Dietary selenium required to achieve body homeostasis and attenuate pro-inflammatory responses in Atlantic salmon post-smolt exceeds the present EU legal limit
Peer reviewed, Journal article
MetadataShow full item record
Original versionAquaculture. 2020, 526:735413 1-14. 10.1016/j.aquaculture.2020.735413
Selenium (Se) supplementation either as inorganic or organic form was evaluated in Atlantic salmon post-smolt in vivo and in vitro. The basal diet was formulated to be low in fish meal and contain 0.24 mg Se kg−1; six other diets with Se inclusion of 0.15, 0.4, 0.7 or 1.1 mg kg−1 as sodium selenite (SS) and 0.15 or 0.4 mg kg−1 as L-selenomethionine (SM) were formulated from the basal diet. The diets were fed to Atlantic salmon post-smolt (mean initial weight, 216 ± 27 g) in triplicate groups (35 fish tank−1) and reared in flow-through seawater (33 ppt) at 10–12 °C for 9 weeks. At the end of the feeding trial, whole fish and tissues were sampled for in vivo assessment; whereas, liver cells and head kidney leukocytes (HKL) were isolated and their primary cultures used for in vitro assessment following exposure to hydrogen peroxide (H2O2), lipopolysaccharide (LPS) or poly I:C (PIC). Growth, feed intake, feed conversion ratio, specific growth rate, hepato-somatic index, proximate composition and mineral concentration of the whole fish (except for Se) were unaffected by dietary Se (p > .05). Hematocrit was significantly higher in fish fed the 0.4 mg Se supplemented feeds, irrespective of the Se source (p = .02). The Se concentration in whole body, liver, muscle, plasma, kidney and liver/kidney Se ratio increased with increasing dietary Se concentration (p < .0001). Level of oxidised glutathione (GSSG) in liver and head kidney followed a quadratic function (p < .05) indicating that the concentrations were lower at intermediate SS supplementation of 0.4 and 0.65 mg Se kg−1 (total Se, 0.65 and 0.87 mg Se kg−1). Impact of Se sources on glutathione redox status was similar. Slope-ratio analysis revealed SM to be more efficient than SS in improving apparent availability, whole body or tissues Se status, Se retention and reducing Se loss to the environment. In vitro, the mRNA expression of p38mapk and aif, in liver cells were affected by the impact of dietary Se, but not by the treatment of H2O2 (p < .05). In the HKL, the LPS and PIC induced pro-inflamatory action of il-1β, cox2, nfkβ and viperin were attenuated by SM supplementation, but not by SS (p < .001). Dietary Se supplementation required to the basal diet containing 0.24 mg Se kg−1 was 0.41 mg Se as SS (total 0.65 mg kg−1) or 0.17 mg Se as SM (total 0.41 mg kg−1) based on body Se homeostasis or tissue Se status. SM inclusion at 0.4 mg kg−1 diet (total, 0.65 mg kg−1) attenuated LPS or PIC induced pro-inflammatory responses in vitro. Overall, Se requirement of Atlantic salmon post smolt was 0.27 mg kg−1 diet, on availale basis. Dietary Se level required to maintain body Se homeostasis and improved health status of Atlantic salmon fed plant-based diets (0.65 mg kg−1 diet) exceed the existing EU maximum limit of 0.5 mg Se kg−1 diet. SM as the Se source in salmon feeds has the potential to improve salmon health and reduce Se emissions from Norwegan salmon farming by 60 to 70%.