We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polylactic acid nanoplastics induced pyroptosis in mice testes by activating TRPM2 through mitochondrial damage
AI summary Read the abstract
Mice given polylactic acid (biodegradable plastic) nanoparticles daily for four weeks showed testes damage, reduced sperm production and lower hormone levels. The nanoparticles triggered oxidative stress, damaged cell structures called mitochondria, disrupted calcium levels, and caused a form of inflammatory cell death in testicular cells, contributing to reproductive harm in the mice.
Polylactic acid (PLA) is currently one of the most widely used bio-based plastics, posing exposure risks to humans through various environmental pathways. Therefore, this study evaluated the effects of PLA nanoparticles (NPs) on the testes and the potential mechanisms involved. C57BL/6 J mice were administered PLA NPs (0.1, 1, and 10 mg/kg/day) for 4 weeks. Additionally, supplementary validation was conducted using transient receptor potential cation channel subfamily m member 2 (TRPM2) knockout models and MitoTEMPO-treated models. PLA NPs induced marked histological damage to the testes, resulting in impaired spermatogenesis and suppressed hormone synthesis. PLA NPs elevated reactive oxygen species levels, exacerbated oxidative stress, and mediated mitochondrial damage. Furthermore, PLA NPs activated TRPM2 and induced calcium ion dysregulation, leading to a significant increase in intracellular calcium levels. The study further revealed that PLA NPs markedly elevated serum IL-1β levels and activated the inflammasome pathway, thereby inducing pyroptosis in mouse testicular cells and resulting in reproductive toxicity. Collectively, these findings indicated that PLA NPs activate the TRPM2 pathway through oxidative stress-induced mitochondrial damage, subsequently inducing calcium dysregulation and causing pyroptosis in mouse testes. Our research provides new insights and evidence for the reproductive toxicity assessment of PLA NPs.
More Papers Like This
Polylactic Acid Micro/Nanoplastic Exposure Induces Male Reproductive Toxicity by Disrupting Spermatogenesis and Mitochondrial Dysfunction in Mice
AI summary Read the abstract
Even so-called "eco-friendly" biodegradable plastic (polylactic acid, or PLA) was found to cause reproductive harm in male mice. After breaking down in the digestive system, tiny PLA nanoparticles crossed into the testes and damaged sperm quality, mitochondria (the energy producers in cells), and hormone levels. This challenges the assumption that biodegradable plastics are safe and highlights potential risks to male fertility.
Disturbance of mitochondrial dynamics led to spermatogenesis disorder in mice exposed to polystyrene micro- and nanoplastics
AI summary Read the abstract
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.
Nrf2-mediated ferroptosis of spermatogenic cells involved in male reproductive toxicity induced by polystyrene nanoplastics in mice
AI summary Read the abstract
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.
A meta-analysis-based adverse outcome pathway for the male reproductive toxicity induced by microplastics and nanoplastics in mammals
AI summary Read the abstract
This meta-analysis of 39 studies mapped the adverse outcome pathway for microplastic and nanoplastic-induced male reproductive toxicity in mammals. Increased reactive oxygen species triggers a cascade of cellular damage including mitochondrial dysfunction, sperm DNA damage, and disrupted hormone signaling, ultimately leading to reduced sperm quality, impaired spermatogenesis, and decreased testosterone levels.
Novel insights into male reproductive toxicity: autophagy-dependent ferroptosis triggered by polylactic acid nanoplastics and copper sulfate
AI summary Read the abstract
Researchers exposed mice to polylactic acid nanoplastics combined with copper sulfate and found that the combination caused significant testicular damage through a process linking autophagy to ferroptosis, a form of iron-dependent cell death. The combined exposure was more damaging than either substance alone, disrupting sperm production and testicular tissue structure. The study suggests that nanoplastics from biodegradable plastics may amplify the reproductive toxicity of environmental heavy metals.
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.