Volume 15, Issue 2 (2013)
JAST 2013, 15(2): 303-310 |
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Nematollahi M A, de Van Pelt H, Komen H. Response to Stress in 17α-hydroxylase Deficient Common Carp (Cyprinus carpio L.). JAST 2013; 15 (2) :303-310
URL: http://jast.modares.ac.ir/article-23-5799-en.html
URL: http://jast.modares.ac.ir/article-23-5799-en.html
1- Department of Fisheries, Faculty Natural Resources, University of Tehran, Chamran St., P. O. Box: 31585-4314, Karaj, Islamic Republic of Iran.
2- Animal Breeding and Genomics Center, Wageningen Institute of Animal Sciences (WIAS), Wageningen University, PO Box: 338, 6700 AH Wageningen, The Netherlands.
2- Animal Breeding and Genomics Center, Wageningen Institute of Animal Sciences (WIAS), Wageningen University, PO Box: 338, 6700 AH Wageningen, The Netherlands.
Abstract: (5806 Views)
The aim of this study was to analyze the stress response during 3 hours net confinement stress and recovery period of 22 hours in normal (STD) and in 17α-hydroxylase deficient common carp (E5). Fish were raised for 6 months and sampled at T0 (control, unstressed), 5 minutes, 20 minutes, 1 hour and 3 hours of exposure to net confinement, and after 1 hour, 4 hours, and 22 hours of recovery. At every sampling time, blood was collected to determine cortisol, corticosterone, glucose, lactate and free fatty acids (FFA) levels (5 fish per strain). Fish and head kidney were weighed before and after dissection, respectively, to determine head kidney somatic Index (HKSI). Morphometric analysis of head kidney tissues indicated that the head kidney somatic index was significantly higher in E5 fish (0.076±0.021) compared with STD fish (0.045±0.015). Also, significant differences in cortisol and corticosterone as well as in glucose, lactate and FFA values were observed between the two strains of E5 and STD. Moreover, the pattern of changes of glucose and FFA during stress and afterward indicated a significant difference compared to the T0. Results support the conclusion that the reduced capacity of ill fish to produce cortisol is caused by a deficiency in 17α-hydroxylase activity. A reduced cortisol output leads to increased stimulation of adrenals by adrenocorticotropic Hormone (ACTH), resulting in increased outputs of corticosterone.
Received: 2013/01/17 | Accepted: 2013/01/17 | Published: 2013/01/17
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