We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polystyrene microplastics disrupt the blood-testis barrier via CEBPB-driven lysosomal autophagy and induce ferroptosis-like injury in human sperm, compromising embryo development
AI summary Read the abstract
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.
Environmental exposure to microplastics, especially polystyrene microplastics (PS-MPs), poses growing concerns for male reproductive health. In this study, we demonstrate that PS-MPs internalize into Sertoli cells, triggering CEBPB-mediated lysosomal hyperactivation and the degradation of tight junction proteins, thereby impairing the structural integrity of the blood-testis barrier (BTB). Concurrently, PS-MPs accumulate in mature human sperm, damaging mitochondrial ultrastructure and inducing ROS-driven lipid peroxidation and ferroptosis-like injury. These alterations result in reductions in motility, DNA integrity, and early embryonic development following intracytoplasmic sperm injection (ICSI). Crucially, the antioxidant N-acetylcysteine (NAC) rescued sperm functional metrics and restored embryo quality. These findings reveal dual cellular pathways, disruption of both the barrier and sperm mitochondrial integrity, by which environmental PS-MPs impair male fertility. The study highlights NAC as a promising intervention and identifies chloroquine as a potent modulator of lysosome-mediated BTB disruption. The environmental relevance of PS-MPs and their mechanistic impact on human reproductive health underscore the urgent need for strategies to reduce pre-fertilization microplastic exposure.
More Papers Like This
Internalized polystyrene nanoplastics trigger testicular damage and promote ferroptosis via CISD1 downregulation in mouse spermatocyte
AI summary Read the abstract
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.
Polyethylene microplastics disrupt focal adhesion kinase (FAK) signaling and sertoli cell metabolism, compromising blood-testis barrier function and spermatogenesis
AI summary Read the abstract
Researchers exposed rats to polyethylene microplastics orally for 56 days and found dose-dependent damage to the blood-testis barrier, a structure critical for protecting developing sperm. The microplastics disrupted key signaling pathways in Sertoli cells, which support sperm development, leading to reduced sperm quality and altered testicular metabolism. The study suggests that polyethylene microplastic exposure may compromise male reproductive function by destabilizing the protective environment around developing sperm cells.
Micro- and nanoplastics in human male reproduction: Immune disruption, blood–testis barrier, and clinic-ready biomarkers
AI summary Read the abstract
This review synthesizes evidence that micro- and nanoplastics have been detected in human testes and semen, with experimental models showing they trigger oxidative stress, NLRP3 inflammasome activation, and disruption of blood-testis barrier tight-junction proteins, collectively impairing sperm production and quality.
Adverse effects and potential mechanisms of polystyrene microplastics (PS-MPs) on the blood-testis barrier
AI summary Read the abstract
This review examines how polystyrene microplastics damage the blood-testis barrier, a critical structure that protects developing sperm cells from harmful substances. Microplastics can break down this barrier through oxidative stress, inflammation, and disruption of gut bacteria, allowing pollutants and immune cells to enter the reproductive system. These findings suggest that microplastic exposure may contribute to declining male fertility, a trend observed globally in recent decades.
Polystyrene microplastics induce male reproductive toxicity in mice by activating spermatogonium mitochondrial oxidative stress and apoptosis
AI summary Read the abstract
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.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.