scholarly journals The effects of CO2 and external buffering on ammonia excretion and Rhesus glycoprotein mRNA expression in rainbow trout

2008 ◽  
Vol 211 (20) ◽  
pp. 3226-3236 ◽  
Author(s):  
C. M. Nawata ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
Mrna Expression ◽  
Ammonia Excretion ◽  
Rhesus Glycoprotein

Ammonia excretion in rainbow trout (Oncorhynchus mykiss): evidence for Rh glycoprotein and H+-ATPase involvement

2007 ◽  
Vol 31 (3) ◽  
pp. 463-474 ◽  
Author(s):  
C. Michele Nawata ◽  
Carrie C. Y. Hung ◽  
Tommy K. N. Tsui ◽  
Jonathan M. Wilson ◽  
Patricia A. Wright ◽  
...  
Keyword(s):  
Boundary Layer ◽  
Rainbow Trout ◽  
Ammonia Excretion ◽  
Pavement Cell ◽  
New Members ◽  
Pavement Cells ◽  
Cdna Sequences ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Ammonia Transport ◽  
Genes Encoding

Branchial ammonia transport in freshwater teleosts is not well understood. Most studies conclude that NH3 diffuses out of the gill and becomes protonated to NH4+ in an acidified gill boundary layer. Rhesus (Rh) proteins are new members of the ammonia transporter superfamily and rainbow trout possess genes encoding for Rh30-like1 and Rhcg2. We identified seven additional full-length trout Rh cDNA sequences: one Rhag and two each of Rhbg, Rhcg1, and Rh30-like. The mRNA expression of Rhbg, Rhcg1, and Rhcg2 was examined in trout tissues (blood, brain, eye, gill, heart, intestine, kidney, liver, muscle, skin, spleen) exposed to high external ammonia (HEA; 1.5 mmol/l NH4HCO3, pH 7.95, 15°C). Rhbg was expressed in all tissues, Rhcg1 was expressed in brain, gill, liver, and skin, and Rhcg2 was expressed in gill and skin. Brain Rhbg and Rhcg1 were downregulated, blood Rh30-like and Rhag were downregulated, and skin Rhbg and Rhcg2 were upregulated with HEA. After an initial uptake of ammonia into the fish during HEA, excretion was reestablished, coinciding with upregulations of gill Rh mRNA in the pavement cell fraction: Rhcg2 at 12 and 48 h, and Rhbg at 48 h. NHE2 expression remained unchanged, but upregulated H+-ATPase (V-type, B-subunit) and downregulated carbonic anhydrase (CA2) expression and activity were noted in the gill and again expression changes occurred in pavement cells, and not in mitochondria-rich cells. Together, these results indicate Rh glycoprotein involvement in ammonia transport and excretion in the rainbow trout while underscoring the significance of gill boundary layer acidification by H+-ATPase.

Retinol Binding Protein in Rainbow Trout: Molecular Properties and mRNA Expression in Tissues

2001 ◽  
Vol 123 (1) ◽  
pp. 51-61 ◽  
Author(s):  
Marei Sammar ◽  
Patrick J. Babin ◽  
Michéle Durliat ◽  
Iris Meiri ◽  
Itai Zchori ◽  
...  
Keyword(s):  
Rainbow Trout ◽  
Mrna Expression ◽  
Binding Protein ◽  
Molecular Properties ◽  
Retinol Binding Protein

Melatonin treatment alters glucosensing capacity and mRNA expression levels of peptides related to food intake control in rainbow trout hypothalamus

2012 ◽  
Vol 178 (1) ◽  
pp. 131-138 ◽  
Author(s):  
Marta Conde-Sieira ◽  
Marta Librán-Pérez ◽  
Marcos A. López Patiño ◽  
José L. Soengas ◽  
Jesús M. Míguez
Keyword(s):  
Rainbow Trout ◽  
Food Intake ◽  
Mrna Expression ◽  
Melatonin Treatment ◽  
Expression Levels ◽  
Mrna Expression Levels ◽  
Intake Control

Acute Ammonia Toxicity and Ammonia Excretion in Rainbow Trout (Salmo gairdneri)

1979 ◽  
Vol 36 (6) ◽  
pp. 621-629 ◽  
Author(s):  
Betty A. Hillaby ◽  
David J. Randall
Keyword(s):  
Rainbow Trout ◽  
Ammonia Excretion ◽  
Hydrogen Ion ◽  
Ammonia Toxicity ◽  
Salmo Gairdneri ◽  
Mean Values ◽  
Arterial Blood ◽  
Blood Ph ◽  
Before And After ◽  
Total Ammonia

