A 100‐day growth trial was executed to determine the dietary selenium (Se) requirement of juvenile gibel carp (Carassius auratus gibelio). Selenomethionine was supplemented to casein‐gelatin diets at 0, 0.1, 0.25, 0.5, 1.0, 2.5 and 5 mg Se kg⁻¹, respectively. Each of these seven semi‐purified diets containing 0.34, 0.47, 0.66, 0.82, 1.23, 2.77 and 5.13 mg Se kg⁻¹ was fed to triplicate groups of gibel carp (2.74 ± 0.02 g) in a flow‐through system. No behaviour abnormalities and no mortality were found in fish exposed to dietary Se concentrations. With the increasing dietary Se supplemented concentrations, weight gain of fish remarkably increased at the levels of ≤1 mg Se kg⁻¹ diet and then showed no significant difference above 1 mg Se kg⁻¹ levels. Although growth performances (weight gain, hepatosomatic index, condition factor and survival) were not impaired in gibel carp fed at above the levels of 2.5 mg Se kg⁻¹, indicators of oxidative stress were changed significantly. Serum superoxide dismutase (SOD) activities significantly declined, hepatic glutathione peroxidase (GPx) activities significantly increased and the tissue Se concentrations significantly raised at the highest supplemented level of 5 mg Se kg⁻¹. A clear linear relationship between Se‐depended GPx activities and hepatic Se concentrations was observed. The present results indicated that the dietary Se requirement for gibel carp is 1.18 mg Se kg⁻¹ diet based on weight gain, GPx activities and tissue accumulation.

Se is an essential micronutrient required for normal growth, development and antioxidant defence. The objective of the present study was to assess the impact of dietary Se sources and levels on the antioxidant status of rainbow trout (Oncorhynchus mykiss) fry. First-feeding fry (initial body weight: 91 mg) were fed either a plant- or fishmeal-based diet containing 0·5 or 1·2 mg Se/kg diet supplemented or not with 0·3 mg Se/kg diet supplied as Se-enriched yeast or sodium selenite for 12 weeks at 17°C. Growth and survival of rainbow trout fry were not significantly affected by dietary Se sources and levels. Whole-body Se was raised by both Se sources and to a greater extent by Se-yeast. The reduced:oxidised glutathione ratio was raised by Se-yeast, whereas other lipid peroxidation markers were not affected by dietary Se. Whole-body Se-dependent glutathione peroxidase (GPX) activity was enhanced in fish fed Se-yeast compared to fish fed sodium selenite or non-supplemented diets. Activity and gene expression of this enzyme as well as gene expression of selenoprotein P (SelP) were reduced in fish fed the non-supplemented plant-based diet. Catalase, glutamate–cysteine ligase and nuclear factor-erythroid 2-related factor 2 (Nrf2) gene expressions were reduced by Se-yeast. These results suggest the necessity to supplement plant-based diets with Se for rainbow trout fry, and highlight the superiority of organic form of Se to fulfil the dietary Se requirement and sustain the antioxidant status of fish. GPX and SelP expression proved to be good markers of Se status in fish.

Previous studies have found that vitamin C (VC) has protective effects in fish. However, the efficacy of VC on hypoxia-induced liver injury in fish remains unknown. Therefore, to investigate the protective mechanism of VC on liver injury after acute hypoxic stimulation in fish, gibel carp were fed a diet containing VC for eight weeks, then were subjected to acute hypoxia stimulation. The specific growth rate of fish was increased by the supplementation of VC. Plasma stress markers (glucose, lactic acid, and cortisol) were decreased by the VC supplementation. Moreover, the levels of the inflammatory cytokines (tnf-α, il-2, il-6, and il-12) were increased by enhancing the Nrf2/Keap1 signaling pathway. Upregulation of the antioxidant enzymes activity (CAT, SOD, and GPx); T-AOC; and anti-inflammatory factors (il-4 and tgf-β) highlighted the antioxidant and anti-inflammatory activities of VC. The results showed that VC reduced the apoptotic index of the fish hypothalamus. The expression of GRP78 protein in the liver and endoplasmic reticulum stress and apoptosis induced by hypoxia were inhibited by VC. Taken together, the results indicate that VC can attenuate oxidative damage, inflammation, and acute hypoxia induced apoptosis in gibel carp via the Nrf2/Keap1 signaling pathway. The results identify a new defense strategy of gibel carp in response to hypoxic conditions.