We evaluated the individual and combined effects of salinity and alkalinity on gill Na⁺/K⁺-ATPase enzyme activity, plasma ion concentration, and osmotic pressure inLuciobarbus capito. Increasing salinity concentrations (5, 8, 11, and 14 g/L) were associated with an initial increase and then decrease inL. capitogill Na⁺/K⁺-ATPase activity. Activity was affected by the difference between internal and external Na⁺ion concentrations and osmotic pressure (P<0.05). Both plasma ion (Na⁺, K⁺, and Cl⁻) concentration and osmotic pressure increased significantly (P<0.05). An increase in alkalinity (15, 30, 45, and 60 mM) caused a significant increase in plasma K⁺and urea nitrogen concentrations (P<0.05) but had no effect on either plasma osmotic pressure or gill filament ATPase activity. In the two-factor experiment, the saline-alkaline interaction caused a significant increase in plasma ion (Na⁺, Cl⁻, and urea nitrogen) and osmotic pressure (P<0.05). Variance analysis revealed that salinity, alkalinity, and their interaction significantly affected osmotic pressure, with salinity being most affected, followed by alkalinity, and their interaction. Gill filament ATPase activity increased at first and then decreased; peak values were observed in the orthogonal experiment group at a salinity of 8 g/L and alkalinity of 30 mM.

Cadmium (Cd) poses a great threat to the breeding of aquatic economic animals. The present study aimed to explain the antagonistic effects of selenium-enriched Lactobacillus plantarum (SL) on Cd toxicity through the expression of oxidative and inflammatory factors. A total of 225 Bulatmai barbel Luciobarbus capito (L. capito) were divided into 3 groups, namely, the control group, the Cd group (Cd, 0.05 mg·L⁻¹), and the SL + Cd group (Cd, 0.05 mg·L⁻¹; Nano Se, 5 mg·kg⁻¹; L. plantarum, 10⁵ CFU·g⁻¹). The experiment lasted for 28 d, Sampling at 14 and 28 d, respectively. The results showed that Cd exposure caused obvious pathological damage to the liver and kidney, and the serum parameter ALT increased significantly (p < 0.05). In the Cd group, the concentration of Cd in the kidney was significantly increased (p < 0.05), and the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) in the kidney and gill were significantly decreased; malonaldehyde (MDA) increased significantly (p < 0.05) Then the mRNA expression levels in the kidney and liver were measured. Cd exposure significantly decreased the mRNA expressions of SOD, CAT, GSH-Px, HO-1, I-κBα, and Nrf2 (p < 0.05). The Cd-treated group showed significantly increased NF-kBp65, TGF-β, IL-8, IL-1, Keap1, and TNF-α expression levels. SL significantly alleviated the changes in the above indicators. The results of this study suggest that SL can trigger the Nrf2 signalling pathway and NF-kB signalling pathway to alleviate Cd toxicity. SL might be a potential drug for the treatment of Cd poisoning.