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Long-term exposure to polystyrene nanoparticles at environmentally relevant concentration causes suppression in heme homeostasis signal associated with transgenerational toxicity induction in Caenorhabditis elegans
Summary
Researchers showed in C. elegans that nanopolystyrene exposure suppresses the hemoglobin-related gene glb-18 across generations, and that this disruption of heme homeostasis transgenerationally impairs an intestinal protective pathway (HRG-4/HRG-1/ATFS-1/HSP-6) — linking nanoplastic exposure to heritable toxicity through an epigenetic-like mechanism.
Heme homeostasis related signaling participates in inducing a protective response when controlling nanopolystyrene toxic effects in parental generation. However, whether the heme homeostasis signal is involved in regulation of transgenerational toxicity of nanopolystyrene toxicity is still unclear. Herein, with the model organism of Caenorhabditis elegans, 0.1-10 μg/L nanopolystyrene particles (PS-NPs) at 20-nm treatment downregulated glb-18, and the decrease was also discovered in the offspring following PS-NPs exposure. Germline glb-18 RNAi induced susceptive property to transgenerational PS-NPs toxicity, suggesting that a decreased GLB-18 level mediated induction of transgenerational toxicity. Importantly, germline GLB-18 transgenerationally activated the function of intestinal HRG-4 in controlling transgenerational PS-NPs toxicity. In transgenerational toxicity control, HRG-1/ATFS-1/HSP-6 was recognized to be the downstream pathway of HRG-4. Briefly, germline GLB-18 in P0 generation can transgenerationally activate the downstream intestinal HRG-4/HRG-1/ATFS-1/HSP-6 pathway among offspring for controlling the transgenerational toxicity of PS-NPs. Findings in the present work strengthens the possible association of heme homeostasis signal changes with transgenerational nanoplastic toxicity within the organisms.