Long-term exposure to polystyrene nanoparticles causes transgenerational toxicity by affecting the function and expression of MEV-1 and DAF-2 signals in Caenorhabditis elegans

In this study, we determined the roles of oxidative stress and related signals in mediating transgenerational toxicity of 30 nm polystyrene nanoparticles (PS-NPs) in Caenorhabditis elegans. Using brood size and locomotion behavior as endpoints, exposure to 1-100 mu g/L PS-NPs caused transgenerational toxicity. Meanwhile, the activation of reactive oxygen species (ROS) was also observed transgenerationally after exposure to 1-100 mu g/L PS NPs. After exposure to 1 mu g/L PS-NPs, the transgenerational toxicity was monitored until F2 generation (F2-G) and recovered at F3-G. At the F1-G of 1 mu g/L PS-NPs-exposed nematodes, RNAi knockdown of daf-2 with function to inhibit oxidative stress suppressed the transgenerational toxicity and increased the mitochondrial SOD-3 expression. In contrast, at F3-G of 1 mu g/L PS-NPs-exposed nematodes, RNAi knockdown of mev-1 with function to induce oxidative stress promoted locomotion and brood size, and suppressed the SOD-3 expression. Moreover, we observed the dynamic expressions of mev-1, daf-2, and sod-2 transgenerationally after exposure to 1 mu g/L PS-NPs at P0-G, which further suggested the involvement of MEV-1, DAF-2, and SOD-3 in affecting induction of transgenerational PS-NP toxicity. Therefore, we provided the evidence to suggest the roles of oxidative stress activation and related molecular signals in mediating induction of transgenerational PS-NP toxicity. Our data highlights the crucial function of oxidative stress-related signals during induction of transgenerational PS NP toxicity.

Automated summary

This study investigates the roles of oxidative stress and related signals in mediating transgenerational toxicity of 30 nm polystyrene nanoparticles in Caenorhabditis elegans. The results show that exposure to polystyrene nanoparticles causes transgenerational toxicity and activation of oxidative stress. Knockdown experiments suggest the involvement of specific genes in the induction and recovery of transgenerational toxicity.