Nanoparticles like nano silica (E551) are commonly used as food additives although bio-interactions with the gut are not well understood. Nutrients, like oligopeptides, together with nano silica are taken up via the same route via the pharynx to the intestinal tract. At the apical domain of intestinal cells, oligopeptides are transferred by the OPT-2/PEP-2 transporter to the cytoplasm and degraded downstream by hydrolases to provide amino acids for protein biosynthesis. For analyses of the peptide transport, the fluorophore-conjugated dipeptide B-Ala-Lys (AMCA) was used which normally distributes diffusely throughout the cytoplasm. Exposure with nano silica lead to an altered morphology of the intestine and disturbed peptide trafficking. Dipeptides accumulated in spherical subdomains that grow over time to a diameter of ≥6 microm. The peptide subdomains did not colocalize with known organelles such as gut granules and formed independently of the insulin/IGF-1 receptor (DAF-2) signaling pathway. Mutation of the
daf-2 tyrosine kinase domain showed distinct patterns of peptide subdomains along the apical membrane of intestinal cells which indicated specific trafficking defects (Piechulek et al., 2019). We suggest that nano silica-induced peptide subdomains represent new compartments of dipeptide storage leading to the inhibition of hydrolysis and peptide metabolism which in turn results in a decline of translation. Aberrant segregation of dipeptides by phase separation leads to a petite phenotype resembling OPT-2/PEP-2 transporter deficient mutants. In addition, nano silica induce global amyloid protein aggregation that segregates components of the protein homeostasis to an insoluble aggregome. Candidate proteins include components of the translational machinery and ribosomal RNA processing (Scharf et al., 2016). Taken together, the results suggest that impairment of translation occurred by a lack of amino acid supply and amyloid segregation of proteins critically involved in protein synthesis. As translation was shown to be involved in the generation of both, premature aging and neurodegenerative diseases, further investigation of its role in the organ-cross talk between intestine and the neural system in xenobiotic-exposed C. elegans is required.