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Polyethylene nanoplastics cause reproductive toxicity associated with activation of both estrogenic hormone receptor NHR-14 and DNA damage checkpoints in C. elegans
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Researchers found that polyethylene nanoplastics caused reproductive damage in the roundworm C. elegans by activating a hormone receptor and DNA damage pathways, leading to fewer offspring and increased cell death in reproductive tissues. Importantly, the damage was caused by the plastic particles themselves, not by chemicals leaching from them. Since polyethylene is the most common plastic in everyday products, these findings raise concerns about how nanoplastic exposure could affect reproductive health.
As the most commercial polymer, the polyethylene nanoparticle (PE-NP) has been discharged into the environment and poses potential risks to organisms. However, the possible reproductive toxicity of PE-NP and underlying mechanisms remain largely unknown. In this study, Caenorhabditis elegans was employed as the animal model to effects of PE-NP (100 nm) and their leachates on reproduction and underlying mechanisms. Nematodes were exposed to PE-NP at 0.1-100 μg/L from L1-larvae to adult day 1 (approximately 4.5 days). Both brood size and number of fertilized eggs in uterus were decreased by 10 and 100 μg/L PE-NP, but could not be affected by their leachates. In addition, number of mitotic cells, length, and area of gonad were reduced by 10 and 100 μg/L PE-NP, but were not altered by their leachates. Accompanied with alteration in expressions of genes (egl-1, ced-9, ced-4, and ced-3) governing cell apoptosis, germline apoptosis was enhanced by PE-NP. Meanwhile, DNA damage was involved in the enhancement germline apoptosis after PE-NP exposure. PE-NP further increased expression of nhr-14 encoding estrogenic hormone receptor, and RNAi of nhr-14 suppressed PE-NP reproductive toxicity. Moreover, RNAi of nhr-14 decreased expression of egl-1, ced-4, ced-3, and mrt-2 in PE-NP exposed nematodes. Therefore, exposure to PE-NPs rather than in their leachates potentially caused reproductive toxicity by activating both estrogenic hormone receptor NHR-14 and DNA damage checkpoints (CLK-2, HUS-1, and MRT-2) in nematodes. These findings provide important insights into the exposure risk of PE-NPs on reproduction of environmental organisms.
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