Polyethylene nanoplastics cause reproductive toxicity associated with activation of both estrogenic hormone receptor NHR-14 and DNA damage checkpoints in C. elegans

Abstract

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.