fertility: Insights From an In Vivo Study and In Vitro Sertoli Cell Culture
This study found that polystyrene microplastics caused reproductive damage in male mice, disrupting the cells that support sperm development (Sertoli cells). The microplastics interfered with normal reproductive function in both live mice and cell cultures. These findings add to growing evidence that microplastic exposure could contribute to declining male fertility, a trend already observed in humans worldwide.
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.
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.
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.
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.
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.
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 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.
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.
Chronic Polystyrene Microplastic Exposure Reduces Testosterone Levels in Mice through Mitochondrial Oxidative Stress and BAX/BCL2-Mediated Apoptosis
This mouse study found that oral exposure to polystyrene microplastics for four weeks significantly lowered testosterone levels by damaging the cells in the testes that produce it. The microplastics caused mitochondrial damage, oxidative stress, and triggered cell death in these testosterone-producing cells. These findings suggest that chronic microplastic exposure could contribute to declining male hormone levels and fertility issues.
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.
Chronic toxic effects of polystyrene microplastics on reproductive parameters of male rats
Researchers studied the chronic toxic effects of polystyrene microplastics on the reproductive system of male rats over 90 days. The study found significant reductions in sperm volume, motility, epididymal count, and serum testosterone levels, along with disrupted testicular architecture and decreased antioxidant capacity. The findings suggest that chronic microplastic exposure may adversely affect male reproductive parameters in mammals.
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.
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 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.
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.
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.