An unknown structure in the chloride cells of the gill epithelium of the rainbow trout (Salmo gairdneri)

1973 ◽  
Vol 146 (2) ◽  
pp. 293-295 ◽  
Author(s):  
P. D. Abel
Keyword(s):  
Rainbow Trout ◽  
Chloride Cells ◽  
Salmo Gairdneri ◽  
Gill Epithelium ◽  
Unknown Structure

Deposition of aluminum in the gill epithelium of rainbow trout (Salmo gairdneri Richardson) subjected to sublethal concentrations of the metal

1987 ◽  
Vol 65 (3) ◽  
pp. 647-656 ◽  
Author(s):  
John H. Youson ◽  
Christine M. Neville
Keyword(s):  
Rainbow Trout ◽  
Epithelial Cells ◽  
Organic Acid ◽  
Control Fish ◽  
Chloride Cells ◽  
Salmo Gairdneri ◽  
Gill Epithelium ◽  
Epithelial Surface ◽  
X Ray ◽  
Sublethal Concentrations

Rainbow trout (Salmo gairdneri Richardson) were exposed to acid and sublethal concentrations of inorganic aluminum (1.6 μM at pH 6.1; 2.8 μM at pH 5.5, 5.0, and 4.5); aluminum was also administered in combination with organic acid at pH 4.5 and 5.0. The gill epithelium was examined by transmission electron microscopy and by electron probe X-ray microanalysis. Control fish at pH 7.3 without aluminum showed normal morphology but increased acidity and (or) decreased hardness resulted in a greater exposure of chloride cells at the epithelial surface. All fish exposed to aluminum had electron-dense particles on the surface of the respiratory (pavement) epithelial cells and chloride cells of the gills and most cells had these deposits in varying concentrations within cytoplasmic vacuoles and dense bodies. It was shown by X-ray microanalysis that the deposits contained aluminum. Increased acidity did not alter the pattern of distribution of aluminum particles but a heavy concentration of this metal followed the addition of organic acid. The accumulation of aluminum on and within epithelial cells and increased exposure of chloride cells in the gills could reflect decreased oxygen uptake and increased ion loss in trout, and probably are responsible for the toxicity of aluminum to fish in an acid environment.

Aspects of purine metabolism in the gill epithelium of rainbow trout, Salmo gairdneri richardson

1979 ◽  
Vol 62 (1) ◽  
pp. 31-40 ◽  
Author(s):  
Claude Leray ◽  
Jean P. Raffin ◽  
Christine Winninger
Keyword(s):  
Rainbow Trout ◽  
Purine Metabolism ◽  
Salmo Gairdneri ◽  
Gill Epithelium

Zinc Influx Across the Isolated, Perfused Head Preparation of the Rainbow Trout (Salmo gairdneri) in Hard and Soft Water

1988 ◽  
Vol 45 (12) ◽  
pp. 2206-2215 ◽  
Author(s):  
Douglas J. Spry ◽  
Chris M. Wood
Keyword(s):  
Steady State ◽  
Rainbow Trout ◽  
Hard Water ◽  
Soft Water ◽  
Chloride Cells ◽  
Salmo Gairdneri ◽  
First Order ◽  
Scanning Electron Micrography ◽  
Primary Substrate ◽  
Stimulation Of

At a waterborne [Zn] of 1.9 mg∙L−1 in hard water (~1 mmol Ca∙L−1), Zn influx across an isolated, saline-perfused head preparation of rainbow trout (Salmo gairdneri) was about 1.5 nmol∙kg−1∙h−1 through the lamellar pathway and about 1 nmol∙kg−1∙h−1 through the filamental route. Flux rates came rapidly to steady state in both pathways. Trout preexposed to artificial soft water (~0.05 mmol Ca∙L−1) for 5 d showed differential stimulation of flux rates to about 42 and 5 nmol Zn∙kg−1∙h−1 through the lamellar and filamental pathways, respectively. Under these conditions, steady-state fluxes across the lamellae did not occur until 15–20 min after the start of perfusion. Preparations from hardwater-acclimated trout tested in soft water gave typical hardwater fluxes showing that these changes in influx were not simply due to acute exposure of the gill surface to low waterborne [Ca]. Influxes in softwater trout, studied over [Zn] from 0.4 to 7.5 mg Zn∙L−1, revealed a saturable, first-order uptake with apparent Jmax and Km of 150 nequiv∙kg−1∙h−1 and 1.5 mg Zn∙L−1 (23 μmol∙L−1), respectively. Because the apparent Km is in the toxic range, Zn is clearly not the primary substrate. Scanning electron micrography revealed hypertrophy and increased apical exposure of chloride cells; this stimulation, coupled with the increase in Zn influx, suggests that chloride cells may be the site of entry of Zn across the gill.

scholarly journals The pattern of carbon dioxide excretion in the rainbow trout Salmo gairdneri

1978 ◽  
Vol 72 (1) ◽  
pp. 17-24
Author(s):  
M. S. Haswell ◽  
D. J. Randall
Keyword(s):  
Carbon Dioxide ◽  
Rainbow Trout ◽  
Carbonic Anhydrase ◽  
Severe Anaemia ◽  
Salmo Gairdneri ◽  
Gill Epithelium ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
O2 Delivery ◽  
Co2 Excretion

1. Patterns of carbon dioxide excretion were investigated in rainbow trout (Salmo gairdneri). 2. The loss of erythrocytic carbonic anhydrase caused by severe anaemia does not affect acid/base regulation or the ability of fish to excrete CO2. 3. Bicarbonate excretion across the saline-perfused gills of trout is significant even though residence time for the saline in the gills is only 1--3 s. CO2 excretion across these saline-perfused gills is blocked by the carbonic anhydrase inhibitor, diamox. 4. The excretion of CO2 in fish is via the movement of plasma bicarbonate into the gill epithelium where branchial carbonic anhydrase catalyses the production of CO2. Fish can adjust pH by regulating bicarbonate movement across the gills. 5. The erythrocytic carbonic anhydrase is not necessary for CO2 excretion in the gills but is involved in facilitating Bohr and Root shifts to augment O2 delivery in the tissues.

