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61,005 resultsShowing papers similar to Evaluation of polyethylene microplastics toxicity using Nrf2/ARE and MAPK/Nrf2 signaling pathways
ClearPolystyrene microplastics induce blood–testis barrier disruption regulated by the MAPK-Nrf2 signaling pathway in rats
Researchers fed rats polystyrene microplastics for 90 days and found significant damage to male reproductive health, including reduced sperm quality, damaged sperm-producing tissue, and increased cell death. The study identified a specific molecular pathway where microplastics triggered oxidative stress that disrupted the blood-testis barrier, a critical protective structure in the testes. These findings provide new evidence that microplastic exposure may pose risks to male reproductive function.
Polystyrene microplastics induce blood-testis barrier disruption regulated by MAPK-Nrf2 signaling pathway in rats
Researchers found that polystyrene microplastics (PS-MPs) disrupted the blood-testis barrier in male rats after 90 days of exposure, with higher doses (0.15 and 1.5 mg/d) causing significant spermatogenic cell apoptosis and reduced sperm motility through activation of the MAPK-Nrf2 signaling pathway.
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.
Role of the Nrf2 Signaling Pathway in Ovarian Aging: Potential Mechanism and Protective Strategies
This review explores how the Nrf2 signaling pathway, a key defense system against oxidative stress, plays a role in ovarian aging, which leads to menopause, reduced fertility, and health risks like osteoporosis. While not focused on microplastics specifically, the Nrf2 pathway is one of the main systems that microplastics disrupt when they accumulate in reproductive tissues. Understanding this pathway helps explain how environmental pollutants like microplastics could accelerate ovarian aging and harm fertility.
Mitigative potential of kaempferide against polyethylene microplastics induced testicular damage by activating Nrf-2/Keap-1 pathway
Researchers tested whether kaempferide, a natural plant compound with antioxidant properties, could protect against testicular damage caused by polyethylene microplastics in rats. They found that the microplastics triggered significant oxidative stress and tissue damage in the testes, but kaempferide treatment substantially reduced these harmful effects by activating a key protective cellular pathway. The study suggests that natural antioxidant compounds may help counteract some of the reproductive harm associated with microplastic exposure.
Adverse effects of microplastics and oxidative stress-induced MAPK/Nrf2 pathway-mediated defense mechanisms in the marine copepod Paracyclopina nana
Researchers studied how nano- and micro-sized polystyrene particles affect a tiny marine crustacean called a copepod at the molecular level. They found that the smallest particles caused the most severe oxidative stress and triggered cellular defense pathways, with effects worsening at higher concentrations. The study suggests that microplastics can disrupt the internal chemistry of marine organisms even at sizes too small to see with the naked eye.
The Antioxidative Action of ZTP by Increasing Nrf2/ARE Signal Pathway
This study investigated the antioxidant properties of a compound called ZTP and its ability to protect against oxidative stress in brain tissue. While focused on neuroprotection rather than microplastics, oxidative stress is one of the primary mechanisms by which microplastics are thought to cause cellular damage.
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.
Polystyrene microplastics induce apoptosis in chicken testis via crosstalk between NF-κB and Nrf2 pathways
Researchers found that polystyrene microplastics caused testicular damage in chickens through crosstalk between inflammatory and antioxidant defense pathways. Exposure to microplastics through drinking water disrupted the blood-testis barrier, triggered oxidative stress by inhibiting the Nrf2 pathway, activated inflammatory signaling through NF-kB, and ultimately induced cell death in testicular tissue.
A meta-analysis-based adverse outcome pathway for the male reproductive toxicity induced by microplastics and nanoplastics in mammals
This meta-analysis of 39 studies mapped the adverse outcome pathway for microplastic and nanoplastic-induced male reproductive toxicity in mammals. Increased reactive oxygen species triggers a cascade of cellular damage including mitochondrial dysfunction, sperm DNA damage, and disrupted hormone signaling, ultimately leading to reduced sperm quality, impaired spermatogenesis, and decreased testosterone levels.
Polyethylene microplastics disrupt renal function, mitochondrial bioenergetics, redox homeostasis, and histoarchitecture in Wistar rats
Researchers gave rats polyethylene microplastics orally for 28 days and found dose-dependent kidney damage, including impaired filtration, electrolyte imbalances, and tissue inflammation. The microplastics depleted antioxidant defenses, increased oxidative stress markers, and disrupted mitochondrial energy production in kidney cells, identifying the kidneys as a critical target of microplastic toxicity.
