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Polyethylene terephthalate microplastics impair erectile function through macrophage mediated cGAS-STING ferroptosis
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Researchers investigated the impact of PET microplastic exposure on erectile function using human tissue samples, a rat model, and cell assays. The study found that patients with erectile dysfunction had higher microplastic burden in corpus cavernosum tissue, and that chronic PET microplastic exposure in rats triggered a specific inflammatory pathway involving macrophage ferroptosis that led to vascular dysfunction.
Microplastic pollution is a global concern, yet its impact on male reproductive health remains unclear. We assessed chronic polyethylene terephthalate (PET) microplastic exposure using human corpus cavernosum (CC) tissues, a rat model, and cell assays. MPs were quantified in CC from 10 patients; those with erectile dysfunction (ED) showed a higher MP burden, with PET predominant. In rats, chronic PET-MP exposure dose-dependently impaired erectile function, increased fibrosis, and reduced smooth muscle. Mechanistically, PET-MPs localized to macrophage mitochondria, causing depolarization and ROS generation, mtDNA leakage, cGAS-STING activation, and macrophage ferroptosis. This ferroptotic signaling amplified inflammation, promoted M1 polarization, and triggered endothelial-to-mesenchymal transition, leading to vascular dysfunction and ED. Depleting macrophages or inhibiting cGAS-STING or ferroptosis reduced inflammation and partially rescued erectile responses. Together, these data identify a cGAS-STING-ferroptosis axis linking environmental MP exposure to ED and suggest upstream innate-immune and ferroptosis pathways as therapeutic targets.
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Polystyrene nanoplastics exposure causes erectile dysfunction in rats
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Researchers exposed rats to polystyrene nanoplastics through oral ingestion for 28 days and found that the particles accumulated in penile tissue and impaired erectile function. The nanoplastics caused oxidative stress, inflammation, and damage to the smooth muscle and blood vessel lining in erectile tissue. The study suggests that nanoplastic exposure may represent a previously unrecognized risk factor for reproductive health issues.
From Prenatal Exposure to Adult Sexual Dysfunction: The Impact of Plastic-Derived Endocrine Disruptors on Testosterone Homeostasis and Erectile Function
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Everyday plastics — found in food packaging, containers, and countless consumer products — contain chemicals that can interfere with hormone signaling, and this review pulls together existing research suggesting they may lower testosterone and contribute to erectile dysfunction. The disruption seems to start as early as the womb, potentially affecting how the male reproductive system develops, and continues into adulthood by damaging blood vessels, promoting inflammation, and altering metabolism. While more research is needed to confirm direct cause-and-effect in humans, this is a good reminder to minimize plastic exposure where possible, especially around food and drink.
Internalized polystyrene nanoplastics trigger testicular damage and promote ferroptosis via CISD1 downregulation in mouse spermatocyte
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Researchers found that polystyrene nanoplastics cause testicular damage in mice through a cell death process called ferroptosis. The nanoplastics triggered the breakdown of iron-storage proteins and reduced levels of a protective mitochondrial protein called CISD1 in sperm cells. The study suggests that nanoplastic exposure may contribute to male reproductive harm by driving excess iron into mitochondria.
Testicular mitochondrial redox imbalance and impaired oxidative phosphorylation underlie microplastic-induced testicular dysfunction in Wistar rats
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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.
Polystyrene microplastics disrupt the blood-testis barrier via CEBPB-driven lysosomal autophagy and induce ferroptosis-like injury in human sperm, compromising embryo development
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Researchers found that polystyrene microplastics disrupt male fertility through two parallel mechanisms—triggering CEBPB-driven lysosomal degradation of tight junction proteins in Sertoli cells to breach the blood-testis barrier, and inducing mitochondrial damage and ferroptosis-like lipid peroxidation in sperm—with both effects reducing embryo development quality after ICSI, and N-acetylcysteine rescuing sperm function.
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