Effects of Perfusate HCO3− and Pco2 on Chloride Uptake in Perfused Gills of Rainbow Trout (Salmo gairdneri)

1984 ◽  
Vol 41 (12) ◽  
pp. 1768-1773 ◽  
Author(s):  
S. F. Perry ◽  
P. Payan ◽  
J. P. Girard
Keyword(s):  
Rainbow Trout ◽  
Carbonic Anhydrase ◽  
Chloride Transport ◽  
Salmo Gairdneri ◽  
Gill Epithelium ◽  
Major Pathway ◽  
Chloride Uptake ◽  
Transport Inhibitors ◽  
Initial Results ◽  
Stimulation Of

Experiments were conducted using a saline-perfused trout (Salmo gairdneri) head preparation in an attempt to determine the origin of HCO3− involved in gill apical Cl−/HCO3− exchange, the possibilities being plasma CO2 or HCO3−. Initial results showed that branchial Cl− influx was stimulated both by increased perfusate [HCO3−] and Pco2. Subsequent experiments employing the chloride transport inhibitors, SITS and thiocyanate, indicated that stimulation of Cl− influx by HCO3− probably was due to gill hemodynamic alterations and not to increased entry of HCO3− into the gill epithelium. We conclude that CO2 entry into the gill epithelium from plasma and its subsequent hydration to HCO3− and H+, by carbonic anhydrase, is a major pathway by which HCQ3− for Cl−/HCO3− exchange is generated.

Ultrastructural and Clinicopathological Studies on the Toxicity of Cationic Acrylamide-based Flocculant to Rainbow Trout

1987 ◽  
Vol 24 (1) ◽  
pp. 34-43 ◽  
Author(s):  
M. Albassam ◽  
J. Moore ◽  
A. Sharma
Keyword(s):  
Rainbow Trout ◽  
Epithelial Cells ◽  
Blood Vessels ◽  
Cell Injury ◽  
Basement Membranes ◽  
Chloride Cells ◽  
Salmo Gairdneri ◽  
Apical Plasma Membrane ◽  
Plasma Sodium ◽  
Secondary Lamellae

Rainbow trout (Salmo gairdneri) of two age groups were exposed to a cationic acrylamide-based flocculant at various concentrations in static bioassay chambers. At lethal concentrations the flocculant produced severe gill alterations in all fish. The principal alterations were necrosis and separation of the respiratory epithelial cells covering secondary lamellae. Many necrotic chloride cells were also seen, their apical plasma membrane was destroyed, and mitochondria were swollen with separated cristae. An influx of a large amount of fluid into the interstitial spaces caused partial or complete separation of subepithelial spaces from the covering epithelial cells and basement membranes of underlying blood vessels. Clinicopathological alterations included marked decreases in blood pH, partial pressure of oxygen, bicarbonate and plasma sodium, and chloride concentrations. Hematocrit, total protein, and blood glucose were increased. Fish exposed to sublethal concentrations had gill alterations characterized by hypercellularity and thickening of the secondary lamellae. These were due to undifferentiated cell proliferation and macrophage and lymphocyte infiltration between the covering epithelial cells and the underlying blood vessels. Macrophages and undifferentiated cells had large phagolysosomes containing cytoplasmic organelles, an indication of cell injury and increased turnover.

Fixation Artifacts in Rainbow Trout (Salmo gairdneri) Gills: A Morphometric Evaluation

1989 ◽  
Vol 46 (5) ◽  
pp. 780-785 ◽  
Author(s):  
D. J. Speare ◽  
H. W. Ferguson
Keyword(s):  
Rainbow Trout ◽  
Epithelial Cell ◽  
Chloride Cells ◽  
Salmo Gairdneri ◽  
Histopathological Changes ◽  
Whole Mount ◽  
Gill Lamellae ◽  
Linear Manner ◽  
Morphometric Evaluation ◽  
Fixation Delay

Epithelial capillary separation (E.C.S.) and epithelial cell hypertrophy (E.H.) of the gill lamellae of fish are two histopathological changes frequently described in association with toxic insults. Both of these gill changes increased in a significant linear manner over delay periods of 20–900 s from death to first entering either Bouin's or 10% formalin fixative. E.C.S. also occurred rapidly when gills were examined as whole mount preparations. The presence of occasional necrotic epithelial and chloride cells resembled apoptosis and is not in itself abnormal, nor did the type of fixative used or fixation delay have an effect on their extent. Gills from fish killed by either MS-222 or cervical spinal severance were similar, except that the latter also had multifocal lamellar telangiectasis. We conclude that E.C.S. and E.H. are readily mimicked by preparation and postmortem artifacts that occur rapidly after death when this is caused by either MS-222 or spinal severance. Bouin's fixative should be used to minimize these changes.

Sign in / Sign up

Export Citation Format

Share Document