We employed an in vivo Caenorhabditis elegans assay system to perform SOLiD sequencing analysis to identify the possible microRNA (miRNA) targets of multi-walled carbon nanotubes (MWCNTs). Bioinformatics analysis on targeted genes for the identified dysregulated miRNAs in MWCNT exposed nematodes demonstrates their involvement in many aspects of biological processes. We used loss-of-function mutants for the identified dysregulated miRNAs to perform toxicity assessment by evaluating functions of primary and secondary targeted organs, and found the miRNA mutants with susceptible or resistant property towards MWCNT toxicity. Both the physiological state of the intestine and defecation behavior were involved in the control of the susceptible or resistant property occurrence for specific miRNA mutants towards MWCNT toxicity. This work provides the molecular basis at the miRNA level for future chemical design to reduce the nanotoxicity of MWCNTs and further elucidation of the related toxicological mechanism.
Lactic acid bacteria (LAB) is safe and useful for food and feed fermentation. We employed Caenorhabditis elegans to investigate the possible beneficial effect of LAB (Lactobacillus bulgaricus) pretreatment against toxicity of graphene oxide (GO) and the underlying mechanisms. LAB prevented GO toxicity on the functions of both primary and secondary targeted organs in wild-type nematodes. LAB blocked translocation of GO into secondary targeted organs through intestinal barrier by maintaining normal intestinal permeability in wild-type nematodes. Moreover, LAB prevented GO damage on the functions of both primary and secondary targeted organs in exposed nematodes with mutations of susceptible genes (sod-2, sod-3, gas-1, and aak-2) to GO toxicity by sustaining normal intestinal permeability. LAB also sustained the normal defecation behavior in both wild-type nematodes and nematodes with mutations of susceptible genes. Therefore, the beneficial role of LAB against GO toxicity under different genetic backgrounds may be due to the combinational effects on intestinal permeability and defecation behavior. Moreover, the beneficial effects of LAB against GO toxicity was dependent on the function of ACS-22, homologous to mammalian FATP4 to mammalian FATP4. Our study provides highlight on establishment of pharmacological strategy to protect intestinal barrier from toxicity of GO.
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