Effects of chloride, sulfate, and bicarbonate stress on mortality rate, gill tissue morphology, and gene expression in mandarin fish (Siniperca chuatsi)

The mandarin fish Siniperca chuatsi is a freshwater fish that is endemic to East Asia. To study the different damages and molecular mechanisms caused by different salt (NaCl, Na2SO4, and NaHCO3) on Siniperca chuatsi, the fish were subjected to NaCl, Na2SO4, and NaHCO3 stresses with different concentration for 96 h for mortality assessment, moreover, the fish were exposed to these salt stresses with equal sodium ion concentration (Na+ = 210 mmol/L), then gill morphological changes were observed and gene expression was analyzed by high-throughput transcriptome sequencing and real-time quantitative PCR (qRT-PCR). The results showed that mandarin fish tolerated NaCl and Na2SO4 better than NaHCO3. NaHCO3 stress caused more damage to gill than NaCl and Na2SO4 stress. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses indicated that differentially expressed genes were enriched in damage and apoptosis upon NaHCO3 stress, whereas they were enriched in energy and immune-related pathways upon NaCl and Na2SO4 stress. Hub genes were different under all three stresses. MAPK pathway genes showed a trend in up-regulated expression under all salt stresses, but the expression patterns varied with time during salt exposure and freshwater recovery stage. Taken together, this study demonstrated the variation in the effects of NaCl, Na2SO4, and NaHCO3 stress on mandarin fish. The MAPK signaling pathway is important for regulating the response to salt stress.

Automated summary

This study investigated the effects of different salt stresses (NaCl, Na2SO4, and NaHCO3) on mandarin fish and found that mandarin fish tolerated NaCl and Na2SO4 better than NaHCO3. Gill morphological changes and gene expression analysis revealed that different pathways were enriched under different salt stresses, with the MAPK signaling pathway playing a key role in regulating the response to salt stress.