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61,005 resultsShowing papers similar to OX-LDL promotes insufficient autophagy and apoptosis of ovarian granulosa cells through regulation ROS-mediated PI3K/Akt/mTOR pathway
ClearHigh Prolactin Concentration Induces Ovarian Granulosa Cell Oxidative Stress, Leading to Apoptosis Mediated by L-PRLR and S-PRLR
This paper is not relevant to microplastics research — it investigates how high prolactin concentrations induce oxidative stress and apoptosis in ovine ovarian granulosa cells, a reproductive endocrinology study.
Beyond apoptosis: evidence of other regulated cell death pathways in the ovary throughout development and life
This review explores different types of programmed cell death in the ovary beyond the well-known process of apoptosis, and their roles in ovarian development and function throughout a woman's life. While not focused on microplastics directly, these cell death pathways are important because emerging research shows that microplastic and nanoplastic exposure can trigger abnormal cell death in ovarian tissue. Understanding these pathways is key to assessing how environmental pollutants may affect female fertility.
Ox-LDL induced endothelial progenitor cells oxidative stress via p38/Keap1/Nrf2 pathway
This cell biology study investigated how oxidized low-density lipoprotein (ox-LDL) triggers oxidative stress and cell death in endothelial progenitor cells through a specific signaling pathway. While not directly about microplastics, the study is relevant because microplastics are known to trigger similar oxidative stress pathways in cardiovascular tissues.
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.
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 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.
Ferroptosis: First evidence in premature duck ovary induced by polyvinyl chloride microplastics
Researchers discovered that polyvinyl chloride microplastics caused premature ovarian damage in ducks through a cell death process called ferroptosis, which involves iron-dependent oxidative damage. Higher microplastic concentrations led to iron accumulation, increased oxidative stress, and structural damage to ovarian tissue. This is the first evidence linking microplastic exposure to ferroptosis in the avian reproductive system.
Polystyrene microplastics impair mouse oocyte maturation by interfering with fatty acid oxidation
Researchers exposed female mice to polystyrene microplastics via oral dosing for 35 days and found that high doses impair oocyte maturation by upregulating SIRT4 and suppressing fatty acid oxidation, with downstream effects including spindle abnormalities, endoplasmic reticulum stress, and accelerated ovarian aging.
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-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.
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 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.
Exposição De Microplásticos E Nanoplásticos Ao Tecido Ovariano: Uma Revisão Integrativa
This integrative review examines the impact of micro- and nanoplastics on female ovarian tissue, synthesizing animal model studies showing damage to follicular structures, increased oxidative stress, and disrupted reproductive hormone signaling.
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: unraveling the signaling pathways involved in reproductive health
This review examines the effects of microplastics on male and female reproductive health, focusing on the metabolic pathways involved in compromised gamete quality, toxicity, apoptosis, and DNA damage. Evidence indicates that microplastics can increase oxidative stress leading to developmental abnormalities, epigenetic changes, and reduced gamete quality, though research on mammalian and human reproductive effects remains limited compared to studies in aquatic organisms.
Microplastics in ovarian function and ozone-based mitigation strategies: Emerging evidence and translational implications
This review synthesized emerging evidence that microplastics accumulate in human follicular fluid, oocytes, placenta, and semen, causing oxidative stress, mitochondrial dysfunction, and meiotic disruption in reproductive cells, and discussed ozone-based strategies as potential mitigation approaches.
Microplastics (MPs) exposure impairs porcine oocyte quality by triggering oxidative stress-directed DNA damage and apoptosis with metabolomic alterations
Researchers exposed pig egg cells (oocytes) to microplastics and found significant damage to their quality, including problems with cell division and chromosome structure. The microplastics disrupted important metabolic processes, leading to oxidative stress, DNA damage, and cell death. Since pig reproductive biology is similar to humans, these findings raise concerns that microplastic exposure could harm female fertility.
P-266 Profiling redox effects induced by micro-nanoplastics in the female reproductive system: insights from human granulosa cells
Researchers showed that nano- and microplastics are taken up by human granulosa cells and cause changes in viability, energy production, and antioxidant responses. The findings provide early evidence that plastic particles can interfere with cellular redox balance in the female reproductive system.
Polystyrene nanoplastics induce ovarian injury by PI3K-Akt pathway-driven macrophage extracellular trap formation
Researchers showed that polystyrene nanoplastics accumulate in mouse ovaries, triggering macrophage infiltration and the formation of macrophage extracellular traps (METs) via the PI3K-Akt signaling pathway, which in turn cause pyroptosis (inflammatory cell death) in granulosa cells and follicular loss — effects reversible with a PI3K inhibitor.
Microplastics and nanoplastics in follicular fluid are associated with diminished ovarian reserve: clinical and molecular insights
Researchers found that microplastics and nanoplastics present in follicular fluid are associated with diminished ovarian reserve in women. The study provides evidence suggesting that exposure to these particles may harm female ovarian function. The findings point to the environment-gut-ovarian axis as a potential pathway through which micro- and nanoplastic exposure could contribute to reproductive health concerns.
Exposição De Microplásticos E Nanoplásticos Ao Tecido Ovariano: Uma Revisão Integrativa
This integrative review (in Portuguese) examines published evidence on the effects of micro- and nanoplastic exposure on female ovarian tissue morphology, finding disrupted folliculogenesis, oxidative stress, and hormonal interference reported across animal model studies.
Reproductive toxicity of microplastics role of oxidative stress in cellular and molecular damage
This review synthesizes in vitro, in vivo, and epidemiological evidence on how microplastics cause reproductive toxicity, focusing on oxidative stress as the central mechanism. MPs infiltrate reproductive tissues, generate reactive oxygen species, and disrupt gametogenesis, hormone regulation, and embryonic development across multiple species.
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.
Developmental and reproductive toxic effects of exposure to microplastics: A review of associated signaling pathways
This review examines how microplastic exposure affects reproductive and developmental health across multiple species, focusing on the biological signaling pathways involved. Researchers found that microplastics can trigger oxidative stress, inflammation, and hormonal disruption through specific cellular pathways, leading to reduced fertility and abnormal development. The study provides a molecular-level framework for understanding why microplastics may pose risks to reproductive health.