We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polystyrene nanoplastics induced transgenerational reproductive toxicity in Caenorhabditis elegans through enhanced DNA damage accompanied by DNA repair inhibition
Summary
Researchers exposed roundworms (C. elegans) to polystyrene nanoplastics at environmentally relevant concentrations and found that reproductive harm persisted across multiple generations, even after exposure stopped. The nanoplastics caused DNA damage while simultaneously suppressing the organisms' DNA repair mechanisms, creating a compounding effect. The study suggests that nanoplastic exposure may have lasting consequences that are passed down through generations, amplifying harm beyond the originally exposed organisms.
Microplastics (MPs) are omnipresent environmental pollutants posing potential impacts on organisms. To explore the transgenerational effects of polystyrene nanoplastics (PS-NPs) and the molecular mechanisms at environmental relevant concentrations, Caenorhabditis elegans (C.elegans) was applied as an in vivo model. Worms were incubated with PS-NPs at environmental concentrations from L1 larvae stage, while subsequent generations (F1 -F3) were maintained under non-exposure condition. Reproductive potential was estimated based on brood size, fertilized eggs, oocytes, and germline apoptosis. Results indicated that PS-NPs induced transgenerational toxicity in inhibiting reproductive ability, impairing gonad development, and promoting germline apoptosis. And these adverse effects were associated with dysregulated expression of apoptosis-related genes. Furthermore, DNA damage was participated in enhancing germline apoptosis through activating DNA damage checkpoint kinase ATL-1 and p53 ortholog CEP-1. Additionally, PS-NPs reduced the expression of DNA recombination repair protein RAD-51 across generations. This study demonstrates that reproductive toxicity evoked by PS-NPs can be transmitted to offspring by inducing DNA damage through activating ATL-1 and CEP-1, while simultaneously inhibiting DNA repair.