Effects of short-term salt exposure on gill damage, serum components and gene expression patterns in juvenile Largemouth bass (Micropterus salmoides)

Abstract

The Largemouth bass (Micropterus salmoides; LMB) is a freshwater fish that plays a significant role in aquaculture, and its cultural base is expanding into inland saline water areas. To study the effect of short-term salt exposure on LMB, fish with an average body weight of 11.69 (±1.82) g were cultured for 14 days at three different salt concentrations (0 ‰, 6 ‰, and 12 ‰). After 14 days, the second gill arch was collected for tissue sectioning and transcriptome sequencing, while serum samples were collected to analyze serum components. The results showed that the mortality rate in the 0 ‰ and 6 ‰ groups was 0 %, whereas the mortality rate in the 12 ‰ group was 62 %. In the gill tissue sections, no apparent damage was observed in the 0 ‰ and 6 ‰ groups. However, in the 12 ‰ group, the secondary lamellae became shorter, thicker, and exhibited a disordered arrangement. The serum component test results showed that osmolality and K+ significantly increased in the 12 ‰ group, while Na+, K+, and Cl− concentrations showed slight increases, but the differences were not significant. Comparative transcriptome analysis revealed that, along the salinity gradient, gene expression exhibited five profiles. Genes related to ion transport and immunity were highly expressed in the 6 ‰ and 12 ‰ groups, while genes associated with biosynthesis and ATP production showed decreased expression levels as salinity increased. Notably, seven solute carrier genes, two Na+/K+-ATPase genes, and two insulin-like growth factor genes were significantly highly expressed in the 12 ‰ salinity group, playing important roles in the transmembrane transport of ions. Based on the results, the LMB can acclimatize to a salt concentration of at least 6 ‰. However, exposure to 12 ‰ salinity can lead to a series of adverse effects, including organ damage, reduced energy metabolism efficiency, and disruption of ion homeostasis.