Effects of cadmium exposure on metabolism, antioxidant defense, immune function, and the hepatopancreas transcriptome of Cipangopaludina cathayensis.

Cadmium (Cd) is a common contaminant in aquatic environments. However, little is known about the mechanisms underlying Cd toxicity in the freshwater snail Cipangopaludina cathayensis (Heude, 1890). This study to investigate the toxic effects of Cd on the standard metabolism, antioxidant activities, immune function, and hepatopancreas transcriptome profiles of C. cathayensis. C. cathayensis was exposed to 0.25, 0.5, 1.0, or 1.5 mg/L Cd for 3 h, with results showing that Cd significantly inhibited oxygen consumption and ammonia excretion and disrupted the respiratory metabolism of C. cathayensis. In addition, the O:N ratio dropped below 7, indicating that C. cathayensis may rely exclusively on proteins as an energy source under Cd stress. To understand how Cd impacts the antioxidant activities, immune function, and transcriptional profiles, C. cathayensis were exposed to 0.5 (low exposure, L14) or 1.5 (high exposure, H14) mg/L Cd for 14 days. Our results indicate that Cd exposure leads to oxidative stress and immunosuppression, with the latter effect being larger for exposure to higher Cd concentrations. A total of 2172 differentially expressed genes (DEGs) were identified by transcriptome analysis of the hepatopancreas, of which 885 were upregulated and 1287 were downregulated. Gene ontology and KEGG analyses revealed that the DEGs in the H14 group are enriched for energy generation terms and the "oxidative phosphorylation" pathway, respectively. Therefore, up-regulation of energy metabolism may be an adaptive strategy under Cd stress. Moreover, several genes involved in antioxidant activity were downregulated, whereas genes related to reactive oxygen species generation were upregulated. In addition, many immunity-related genes were identified within the DEGs, indicating that Cd toxicity may affect immune defense. Further, DEGs in the H14 group were enriched for disease-associated pathways. Taken together, our results indicate that Cd exposure leads to metabolic disorders, oxidative stress, and immunosuppression and thus may potentially contribute to disease outbreaks.