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61,005 resultsShowing papers similar to Polystyrene microplastics impair mouse oocyte maturation by interfering with fatty acid oxidation
ClearPolystyrene nanoplastics induce apoptosis, autophagy, and steroidogenesis disruption in granulosa cells to reduce oocyte quality and fertility by inhibiting the PI3K/AKT pathway in female mice
Researchers found that polystyrene nanoplastics (tiny plastic particles under 1 micrometer) impair egg cell quality in female mice by damaging the ovarian support cells that help eggs mature, triggering cell death and disrupting hormone production. These findings raise important questions about the potential reproductive risks of nanoplastic exposure in women.
Polystyrene microplastics induced female reproductive toxicity in mice
Researchers exposed female mice to polystyrene microplastics for 35 days and found the particles accumulated in multiple organs including the ovaries, where they caused inflammation and oxidative stress. The microplastics reduced egg quality by lowering protective antioxidants, disrupting mitochondrial function, and altering calcium levels in the cells. This study provides evidence that microplastic exposure could harm female fertility by directly damaging the ovaries and the eggs they produce.
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.
Exposure to microplastics leads to a defective ovarian function and change in cytoskeleton protein expression in rat
Researchers exposed female rats to polystyrene microplastics over multiple reproductive cycles and found, for the first time, that the particles accumulated in different parts of the ovarian tissue. The microplastics reduced ovarian weight, disrupted the normal development of egg follicles, altered the reproductive cycle, and lowered estrogen levels. The study suggests these effects are driven by oxidative stress and changes in key structural proteins within the ovary.
Polystyrene nanoplastic exposure actives ferroptosis by oxidative stress-induced lipid peroxidation in porcine oocytes during maturation
Researchers found that polystyrene nanoplastics trigger ferroptosis — a form of iron-dependent cell death driven by fat oxidation — in pig egg cells, disrupting their maturation and reproductive viability. This finding raises concerns about nanoplastic exposure potentially impairing fertility by damaging the eggs needed for reproduction.
Polystyrene nanoplastics induce ovarian granulosa cell senescence via autophagy suppression
Researchers found that polystyrene nanoplastics induce premature cellular aging (senescence) in human ovarian granulosa cells by suppressing autophagy, triggering inflammatory signaling and mitochondrial dysfunction, and that restoring autophagy with rapamycin reversed these effects — pointing to a potential mechanism linking nanoplastic exposure to accelerated ovarian aging.
Polystyrene microplastics cause granulosa cells apoptosis and fibrosis in ovary through oxidative stress in rats
Researchers exposed female rats to polystyrene microplastics at different concentrations for 90 days and examined the effects on their ovaries. The study found that microplastic exposure caused cell death and tissue scarring in the ovaries through oxidative stress, suggesting that microplastics may have implications for female reproductive health.
Polystyrene nanoplastics exposure triggers spermatogenic cell senescence via the Sirt1/ROS axis
Male mice exposed to polystyrene nanoplastics for 60 days showed damaged sperm-producing cells that displayed signs of premature aging, linked to a specific molecular pathway involving the Sirt1 protein and oxidative stress. This study adds to growing evidence that nanoplastic exposure may harm male reproductive health by accelerating the aging of cells responsible for sperm production.
Polystyrene Microplastics Induced Ovarian Toxicity in Juvenile Rats Associated with Oxidative Stress and Activation of the PERK-eIF2α-ATF4-CHOP Signaling Pathway
Researchers exposed juvenile female rats to polystyrene microplastics and found significant ovarian damage, including increased follicle death and reduced hormone levels. The microplastics triggered oxidative stress and activated a specific cellular stress pathway that led to programmed cell death in ovarian tissue. The study suggests that early-life microplastic exposure may pose risks to reproductive development in mammals.
Microplastics exposure causes premature ovarian aging via inducing mitochondrial dysfunction
Researchers found that microplastic exposure in mice accelerated ovarian aging, characterized by increased expression of aging markers, elevated fibrosis, and inflammatory damage. The microplastics caused mitochondrial dysfunction that reduced ovarian reserve and compromised oocyte quality and embryo development. Notably, supplementation with the amino acid L-arginine significantly mitigated the aging effects, suggesting a potential protective strategy for reproductive health against microplastic exposure.
Polystyrene microplastics impaired decidualization in mice via oxidative stress and inflammation and disrupted the reproductive function of their female offspring
Mouse experiments found that polystyrene microplastics impaired uterine decidualization and embryo implantation via oxidative stress and inflammation, and that maternal PS-MP exposure also disrupted the reproductive function of female offspring.
The ovarian-related effects of polystyrene nanoplastics on human ovarian granulosa cells and female mice
This study tested the effects of polystyrene nanoplastics on both human ovarian cells in the lab and on female mice. The nanoplastics accumulated in ovarian tissue, caused cell death, disrupted hormone levels, and reduced egg quality and fertility in mice. These findings suggest that nanoplastic exposure could threaten female reproductive health by damaging the ovaries.
