Salicylate impacts the physiological responses to an acute handling disturbance in rainbow trout.
While salicylates (non-steroidal anti-inflammatory drugs) have been detected in the aquatic environment, few studies have focused on the mechanism of action of these pharmaceuticals on aquatic organisms. We reported previously that salicylate disrupted the acute trophic hormone-stimulated corticosteroidogenesis in rainbow trout (Oncorhynchus mykiss) interrenal tissue in vitro. Here, we tested the hypothesis that this drug will inhibit the adaptive plasma cortisol response and the associated metabolic response to an acute stressor in trout. Fish were fed salicylate-laced feed (100 mg/kg body weight) for 3 days, subjected to an acute (5 min) handling disturbance and sampled 1, 4 and 24 h after the stressor exposure. Salicylate treatment attenuated the stressor-induced plasma cortisol but not glucose or lactate elevations. The disruption of cortisol response corresponded with a significant reduction in transcript levels of the steroidogenic acute regulatory protein (StAR), but not peripheral-type benzodiazepine receptor, cytochrome P450 side-chain cleavage or 11beta-hydroxylase. Salicylate did not modify the stressor-induced elevation of brain glucocorticoid receptor (GR) protein expression, while liver GR protein content was reduced. Salicylate impact on liver metabolic capacity involved depressed liver glycogen content, whereas no significant changes in liver hexokinase, glucokinase, lactate dehydrogenase, pyruvate kinase, phosphoenolpyruvate carboxykinase, aspartate aminotransferase and alanine aminotransferase activities were observed. Taken together, salicylate impairs the stressor-mediated plasma cortisol response and the associated liver metabolic capacity in trout. The mode of action of salicylate involves disruption of StAR and liver GR, two key proteins critical for cortisol production and target tissue responsiveness to this steroid, respectively.
Gravel
Amélie
A
Department of Biology, University of Waterloo, Waterloo, Ontario, Canada N2L 3G1.
Vijayan
Mathilakath M
MM
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000633:toxicity*; D001786:Blood Glucose / Q000032:analysis; D001921:Brain / Q000187:drug effects; D001923:Brain Chemistry / Q000187:drug effects; D005393:Fish Diseases / Q000209:etiology / Q000503:physiopathology; D005786:Gene Expression Regulation / Q000187:drug effects; D005947:Glucose / Q000032:analysis; D006234:Handling, Psychological; D006854:Hydrocortisone / Q000097:blood; D019344:Lactic Acid / Q000097:blood; D008099:Liver / Q000737:chemistry / Q000187:drug effects / Q000201:enzymology; D008112:Liver Glycogen / Q000032:analysis; D017686:Oncorhynchus mykiss / Q000502:physiology*; D010750:Phosphoproteins / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D011965:Receptors, Glucocorticoid / Q000187:drug effects; D012459:Salicylates / Q000008:administration & dosage / Q000633:toxicity*; D013312:Stress, Physiological / Q000209:etiology / Q000503:physiopathology / Q000662:veterinary; D013997:Time Factors; D014874:Water Pollutants, Chemical / Q000008:administration & dosage / Q000633:toxicity*; D000098682:Steroidogenic Acute Regulatory Protein
D000894:Anti-Inflammatory Agents, Non-Steroidal; D001786:Blood Glucose; D008112:Liver Glycogen; D010750:Phosphoproteins; D011965:Receptors, Glucocorticoid; D012459:Salicylates; D014874:Water Pollutants, Chemical; D000098682:Steroidogenic Acute Regulatory Protein; D019344:Lactic Acid; D005947:Glucose; D006854:Hydrocortisone