Abstract
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.
Highlights
Caenorhabditis elegans, a free-living and abundant soil nematodes, is well-characterized structurally and genetically[21,22]
The height image from atomic force microscopy (AFM) assay indicates that the thickness of the prepared graphene oxide (GO) was about 1.0 nm in topographic height (Fig. 1c)
After Lactic acid bacteria (LAB) pretreatment, the GO (100 mg/L) exposed wild-type nematodes showed the similar triglyceride content to that in control wild-type nematodes (Fig. 4b). These results suggest that LAB pretreatment may potentially block the formation of hyper-permeable intestinal barrier in GO exposed nematodes
Summary
Caenorhabditis elegans, a free-living and abundant soil nematodes, is well-characterized structurally and genetically[21,22]. Our previous study has indicated the crucial role of biological barrier of intestine to be against the possible toxicity from ENMs in nematodes[28]. Previous studies have further demonstrated that GO exposure could result in toxicity on the functions of both primary (such as intestine) and secondary (such as neuron and reproductive organs) targeted organs in nematodes[34,35,36]. The observed GO toxicity may be largely due to the combinational effects of oxidative stress, impaired intestinal barrier, and prolonged defecation cycle length in nematodes[37]. Our study will provide the insights on the establishment of pharmacological strategy in order to protect the intestinal barrier from the adverse effects of GO in organisms
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