Polystyrene microplastics lead to pyroptosis and apoptosis of ovarian granulosa cells via NLRP3/Caspase-1 signaling pathway in rats
In a 90-day study, female rats exposed to polystyrene microplastics had fewer healthy ovarian follicles, increased oxidative damage, and elevated inflammation in their ovaries. The microplastics triggered a type of inflammatory cell death called pyroptosis in the cells surrounding eggs, along with increased programmed cell death. These findings suggest that microplastic exposure could harm female fertility by damaging the ovaries and the cells needed for healthy egg development.
Effect of polystyrene nanoplastics on in vitro maturation of pig cumulus-encosed oocytes
Researchers exposed pig egg cells to polystyrene nanoplastics during laboratory maturation and found that while the eggs still completed their basic development stages, the nanoplastics significantly increased harmful reactive oxygen species levels. This oxidative stress reduced the quality of resulting embryos, as indicated by fewer cells per embryo, suggesting nanoplastic exposure could be a concern for reproductive health.
Maternal exposure to polystyrene nanoplastics leads to ovotoxicity in female mouse offspring
Researchers exposed pregnant mice to polystyrene nanoplastics throughout mating, pregnancy, and nursing, then examined the ovaries of their female offspring. They found that maternal nanoplastic exposure significantly reduced ovarian weight and follicle numbers in the offspring and lowered the expression of key antioxidant genes. The study suggests that nanoplastic exposure during pregnancy may pose risks to the reproductive development of female offspring.
Polystyrene-microplastics and DEHP co-exposure induced DNA damage, cell cycle arrest and necroptosis of ovarian granulosa cells in mice by promoting ROS production
Researchers found that co-exposure to polystyrene microplastics and DEHP (a common plastic additive) caused more damage to mouse ovarian cells than either pollutant alone, triggering excessive oxidative stress that led to DNA damage, cell cycle arrest, and cell death. These findings suggest that microplastics combined with their chemical additives may pose a synergistic threat to female reproductive health.
Effects of polystyrene nanoplastics on the female reproductive system in mice: Implications for ovarian function and follicular development
Researchers exposed female mice to polystyrene nanoplastics orally for 29 days and examined the effects on their reproductive systems. They found that nanoplastic exposure disrupted estrous cycles, impaired follicle development, and altered hormone levels in a dose-dependent manner. The study suggests that nanoplastics, due to their extremely small size, may cross biological barriers and accumulate in reproductive tissues, raising concerns about potential effects on fertility.
Exposure to Polystyrene Nanoplastics Compromise Ovarian Reserve Function and Endometrial Decidualization in Early Pregnant Mice
Female mice exposed to polystyrene nanoplastics for 90 days before pregnancy had fewer successful pregnancies, smaller pups, and damaged ovaries with reduced egg counts. The nanoplastics disrupted key reproductive hormones and interfered with the uterine process needed for embryo implantation. This study raises concerns that nanoplastic exposure through food and water could harm female fertility and pregnancy outcomes in humans.
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.
Melatonin mitigates polystyrene nanoplastics-induced impairment of oocyte maturation in mice
Researchers found that polystyrene nanoplastics impair egg cell maturation in mice by causing excessive oxidative stress, mitochondrial dysfunction, and disrupting the structural machinery needed for proper cell division. They then tested whether melatonin could counteract these effects and found that melatonin treatment significantly alleviated the damage by restoring mitochondrial function and reducing oxidative stress. The study suggests that melatonin may offer a protective strategy against nanoplastic-induced reproductive harm.
Intergenerational and transgenerational reproductive toxicity of polystyrene microplastics in female mice
Female mice were exposed to polystyrene microplastics during lactation and researchers tracked reproductive outcomes in both exposed mothers and their offspring through multiple generations, finding that even at doses comparable to human infant bottle-feeding exposure, microplastics induced ovarian damage and reduced fertility that persisted across generations.
Polystyrene nanoplastics disrupt ovarian development via cytoskeletal remodeling and epigenetic reprogramming particularly in granulosa cells
Researchers used single-cell RNA sequencing to map polystyrene nanoplastic toxicity in mouse ovaries, identifying granulosa cells as the primary target and showing that 100 nm particles trigger F-actin cytoskeletal remodeling, STAT1-driven epigenetic reprogramming, and necroptosis, disrupting follicle development and hormone production.
Characterization of microplastics in human follicular fluid and assessment of their potential impact on mouse oocyte maturation in vitro
Scientists found microplastics in human follicular fluid, the liquid surrounding eggs in the ovaries, after analyzing samples from 19 women. When they tested how these particles affect egg development in mice, they found that certain types of microplastics reduced the ability of eggs to mature properly, raising concerns about potential effects on fertility.
In vitro effects of polystyrene microplastics exposure on adipose tissue dysfunction
Researchers exposed adipose tissue cells to polystyrene microplastics and found that the effects depended on the developmental stage of the cells. While fully mature fat cells showed minimal changes, microplastics exposure during the differentiation process significantly promoted fat cell enlargement, triggered oxidative stress, endoplasmic reticulum stress, and inflammatory responses. The findings suggest that microplastics may be more disruptive to fat tissue during its formation than after it has matured.