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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.
Our results indicate that PS-NPs cause mouse testicular damage through ferroptosis. Mechanistically, we confirmed that PS-NPs trigger NCOA4-mediated ferritinophagy and CISD1 downregulation in spermatocyte, which aggravates the flow of ferrous iron from the cytoplasm to the mitochondria.
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Nrf2-mediated ferroptosis of spermatogenic cells involved in male reproductive toxicity induced by polystyrene nanoplastics in mice
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When polystyrene nanoplastics were injected into the bloodstream of mice, they accumulated in the testes and caused significant damage to sperm-producing cells through a process called ferroptosis, a type of iron-dependent cell death. The nanoplastics disrupted a key protective pathway (Nrf2) that normally prevents this type of cell death. These findings suggest that nanoplastic exposure could harm male fertility by directly damaging the cells responsible for producing sperm.
Polystyrene nanoplastics disrupt iron homeostasis by promoting FPN1 ubiquitination in GC-2spd(ts) cells
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Researchers showed that polystyrene nanoplastics induce ferroptosis — an iron-dependent form of cell death — in mouse sperm precursor cells by promoting the ubiquitin-tagged degradation of the iron-export protein ferroportin1, causing iron to accumulate inside cells, driving lipid peroxidation and mitochondrial damage.
Disturbance of mitochondrial dynamics led to spermatogenesis disorder in mice exposed to polystyrene micro- and nanoplastics
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Polystyrene micro- and nanoplastics caused spermatogenesis disorders in mice by disrupting mitochondrial dynamics, triggering excessive mitochondrial fission that activated both apoptosis and pyroptosis pathways in testicular tissue. Nanoplastics caused mitochondrial DNA to leak into the cytoplasm, activating the cGAS-STING inflammatory pathway — a mechanism confirmed by rescue experiments with a mitochondrial fission inhibitor.
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.
Polystyrene microplastics induce male reproductive toxicity in mice by activating spermatogonium mitochondrial oxidative stress and apoptosis
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A mouse study found that polystyrene microplastics significantly reduced sperm count and motility while increasing sperm deformities. The damage was caused by oxidative stress in the energy-producing mitochondria of sperm-forming cells, which triggered cell death -- raising concerns about microplastics' potential impact on male fertility.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.