Dietary supplementation with arachidonic acid in tilapia (Oreochromis mossambicus) reveals physiological effects not mediated by prostaglandins.
This study aims to clarify the role of the polyunsaturated fatty acid arachidonic acid (ArA, 20:4n-6) in the stress response of Mozambique tilapia (Oreochromis mossambicus). ArA is converted into eicosanoids, including prostaglandins, which can influence the response to stressors. Tilapia, a species able to form ArA from its precursor, was supplemented with ArA for 18 days, after which they were confined for 5 min. Acetylsalicylic acid (ASA, COX-inhibitor) was subsequently administered to distinguish ArA-mediated effects from enhanced prostaglandin E(2) (PGE(2)) synthesis. ArA supplemented fish had higher ArA levels in gills and kidneys, and these levels were further enhanced after ASA treatment. Levels of total monounsaturated and polyunsaturated fatty acids as well as docosahexaenoic acid (DHA), eicosapentaenoic acid (EPA), and ArA, were altered 24h after confinement, particularly in the kidneys. ArA supplementation had no effect on basal cortisol levels, while ArA + ASA reduced basal cortisol levels. ArA + ASA augmented the cortisol response to confinement. The combination of ArA + ASA also elevated plasma basal prolactin (tPRL)(177) and 3,5,3'-triiodothyronine (T(3)) levels. Neither ArA nor ASA affected the stress-associated increases in plasma glucose and lactate. Na(+), K(+)-ATPase activity in the gills was reduced after ArA supplementation and was even further suppressed by subsequent ASA treatment. In an additional feeding trial, ArA supplementation enhanced the renal Na(+), K(+)-ATPase activity. In vitro, ArA was a potent inhibitor of the Na(+), K(+)-ATPase activity of gill and kidney homogenates. In contrast, PGE(2) had no effect on branchial ATPase, whereas the effect on renal ATPase activity was concentration dependent. Modifying the dietary intake of ArA alters the response of tilapia to an acute stressor and influences osmoregulatory processes and it is unlikely that these effects are due to an enhanced production of prostaglandins.
Van Anholt
R D
RD
Department of Animal Ecology and Ecophysiology, Faculty of Science, University of Nijmegen, Toernooiveld 1, 6525 ED Nijmegen, The Netherlands. rogier@vananholt.org
Spanings
F A T
FA
Koven
W M
WM
Bonga
S E Wendelaar
SE
D000818:Animals; D016718:Arachidonic Acid / Q000378:metabolism / Q000494:pharmacology*; D001241:Aspirin / Q000494:pharmacology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004032:Diet; D019587:Dietary Supplements; D015232:Dinoprostone / Q000096:biosynthesis / Q000494:pharmacology; D004357:Drug Synergism; D005260:Female; D005880:Gills / Q000378:metabolism; D006854:Hydrocortisone / Q000097:blood; D007668:Kidney / Q000378:metabolism; D008297:Male; D011453:Prostaglandins / Q000502:physiology*; D012149:Restraint, Physical; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000378:metabolism; D013312:Stress, Physiological / Q000209:etiology / Q000378:metabolism; D017210:Tilapia / Q000502:physiology*
D016861:Cyclooxygenase Inhibitors; D011453:Prostaglandins; D016718:Arachidonic Acid; D000254:Sodium-Potassium-Exchanging ATPase; D015232:Dinoprostone; D001241:Aspirin; D006854:Hydrocortisone