Title
Compensatory responses in common carp (**Cyprinus carpio**) under ammonia exposure : additional effects of feeding and exercise Compensatory responses in common carp (**Cyprinus carpio**) under ammonia exposure : additional effects of feeding and exercise
Author
Faculty/Department
Faculty of Sciences. Biology
Publication type
article
Publication
Amsterdam ,
Subject
Biology
Pharmacology. Therapy
Source (journal)
Aquatic toxicology. - Amsterdam
Volume/pages
142(2013) , p. 123-137
ISSN
0166-445X
ISI
000328093900013
Carrier
E
Target language
English (eng)
Full text (Publishers DOI)
Affiliation
University of Antwerp
Abstract
Ammonia is an environmental pollutant that is toxic to all aquatic animals. The toxic effects of ammonia can be modulated by other physiological processes such as feeding and swimming. In this study, we wanted to examine these modulating effects in common carp (Cyprinus carpio). Fish were either fed (2% body weight) or starved (unfed for seven days prior to the sampling), and swimming at a sustainable, routine swimming speed or swum to exhaustion, while being exposed chronically (up to 28 days) to high environmental ammonia (HEA, 1 mg/L ∼ 58.8 μmol/L as NH4Cl at pH 7.9). Swimming performance (critical swimming speed, Ucrit) and metabolic responses such as oxygen consumption rate (MO2), ammonia excretion rate (Jamm), ammonia quotient, liver and muscle energy budget (glycogen, lipid and protein), plasma ammonia and lactate, as well as plasma ion concentrations (Na+, Cl−, K+ and Ca2+) were investigated in order to understand metabolic and iono-regulatory consequences of the experimental conditions. Cortisol plays an important role in stress and in both the regulation of energy and the ion homeostasis; therefore plasma cortisol was measured. Results show that during HEA, Jamm was elevated to a larger extent in fed fish and they were able to excrete much more efficiently than the starved fish. Consequently, the build-up of ammonia in plasma of HEA exposed fed fish was much slower. MO2 increased considerably in fed fish after exposure to HEA and was further intensified during exercise. During exposure to HEA, the level of cortisol in plasma augmented in both the feeding regimes, but the effect of HEA was more pronounced in starved fish. Energy stores dropped for both fed and the starved fish with the progression of the exposure period and further declined when swimming to exhaustion. Overall, fed fish were less affected by HEA than starved fish, and although exercise exacerbated the toxic effect in both feeding treatments, this was more pronounced in starved fish. This suggests that fish become more vulnerable to external ammonia during exercise, and feeding protects the fish against the adverse effects of high ammonia and exercise.
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