Stimulation of Enzymatic Defense Mechanisms and Appearance of Liver Damage in Juvenile Trout ( Oncorhynchus mykiss ) Exposed to Water-Accommodated Trace Petroleum Residues

2002 ◽  
Vol 68 (5) ◽  
pp. 644-651
Author(s):  
A. Rudolph ◽  
R. Yáñez ◽  
L. Troncoso ◽  
R. González
2010 ◽  
Vol 299 (1) ◽  
pp. R33-R41 ◽  
Author(s):  
L. Bouraoui ◽  
E. Capilla ◽  
J. Gutiérrez ◽  
I. Navarro

Primary cultures of rainbow trout ( Oncorhynchus mykiss ) adipocytes were used to examine the main signaling pathways of insulin and insulin-like growth factor I (IGF-I) during adipogenesis. We first determined the presence of IGF-I receptors (IGF-IR) and insulin receptors (IR) in trout preadipocytes ( day 5) and adipocytes ( day 14). IGF-IRs were more abundant and appeared to be in higher levels in differentiated cells than in preadipocytes, whereas IRs were detected in lower but constant levels throughout the culture. The cells were immunoreactive against ERK1/2 MAPK, and AKT/PI3K, components of the two main signal transduction pathways for insulin and IGF-I receptors. Stimulation of MAPK phosphorylation by IGF-I was higher in preadipocytes than in adipocytes, while no effects were observed in MAPK phosphorylation after incubation of cells with insulin. AKT phosphorylation increased in the presence of both insulin and IGF-I, with higher levels of stimulation in adipocytes than in preadipocytes. Activation of both pathways was blocked by the use of specific inhibitors of MAPK (PD98059) and AKT (wortmannin). We describe here, for the first time, the effects of IGF-I and insulin on 2-deoxyglucose uptake in primary culture of trout adipocytes. IGF-I was more potent in stimulating glucose uptake than insulin, and PD98059 and wortmannin inhibited the stimulation of glucose uptake by this growth factor, suggesting that IGF-I plays an important metabolic role in trout adipocytes. Our results suggest that differential activation of the MAPK and AKT pathways are involved in the IGF-I- and insulin-induced effects of trout adipocytes during the various stages of adipogenesis.


1998 ◽  
Vol 275 (2) ◽  
pp. R460-R465 ◽  
Author(s):  
Lena Sundin ◽  
Göran E. Nilsson

By cutting gill filaments in anesthetized rainbow trout ( Oncorhynchus mykiss), observing the bleeding through a stereomicroscope, and using blockers of various known endogenous filament artery vasoconstrictors, we have here attempted to characterize hemostatic mechanisms in gills. The immediate hemostatic response to a cut in a gill filament artery was a local vasoconstriction, stopping the hemorrhage within ∼20 s. In heparinized fish, the hemorrhage recommenced after ∼8 min, suggesting that the vasoconstriction soon subsides and blood clotting becomes responsible for the hemostasis. Antagonists of acetylcholine, adenosine, and serotonin receptors were unable to block the hemostatic vasoconstriction. Also, tetrodotoxin was without effect, indicating a nonnervous origin. By contrast, indomethacin significantly affected the measured bleeding times, suggesting that eicosanoids play a significant role in this process (possibly by stimulating vasoconstriction and/or by inducing local thrombocyte aggregation). By possessing several hundred virtually identical filaments with readily observable vasculature, the fish gill appears to be a good experimental model for studying hemostatic mechanisms.


2003 ◽  
Vol 284 (4) ◽  
pp. R990-R999 ◽  
Author(s):  
Stephen G. Reid ◽  
Steve F. Perry

This study addressed the hypothesis that the secretion of catecholamines from trout ( Oncorhynchus mykiss) chromaffin cells, during hypoxia, is triggered by stimulation of O2 chemoreceptors located within the gills. Sodium cyanide was administered into the inspired water (external cyanide) or injected into the gill circulation (internal cyanide) to pharmacologically stimulate external (water sensing) or internal (blood sensing) O2 chemoreceptors, respectively. Both of these treatments caused an elevation of circulating catecholamine levels. The response to external, but not internal, cyanide was abolished by removal of the first gill arch. Hypoxia produced an increase in circulating catecholamine levels that was unaffected by removal of the first gill arch or by denervation of the pseudobranch. Cyanide and hypoxia both caused the well-documented cardiorespiratory reflexes normally observed in this species. This study demonstrates, for the first time, that gill O2chemoreceptors can initiate the reflex that leads to catecholamine release from the chromaffin cells and that stimulation of internally oriented O2 receptors on all gill arches appears to be the physiologically important mechanism for initiating release.


2010 ◽  
Vol 89 (5) ◽  
pp. 630-639 ◽  
Author(s):  
Giuseppina F Dusio ◽  
Diego Cardani ◽  
Laura Zanobbio ◽  
Martina Mantovani ◽  
Patrizia Luchini ◽  
...  

1994 ◽  
Vol 51 (8) ◽  
pp. 1791-1798 ◽  
Author(s):  
C. J. A. Mitton ◽  
D. G. McDonald

Electrofishing, a technique widely used for fish collection, is a procedure that is often followed by handling and air exposure before fish are released. In this study the pathological and physiological consequences of capture with pulsed DC (pDC) electroshock with and without the additional disturbance of air exposure were examined on rainbow trout (Oncorhynchus mykiss). Electroshocked fish showed no evidence of direct mortality, and skeletal damage was only induced under the most severe conditions (~600-g fish, 600 V, 20 or 40 s). Physiological disturbances induced by pDC, in the absence of physical damage, consisted of lactacidosis and stimulation of the interrenal stress response. The acidosis was likely induced by tetany during immobilization and apnea during immobilization and early recovery. In fact, the physiological disturbances induced by pDC were similar in magnitude and duration to 2–3 min of exhaustive exercise and generally more severe than responses previously reported for nonpulsed (i.e., continous) DC gear. In addition, following pDC, fish appeared to experience a mild narcosis, as was evident by a reduced response to the additional stress of air exposure.


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