Investigating polystyrene nanoplastics-induced reproductive toxicity in vitro: Focus on Nrf2-PKM2-autophagy signaling pathway
This lab study investigated how polystyrene nanoplastics damage male reproductive cells, finding they triggered autophagy (cellular self-digestion) and disrupted key proteins in a signaling pathway important for sperm cell survival. The findings suggest nanoplastics could impair male fertility by causing programmed cell death in testicular cells. This adds to growing evidence that plastic nanoparticles can harm reproductive health.
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.
A critical review on male-female reproductive and developmental toxicity induced by micro-plastics and nano-plastics through different signaling pathways.
This critical review examined how micro- and nanoplastics disrupt male and female reproductive systems and fetal development through multiple signaling pathways, including endocrine disruption, oxidative stress, and epigenetic modification, based on animal and cell studies.
Micro- and nano-plastics activation of oxidative and inflammatory adverse outcome pathways
This review maps the biological harm caused by micro- and nanoplastics to formal toxicity pathways, finding that oxidative stress is a common starting point for damage at every level from cells to whole organisms. Researchers found that in ecological settings, this oxidative damage cascades into growth inhibition and behavioral changes, while in human health contexts it may trigger inflammatory responses. The study highlights that more mammalian research is needed to fully define the health risks of plastic particle exposure.
Testicular mitochondrial redox imbalance and impaired oxidative phosphorylation underlie microplastic-induced testicular dysfunction in Wistar rats
Researchers investigated how polyethylene microplastics affect male reproductive function in rats by examining testicular mitochondrial health. The study found that microplastic exposure disrupted mitochondrial redox balance and impaired oxidative phosphorylation in testicular tissue, providing mechanistic evidence for how microplastics may contribute to male reproductive toxicity.
Adverse effects of pristine and aged polystyrene microplastics in mice and their Nrf2-mediated defense mechanisms with tissue specificity
Researchers exposed mice to pristine and UV-aged polystyrene microplastics via intratracheal instillation and found structural damage to the gut, liver, spleen, and testis. Aged microplastics caused greater functional damage than pristine particles, including increased liver enzymes and cholesterol, reduced antioxidant capacity, and tissue-specific activation of the Nrf2 defense pathway.
Preliminary study of polyethylene microplastics disrupting energy Metabolism, redox Balance, and prefrontal cortex structure in Wistar rats
Researchers examined the neurotoxic effects of polyethylene microplastics on the prefrontal cortex of rats over a 28-day oral exposure period. The study found that microplastic exposure disrupted energy metabolism, impaired mitochondrial redox balance, and triggered inflammatory responses in brain tissue, suggesting that microplastics may pose risks to neurological function.
Exposure to Polypropylene Microplastics Causes Cardiomyocyte Apoptosis Through Oxidative Stress and Activation of the MAPK‐Nrf2 Signaling Pathway
Researchers found that polypropylene microplastics caused heart muscle cell death in both mice and lab-grown cells by triggering oxidative stress and activating specific cell damage pathways. Mice exposed to higher concentrations showed visible heart tissue damage and inflammation. This study is one of the first to demonstrate that microplastic exposure can directly harm the heart, raising concerns about cardiovascular effects in people exposed to microplastics.
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.
Evaluation of the health impacts and deregulation of signaling pathways in humans induced by microplastics
This review evaluates how microplastics disrupt key signaling pathways inside human cells, leading to chronic inflammation, oxidative stress, hormone disruption, and abnormal cell death. Microplastics activate inflammatory pathways like NF-kB and MAPK while interfering with the body's protective stress responses. Understanding these cellular mechanisms is important because they help explain how long-term microplastic exposure could contribute to chronic diseases in humans.
Research Progress in Reproductive Toxicity of Micro- and Nanoplastics on Males and Its Mechanisms
This review summarized research on the reproductive toxicity of micro- and nanoplastics (MNPs) in males, finding that MNPs accumulate in reproductive organs and cause toxicity through oxidative stress, hormonal disruption, and DNA damage, with implications for both animal and human reproductive health.
Reproductive and metabolic toxic effects of polystyrene microplastics in adult female Wistar rats: a mechanistic study
Researchers gave female rats polystyrene microplastics orally for 45 days and found disruptions to both metabolic and reproductive hormone levels, including increased cholesterol, insulin resistance, and altered sex hormones. The microplastics also caused liver fibrosis and elevated inflammatory markers. The study suggests that chronic microplastic exposure may contribute to metabolic and endocrine disruption in mammals.
Consequences of nano and microplastic exposure in rodent models: the known and unknown
This review summarizes what rodent studies have revealed about the health effects of micro and nanoplastic exposure, including inflammation, oxidative stress, metabolic disruption, and reproductive harm. Researchers found that toxic effects depend heavily on particle size, polymer type, shape, and exposure route, making it difficult to draw broad conclusions. The study highlights major gaps in current knowledge and calls for more standardized research to better assess human health risks.