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61,005 resultsShowing papers similar to Expression of RSPH6A in the first wave of rat spermatogenesis and oxidative stress conditions: Attenuation by melatonin
ClearNew Insight on the In Vitro Effects of Melatonin in Preserving Human Sperm Quality
Researchers found that melatonin protects human sperm quality against cadmium-induced oxidative stress in vitro, preserving motility, viability, DNA integrity, and mitochondrial function while reducing lipid peroxidation over 24 hours of exposure.
Melatonin alleviates oxidative stress damage in mouse testes induced by bisphenol A
Researchers investigated whether melatonin could alleviate oxidative stress damage caused by bisphenol A (BPA) exposure in mouse testicular tissue. The study found that melatonin treatment reduced BPA-induced oxidative damage and improved sperm quality indicators, suggesting a potential protective role against the reproductive effects of this common plastic-associated chemical.
Transcriptome-wide m6A profiling reveals mRNA post-transcriptional modification of boar sperm during cryopreservation
Researchers mapped chemical modifications (m6A tags) on messenger RNA in boar sperm during freeze preservation for the first time, finding these epigenetic marks are linked to sperm motility and cell survival — offering new insight into why sperm quality declines during cryopreservation.
Feedback Regulation of sPLA2-COX/5-LOX-Ca2+ in Seminal Plasma and Its Impact on Sperm Quality Parameters
Researchers investigated feedback regulation of the sPLA2-COX/5-LOX-Ca2+ pathway in seminal plasma and its impact on sperm quality parameters. The study found that arachidonic acid metabolism in seminal plasma strongly influences sperm quality, with the PL-AA-COX1 model proposed as a sperm quality predictor and AA/COX1 supplementation shown to protect sperm under heat stress.
Editorial: Mammalian spermatogenesis: genetic and environmental factors
This editorial introduces a research collection on mammalian spermatogenesis, examining both genetic and non-genetic environmental factors that can disrupt the tightly regulated process from spermatogonial proliferation through spermatozoa maturation and lead to male infertility.
Oxidative Stress and Male Fertility: Promising Role of Nutraceuticals
This paper is not about microplastics; it reviews the role of oxidative stress in male infertility and the potential of nutraceuticals (antioxidant-rich dietary supplements) to improve sperm quality and hormonal profiles, with no connection to microplastic research.
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.
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.
Microplastics and male reproductive system: A comprehensive review based on cellular and molecular effects
This comprehensive review examines how microplastics affect the male reproductive system at cellular and molecular levels, drawing on studies from multiple scientific databases. Researchers found that microplastics can damage testicular structure and function, impair spermatogenesis, and disrupt sperm parameters through mechanisms including oxidative stress, inflammation, and activation of cell death pathways. The review highlights that microplastics reduce ATP production and trigger signaling cascades that may contribute to male fertility problems.
A short-term high-fat diet alters rat testicular activity and blood-testis barrier integrity through the SIRT1/NRF2/MAPKs signaling pathways
Researchers found that a short-term high-fat diet in rats caused changes in testicular function and disrupted the blood-testis barrier through specific cell signaling pathways. The study suggests that even moderate metabolic stress from overweight conditions can affect male reproductive health at the molecular level. The findings may help identify potential targets for preventing fertility issues related to metabolic disorders.
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.
Fetal exposure to endocrine disrupting-bisphenol A (BPA) alters testicular fatty acid metabolism in the adult offspring: relevance to sperm maturation and quality
This study showed that prenatal exposure to bisphenol A in rats altered testicular fatty acid metabolism in adult male offspring, reducing levels of polyunsaturated fatty acids essential for sperm quality and function, linking early BPA exposure to lasting male reproductive effects.
MORN2 regulates the morphology and energy metabolism of mitochondria and is required for male fertility in mice
Researchers identified a protein called MORN2 that plays a critical role in shaping mitochondria and supporting their energy production in sperm cells. When this protein was absent in mice, the animals became infertile due to defective mitochondrial structures in their sperm. The study adds to our understanding of the molecular requirements for male reproductive health.
Quantitative analysis and toxicological mechanisms of various male infertility inducers: A network meta-analysis and pharmacological approach.
This network meta-analysis of 201 rodent studies compared nine common male infertility inducers, finding that microplastics caused among the most severe impairments to sperm count and motility — on par with the chemotherapy drug cyclophosphamide. Oxidative stress emerged as a shared mechanistic pathway across all inducers, pointing to it as a key target for understanding and potentially mitigating reproductive harm from environmental exposures.
Rhamnetin alleviates polystyrene microplastics-induced testicular damage by restoring biochemical, steroidogenic, hormonal, apoptotic, inflammatory, spermatogenic and histological profile in male albino rats
Researchers studied whether the plant compound rhamnetin could protect against testicular damage caused by polystyrene microplastics in rats. Microplastic exposure caused significant harm to sperm quality, hormone levels, and testicular tissue through oxidative stress and inflammation. Co-treatment with rhamnetin restored many of these markers, suggesting it may help counteract some of the reproductive harm associated with microplastic exposure.
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.
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.
Microplastics from face mask impairs sperm motility
Researchers fed mice microplastics derived from face masks for 21 days and found that while overall body weight and sperm counts were unaffected, sperm motility was significantly impaired. Gene expression analysis revealed disruptions in pathways related to sperm development, oxidative stress, and inflammation in the testes. The findings suggest that microplastics shed from disposable face masks could pose risks to male reproductive health.
Oxidative Stress and Autophagy: Unraveling the Hidden Threat to Boars’ Fertility
This review examines how oxidative stress affects male livestock reproductive function by disrupting autophagy processes in the testes. The study suggests that oxidative stress-induced autophagy dysfunction can impair spermatogenesis, reduce sperm quality, compromise testosterone synthesis, and damage the blood-testis barrier, with implications for improving livestock breeding outcomes.
The mouse model of induced sperm DNA damage caused by polystyrene microplastics exhibited distinct transcriptomic and proteomic features
Researchers established a mouse model of polystyrene microplastic-induced sperm DNA damage by administering 1 mg/kg/day for 60 days, which significantly elevated the sperm DNA fragmentation index, and characterized the transcriptomic and proteomic profiles associated with this reproductive toxicity.
Melatonin attenuates polystyrene microplastics induced motor neurodevelopmental defect in zebrafish (Danio rerio) by activating nrf2 - isl2a Axis
Researchers found that melatonin protected zebrafish embryos from polystyrene microplastic-induced motor neuron developmental defects by activating the Nrf2-Isl2a signaling pathway, reducing oxidative stress and restoring normal motor neuron axon development.
Evaluation of possible attenuative role of chrysoeriol against polyethylene microplastics instigated testicular damage: A biochemical, spermatogenic and histological study
Researchers investigated whether the plant compound chrysoeriol could protect against testicular damage caused by polyethylene microplastics in a rat model. The study found that microplastic exposure reduced antioxidant enzyme activity and increased inflammation markers, while co-administration of chrysoeriol showed a protective effect by mitigating oxidative stress and preserving sperm quality.
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.
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.