DIKUL - logo
E-resources
Full text
Peer reviewed
  • Integration of transcriptom...
    Xiang, Qian-Qian; Yan, Hui; Luo, Xin-Wen; Kang, Yu-Hang; Hu, Jin-Ming; Chen, Li-Qiang

    Aquatic toxicology, August 2021, 2021-08-00, 20210801, Volume: 237
    Journal Article

    •Transcriptome and metabolome levels of fish gill were triggered by AgNPs after a 24 h exposure.•Most of DEGs and DMs induced by AgNPs can return to control levels after a 7-day recovery.•Morphological changes in gills are reversible after removing the toxicant.•The TCA cycle was one of the key pathways of AgNPs toxicity in the gills.•Released Ag+ was less toxic than silver nanoparticles. Toxic effects of silver nanoparticles (AgNPs) on fish gills have been widely reported but the recoverability of AgNPs-induced fish gill injuries is still unknown. In this study, combined multiomics and conventional toxicological analytical methods were used to investigate the changes in the gills of common carp responses to AgNPs (0.1 mg/L) toxicity after 24 h exposure and 7-day recovery. Conventional toxicological results showed that AgNPs exposure significantly increased silver content in gills and caused epithelial hyperplasia and lamellar fusion. After the recovery period, the silver content in fish gills significantly decreased; accompanied by the disappearance of histopathological characteristics in fish gills. Multiomics results revealed that AgNPs exposure resulted in the differential expression of 687 genes and 96 metabolites in fish gills. These differentially expressed genes (DEGs) and metabolites mainly participate in amino acid, carbohydrate, and lipid metabolisms, and are significantly enriched in the tricarboxylic acid (TCA) cycle. After the recovery period, the number of DEGs and metabolites in gills decreased to 33 and 90, respectively. Moreover, DEGs and metabolites in the TCA cycle recovered to control levels. In summary, the present study found that AgNPs-induced fish gill toxicity showed potential recoverability at molecular and phenotype levels.