Open AccessEffect of the arachidonic acid/vitamin E interaction on the immune response of juvenile Atlantic salmon ( Salmo salar ) challenged against Piscirickettsia salmonis
Author(s) -
Dantagnan P.,
Gonzalez K.,
Hevia M.,
Betancor M.B.,
Hernández A.J.,
Borquez A.,
Montero D.
Publication year - 2017
Publication title -
aquaculture nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.941
H-Index - 79
eISSN - 1365-2095
pISSN - 1353-5773
DOI - 10.1111/anu.12438
Subject(s) - salmo , lysozyme , biology , immune system , vitamin , respiratory burst , arachidonic acid , pathogen , juvenile , immunity , vitamin e , food science , zoology , biochemistry , microbiology and biotechnology , immunology , fish <actinopterygii> , fishery , ecology , enzyme , antioxidant
Atlantic salmon ( Salmo salar ) were fed 6 experimental diets containing three levels of arachidonic acid ( ARA ) (0.18 g kg −1 , 0.28 g kg −1 and 0.63 g kg −1 for low, medium and high levels, respectively) and two levels of vitamin E (150 and 730 mg kg −1 for low and high levels, respectively). At the end of the experimental period, fatty acids in the liver and immunity markers (lysozyme activity, respiratory burst and phagocytic activity) were determined and fish subjected to a challenge test against the salmonid rickettsial syndrome ( SRS ) pathogen. ARA , vitamin E or their interaction did not exert an effect on fish performance, whereas ARA alone clearly increased the deposition of ARA . Dietary vitamin E only enhanced liver vitamin E deposition, while the interaction of ARA and vitamin E influenced lysozyme activity and EPA / ARA ratio pointing out the effect of both nutrients on the fish immune system and metabolism. Only the medium concentration contributed to reducing mortality when the fish were exposed to the SRS pathogen. In conclusion, different levels of supplementation with ARA and vitamin E in the diet had no effect on productivity, but did have effects on immune markers and cumulative mortality when fish were exposed to the SRS pathogen.