Acute ammonia toxicity in rainbow trout (Salmo gairdneri) was studied by intraarterial injection of NH4Cl and NH4HCO3. Hydrogen ion and total ammonia concentrations were measured in blood sampled from the dorsal aorta both before and after injection. Although injection of NH4HCO3 increased arterial blood pH, and injection of NH4Cl decreased arterial blood pH, the same dose of each was required to kill fish. While the un-ionized form of ammonia in water has been shown to be toxic, in the blood either the ionized form or the total ammonia load is toxic to fish. Ammonia levels were measured in pre- and postbranchial blood. Mean values were not significantly different, but paired values indicated a fall in blood ammonia due to excretion across the gills. There appears to be a more rapid excretion of ammonia following NH4HCO3 infusions, which result in higher un-ionized ammonia levels in blood compared with those following NH4Cl infusions. These results are consistent with the hypothesis that ammonia is excreted in the un-ionized form. Key words: un-ionized ammonia, ionized ammonia, gills, pH, blood

scholarly journals Estrogen receptor mRNA expression patterns in the liver and ovary of female rainbow trout over a complete reproductive cycle

2012 ◽  
Vol 178 (3) ◽  
pp. 556-561 ◽  
Author(s):  
James J. Nagler ◽  
Timothy D. Cavileer ◽  
Joseph S. Verducci ◽  
Irvin R. Schultz ◽  
Sharon E. Hook ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Rainbow Trout ◽  
Mrna Expression ◽  
Reproductive Cycle ◽  
Expression Patterns ◽  
Receptor Mrna ◽  
Estrogen Receptor Mrna

The effect of highly alkaline water (pH 9.5) on the morphology and morphometry of chloride cells and pavement cells in the gills of the freshwater rainbow trout: relationship to ionic transport and ammonia excretion

2000 ◽  
Vol 78 (2) ◽  
pp. 307-319 ◽  
Author(s):  
Pierre Laurent ◽  
Michael P Wilkie ◽  
Claudine Chevalier ◽  
Chris M Wood
Keyword(s):  
Rainbow Trout ◽  
Surface Area ◽  
Ammonia Excretion ◽  
Chloride Cells ◽  
Apical Surface ◽  
Influx Rate ◽  
Pavement Cells ◽  
Alkaline Water ◽  
Partial Restoration ◽  
Water Ph

Exposure of rainbow trout (Oncorhynchus mykiss) to alkaline water (pH 9.5) impairs ammonia excretion (JAmm) and gill-mediated ion-exchange processes, as characterized by decreased Cl- (JC1in) and Na+ influx (JNain) across the gill. Scanning electron microscopy suggested that the depression of JC1in was concomitant with an early decrease in the population of the most active chloride cells (CCs), partly compensated for by an increasing number of immature CCs. However, within 72 h after the onset of exposure to alkaline water, there was a 2-fold increase in the fractional apical surface area of CCs that paralleled complete recovery of the maximal Cl- influx rate (JC1max). These results suggest that recovery of JC1max was associated with greater CC surface area, resulting in more transport sites on the gill epithelium. Morphometric analysis of the outermost layer of pavement cells on the lamellar epithelium showed a greater density of microvilli during exposure to alkaline water, which may have contributed to partial restoration of the number of Na+ transport sites (JNamax). Finally, the blood-to-water gill-diffusion distance decreased by 27% after 72 h at pH 9.5, and likely contributed to progressive restoration of ammonia excretion in alkaline water.

Renal expression of the ammonia transporters, Rhbg and Rhcg, in response to chronic metabolic acidosis

2006 ◽  
Vol 290 (2) ◽  
pp. F397-F408 ◽  
Author(s):  
Ramanathan M. Seshadri ◽  
Janet D. Klein ◽  
Shelley Kozlowski ◽  
Jeff M. Sands ◽  
Young-Hee Kim ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Protein Expression ◽  
Mrna Expression ◽  
Collecting Duct ◽  
Broad Band ◽  
Ammonia Excretion ◽  
Intercalated Cells ◽  
Outer Medulla ◽  
Chronic Metabolic Acidosis ◽  
Medullary Collecting Duct

Chronic metabolic acidosis induces dramatic increases in net acid excretion that are predominantly due to increases in urinary ammonia excretion. The current study examines whether this increase is associated with changes in the expression of the renal ammonia transporter family members, Rh B glycoprotein (Rhbg) and Rh C glycoprotein (Rhcg). Chronic metabolic acidosis was induced in Sprague-Dawley rats by HCl ingestion for 1 wk; control animals were pair-fed. After 1 wk, metabolic acidosis had developed, and urinary ammonia excretion increased significantly. Rhcg protein expression was increased in both the outer medulla and the base of the inner medulla. Intercalated cells in the outer medullary collecting duct (OMCD) and in the inner medullary collecting duct (IMCD) in acid-loaded animals protruded into the tubule lumen and had a sharp, discrete band of apical Rhcg immunoreactivity, compared with a flatter cell profile and a broad band of apical immunolabel in control kidneys. In addition, basolateral Rhcg immunoreactivity was observed in both control and acidotic kidneys. Cortical Rhcg protein expression and immunoreactivity were not detectably altered. Rhcg mRNA expression was not significantly altered in the cortex, outer medulla, or inner medulla by chronic metabolic acidosis. Rhbg protein and mRNA expression were unchanged in the cortex, outer and inner medulla, and no changes in Rhbg immunolabel were evident in these regions. We conclude that chronic metabolic acidosis increases Rhcg protein expression in intercalated cells in the OMCD and in the IMCD, where it is likely to mediate an important role in the increased urinary ammonia excretion.

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