The widespread use of silver nanoparticles (AgNPs) has raised public concern due to their potential toxic effects on humans and the environment. Although some studies have evaluated the toxicity of nanomaterials in vertebrates, studies on their hazardous effects on insects are limited. Here we focused on different concentrations of AgNPs to silkworms, a promising model organism, to evaluate their toxic effects by omics analysis. After the silkworms were fed with 100 mg L-1 AgNPs, transcriptomics analysis showed differential expression of 43 genes: 39 upregulated and 4 downregulated. These differentially expressed genes (DEGs) were involved in the digestion process, various metabolic pathways, transmembrane transport and energy synthesis. Proteomic results for silkworms fed with 400 mg L-1 AgNPs revealed 14 significantly differentially expressed proteins: 11 downregulated and 3 upregulated. Reverse transcription-polymerase chain reaction (RT-PCR) results showed that the expression levels of eight proteins were similar to the transcription levels of their corresponding genes. As the AgNPs concentration was increased, the expression of digestive enzymes was downregulated, which damaged the silkworm tissue and suppressed the activity of the enzyme superoxide dismutase and the protein HSP 1, causing oxidative stress and the production of reactive oxygen species, which had toxic effects on the silkworm digestive system. Histopathological results showed that treatment with 400 mg L-1 AgNPs destroyed the basal lamina and the columnar cells, caused adverse effects on tissues and had the potential to induce harmful effects on the digestive system. The data presented herein provide valuable information on the hazards and risks of nanoparticle contamination. Main finding: AgNPs would downregulate some digestive enzymes, damage the tissue of midgut in silkworm, meantime induce the accumulation of reactive oxygen species which may cause oxidative stress.
Keywords: Proteome; Silkworm; Silver nanoparticles; Toxicity; Transcriptome.
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