We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
The crosstalk between M1 macrophage polarization and energy metabolism disorder contributes to polystyrene nanoplastics-triggered testicular inflammation
Summary
Researchers investigated how polystyrene nanoplastics cause testicular inflammation in mice by studying the interplay between immune cell behavior and energy metabolism. They found that nanoplastics triggered a pro-inflammatory immune response involving M1 macrophage activation, disrupted cellular energy processes, and caused testicular tissue damage. The study reveals a specific biological mechanism by which nanoplastic exposure may impair male reproductive health.
Ubiquitous microplastics have become a threat to animal and human health, due to their potential toxicity, persistent nature and consequent bioaccumulation. Supporting evidence elucidates that polystyrene nanoplastics (PS-NPs) can destroy blood-testis barrier integrity, thus causing testicular hypoplasia and impairment of spermatogenesis. Nevertheless, how PS-NPs modulate macrophage polarization-energy metabolism crosstalk has not been fully investigated in testicular tissue. Here, we observed that polystyrene PS-NPs exposure contributes to severe vacuolization in the seminiferous tubules, accompanied by apoptosis of testicular tissue and infiltration of M1 macrophages. Meanwhile, we found that PS-NPs could trigger the M1 polarization phenotype, which activated ROS-macrophage migration inhibitory factor (MIF)/NF-κB signaling that in turn induced apoptosis of GC2 cells in the GC2-macrophage cell coculture model. Simultaneously, we confirmed that PS-NPs exposure increased 3-phospho-D-glycerate, phosphoenolpyruvate and lactate concentrations, accompanied by decreased pyruvate and adenosine triphosphate (ATP) production, likely due to downregulated pyruvate kinase M2 (PKM2) dimer expression. In conclusion, the mechanism of PS-NPs-induced testicular inflammation can be mediated by promoting the infiltration of M1 macrophages, thereby resulting in an ROS burst and subsequent induction of energy metabolism disorders. The current study will provide new insights into PS-NPs-induced male reproductive toxicity and highlight the context-specific roles of testicular macrophages.
Sign in to start a discussion.
More Papers Like This
Polystyrene nanoplastics aggravate reproductive system damage in obese male mice by perturbation of the testis redox homeostasis
Researchers found that polystyrene nanoplastics worsened reproductive damage in male mice already fed a high-fat diet, reducing sperm quality and testosterone production beyond what obesity alone caused. The nanoplastics disrupted the protective blood-testis barrier and increased oxidative stress in reproductive tissues. The study suggests that nanoplastic exposure combined with obesity may create compounding risks to male fertility.
Disturbance of mitochondrial dynamics led to spermatogenesis disorder in mice exposed to polystyrene micro- and nanoplastics
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 induced spermatogenesis disorder via disrupting mitochondrial function through the regulation of the Sirt1-Pgc1α signaling pathway in male mice
Researchers investigated how polystyrene microplastics of different sizes affect sperm development in male mice and found that exposure decreased sperm motility and caused structural abnormalities. The microplastics disrupted mitochondrial function in reproductive cells by interfering with a key energy regulation pathway. The study provides evidence that microplastic exposure may contribute to male reproductive health problems through mitochondrial damage.
Integrated fecal microbiome and metabolome analysis explore the link between polystyrene nanoplastics exposure and male reproductive toxicity in mice
Researchers exposed mice to polystyrene nanoplastics of different sizes and doses, then analyzed fecal microbiome and metabolome changes alongside reproductive outcomes. The study found that nanoplastic exposure disrupted gut microbiota balance and metabolic pathways, which correlated with reduced sperm count, viability, and testosterone levels. The findings suggest that gut microbiota-metabolite disruption may play an important role in nanoplastic-induced male reproductive toxicity.
Polystyrene microplastics induced male reproductive toxicity in mice
Researchers exposed male mice to polystyrene microplastics of different sizes and found that the particles accumulated in testicular tissue and entered reproductive cells. After 28 days of exposure, sperm quality and testosterone levels declined, and tissue examination revealed disorganized sperm-producing cells and inflammation. The study suggests that microplastic exposure may pose risks to male reproductive health in mammals.