Salinity stress is one of the marked influencing factors on the ecophysiology of
aquaculture and is considered an important reason for the retreat of the fish
industry. The current study is an endeavor to elucidate the molecular mechanisms
that underlie the response to salinity stress in common carp. Fish (Average weight
5 ± 2 g)were randomly distributed into two groups; the 1st is a control was exposed
to tap water (0.2 ppt salinity) and the 2nd is a treated was exposed to hypersalinity
(10 ppt salinity) for five days. Serum biochemical indicators including total protein,
albumin, globulins, A/G ratio, blood glucose, cortisone,Na+, K+, andCl- levelswere
evaluated. Besides, Tumor necrosis factor-a, interleukin-1b, corticotropinreleasing
hormone, and catalase enzyme mRNA expression levels were assessed
in lymphoid and immunocompetent organs (liver and spleen) and osmoregulatory
organs (kidney and gills) by using Real-time qPCR. Hypersalinity adversely affected
the biochemical markers; total protein, albumin, and globulins decreased
significantly; however, blood glucose, serum cortisol, and sodium markedly
increased in fish exposed to hypersalinity compared with the control. In
addition, from the molecular point of view, all the evaluated genes were
upregulated at a high expression rate in the liver compared with other studied
organs after the salinity challenge. On the contrary, hypersalinity modulated the
expression of immune-related genes (Tumor necrosis factor-a and interleukin-1b) in the kidney and spleen and upregulated corticotropin-releasing hormone
mRNA in all studied organs except gills. In conclusion, the obtained data
clarified the molecular and biochemical mechanisms of salinity stress on the
liver, kidney, spleen, and gills. Furthermore, it strongly suggests the implication of
neural, endocrine, and immune systems in the responsive mechanisms to the
salinity stress in carp.