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Induction of transgenerational toxicity is associated with the activated germline insulin signals in nematodes exposed to nanoplastic at predicted environmental concentrations
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Researchers found that exposure to polystyrene nanoparticles at environmentally relevant concentrations activated insulin signaling pathways in the nematode C. elegans, and these effects were transmitted to offspring. The study suggests that activation of specific insulin ligands in the germline mediates the transgenerational toxicity of nanoplastics, meaning parental exposure can affect subsequent generations.
Exposure to nanoplastics can induce toxicity on organisms at both parental generation (P0-G) and the offspring. However, the underlying mechanism remains unknown. Using Caenorhabditis elegans as a model organism, exposure to 20-nm polystyrene nanoparticle (PS-NP) (1-100 μg/L) upregulated the expressions of insulin ligands (INS-39, INS-3, and DAF-28), and this increase could be further detected in the offspring after PS-NP exposure. Germline ins-39, ins-3, and daf-28 RNAi induced resistance to transgenerational toxicity of PS-NP, indicating that increase in expression of these three insulin ligands mediated induction of transgenerational toxicity. These three insulin ligands transgenerationally activated function of insulin receptor DAF-2 to control transgenerational toxicity of PS-NP. Exposure to 1-100 μg/L PS-NP further upregulated DAF-2, AGE-1, and AKT-1 expressions and downregulated DAF-16 expression. During transgenerational toxicity control, DAF-16/AKT-1/AGE-1 was identified as downstream signaling cascade of DAF-2. Moreover, transcriptional factor DAF-16 activated two downstream targets of HSP-6 (a mitochondrial UPR marker) and SOD-3 (a mitochondrial SOD) to modulate transgenerational toxicity of PS-NP. Our findings indicate a crucial link between activation of insulin signaling and induction of transgenerational toxicity of nanoplastics at low concentrations in organisms.
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Activation of FGF signal in germline mediates transgenerational toxicity of polystyrene nanoparticles at predicted environmental concentrations in Caenorhabditis elegans
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Using the roundworm C. elegans as a model, researchers investigated how nanoplastic exposure causes toxic effects that persist across generations. They found that polystyrene nanoparticles activate a specific growth factor signaling pathway in reproductive cells, which then transmits harmful effects to offspring. The study provides molecular evidence for how even low, environmentally relevant concentrations of nanoplastics can cause damage that carries over to future generations.
Transgenerational Response of Germline Nuclear Hormone Receptor Genes to Nanoplastics at Predicted Environmental Doses in Caenorhabditis elegans
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Exposure to very low doses of polystyrene nanoplastics in roundworms caused reproductive and developmental problems that persisted across multiple generations through changes in nuclear hormone receptor genes. These receptors control important signaling pathways, and their disruption altered the expression of insulin and other growth signals in offspring that were never directly exposed to nanoplastics. This demonstrates that nanoplastic effects can be inherited through epigenetic mechanisms even at doses found in the environment.
Nanoplastics cause transgenerational toxicity through inhibiting germline microRNA mir-38 in C. elegans
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Researchers used the model organism C. elegans to investigate how nanoplastic exposure causes transgenerational toxicity through effects on germline microRNA. The study found that polystyrene nanoparticles decreased expression of germline miRNA mir-38, and that overexpressing this miRNA conferred resistance to transgenerational toxicity. The findings suggest that nanoplastics can cause heritable toxic effects across generations by disrupting germline gene regulation.
Alteration in Wnt signaling mediates induction of transgenerational toxicity of polystyrene nanoplastics in C. elegans
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Researchers used C. elegans to show that polystyrene nanoplastics disrupt germline Wnt signaling — a cell communication pathway — causing toxicity that persists into the next generation, with the LIN-44/MIG-1 ligand-receptor pair and downstream BAR-1/beta-catenin cascade mediating whether offspring are protected or sensitized to nanoplastic damage.
Nanoplastic at environmentally relevant concentrations activates a germline mir-240-rab-5 signaling cascade to affect the secreted ligands associated with transgenerational toxicity induction in C. elegans
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Researchers found that nanoplastics at levels commonly found in the environment activated a specific genetic signaling pathway in roundworms that caused toxic effects passed down across multiple generations. The nanoplastics triggered changes in gene regulation that affected offspring who were never directly exposed to the plastic particles. This is particularly alarming because it suggests that nanoplastic exposure could have health consequences not just for the individual exposed but for their children and grandchildren through inherited genetic changes.
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