The molecular response of animals to nanoplastic particles is still largely unclear. In this study, we employed a modified prolonged exposure system to investigate the molecular response of Caenorhabditis elegans to nanopolystyrene particles. Exposure to nanopolystyrene particles (1 μg/L) significantly decreased expressions of daf-2 encoding an insulin receptor, age-1 encoding a PI3K, and akt-1 encoding an Akt/PKB, and increased expression of daf-16 encoding a FOXO transcriptional factor in insulin signaling pathway. Among these genes, mutation of daf-2, age-1, or akt-1 induced a resistance to toxicity of nanopolystyrene particles, whereas mutation of daf-16 induced a susceptibility to the toxicity of nanopolystyrene particles. RNAi knockdown of daf-16 could further suppress the resistance of daf-2, age-1, or akt-1 mutant to the toxicity of nanopolystyrene particles. The insulin signaling pathway acted in intestinal cells to regulate the toxicity of nanopolystyrene particles. Moreover, sod-3 encoding a manganese superoxide dismutase, mtl-1 encoding a metallothionein, and gpd-2 encoding a glyceraldehyde-3-phosphate dehydrogenase were identified as downstream targeted genes for daf-16 in the regulation of toxicity of nanopolystyrene particles. Therefore, a signaling cascade of DAF-2-AGE-1-AKT-1-DAF-16-SOD-3/MTL-1/GPD-2 was identified in response to nanopolystyrene particles in nematodes. Additionally, this signaling cascade in the insulin signaling pathway may mediate a protective response for nematodes against the adverse effects from nanopolystyrene particles.
Keywords: Nanopolystyrene; insulin signaling pathway; response.