Branchial chloride cell proliferation in the rainbow trout, Oncorhynchus mykiss: implications for gas transfer

1994 ◽  
Vol 72 (8) ◽  
pp. 1395-1402 ◽  
Author(s):  
Shawn D. Bindon ◽  
James C. Fenwick ◽  
Steve F. Perry
Keyword(s):  
Electron Microscopy ◽  
Cell Proliferation ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Surface Area ◽  
Chloride Cell ◽  
Gas Transfer ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Treated Fish ◽  
Fractional Surface

The effects of branchial chloride cell proliferation on ion transport capability and gill morphometry were evaluated in the rainbow trout, Oncorhynchus mykiss, to test the hypothesis that chloride cell (CC) proliferation benefits ionic regulation at the expense of efficient gas transfer. The extent of hormone-induced CC proliferation (using ovine growth hormone (oGH), cortisol, or a combination of both) on the gill filament epithelium was assessed by determining the fractional surface area of exposed cells using scanning electron microscopy. Cortisol and oGH were equally effective in increasing CC fractional surface area (~2×), owing to the enlargement of individual CCs. The combined cortisol/oGH treatment resulted in an even greater increase in CC fractional area (~6×), as both the size and number of CCs increased. Sham injections were without effect on CC surface area or number. Significant increases in Na+ (Jin Na+) and Cl− uptake (Jin Cl−) were observed after all hormone treatments and were correlated positively with the increases in the CC fractional surface area. These findings support the view that CC proliferation enhances branchial ion transport capability. Lamellar epithelial thickness (measured by transmission electron microscopy) was increased in hormone-treated fish, while lamellar surface area (measured using light microscopy) was unaffected. The area of the interlamellar water channels (calculated from light micrographs) was significantly reduced in hormone-treated fish. These results suggest that, in trout, a compromise is made between the efficiency of ion regulation and gas transfer in which the enlargement/proliferation of CCs may impede gas transfer.

scholarly journals THE EFFECTS OF BRANCHIAL CHLORIDE CELL PROLIFERATION ON RESPIRATORY FUNCTION IN THE RAINBOW TROUT ONCORHYNCHUS MYKISS

1994 ◽  
Vol 197 (1) ◽  
pp. 47-63
Author(s):  
S Bindon ◽  
K Gilmour ◽  
J Fenwick ◽  
S Perry
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Partial Pressure ◽  
Respiratory Function ◽  
Chloride Cell ◽  
Control Fish ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Arterial Blood ◽  
Environmental Hypoxia ◽  
Treated Fish

The objectives of this study were to induce chloride cell (CC) proliferation on the gill lamellae of rainbow trout Oncorhynchus mykiss and to evaluate the consequences for respiratory function. Chronic elevation of hormone levels was used to induce CC proliferation; fish were injected with a combination of cortisol (8 mg kg-1 intramuscularly every day for 10 days) and ovine growth hormone (2 mg kg-1 intraperitoneally every second day for 10 days). The extent of CC proliferation was quantified using scanning electron microscopy and a two-dimensional analysis. An extracorporeal preparation in combination with environmental hypoxia was used to assess the effects of CC proliferation on respiratory function. Arterial blood was routed from the coeliac artery through an external circuit in which pH (pHa), partial pressure of oxygen (PaO2) and partial pressure of carbon dioxide (PaCO2) were monitored continuously. Environmental hypoxia was imposed by gassing a water equilibration column supplying the experimental chamber with N2. The hormone treatment increased the average CC surface area by 2.7-fold and CC density by 2.2-fold; the combined effect was a fivefold increase in CC fractional area. While the PaO2 values of hormone-treated and control fish were similar at PwO2>12.0 kPa, the arterial O2 tensions of treated fish were significantly lower than those of the control group for PwO2¾12.0 kPa. In comparison with control fish at all environmental O2 tensions, the hormone-treated fish exhibited elevated PaCO2 values and a significant acidosis. The effects of CC proliferation on blood gas variables in hormone-treated fish were accompanied by a significantly elevated ventilation amplitude and a lowered ventilation frequency. The results of this study demonstrated (i) that impairment of respiratory gas transfer coincides with CC proliferation, (ii) that O2 and CO2 transfer are influenced differently and (iii) that partial compensation is achieved through physiological adjustments.

Metabolic Costs and Physiological Consequences of Acclimation to Aluminum in Juvenile Rainbow Trout (Oncorhynchus mykiss). 2: Gill Morphology, Swimming Performance, and Aerobic Scope

1994 ◽  
Vol 51 (3) ◽  
pp. 536-544 ◽  
Author(s):  
Rod W. Wilson ◽  
Harold L. Bergman ◽  
Chris M. Wood
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Surface Area ◽  
Swimming Performance ◽  
Mucous Cell ◽  
Aerobic Scope ◽  
Fourfold Increase ◽  
Juvenile Rainbow Trout ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Oxygen Requirements

Juvenile rainbow trout (Oncorhynchus mykiss, 5–13 g) were chronically exposed to sublethal Al (38 μg∙L−1) in acidified soft water (Na+ = 85, Ca2+ = 28 μEq∙L−1, pH 5.2–5.4) for 36 d. Acclimation (increased resistance to challenge with 162 μg Al∙L−1 Al at pH 5.2) occurred after 5 d and was associated with a fourfold increase in gill mucous cell density and reduction in apparent lamellar surface area; initially elevated blood–water diffusion distances returned to normal after 34 d, but the reduction in apparent surface area persisted. Chronic exposure to acid alone (pH 5.2, same water chemistry) caused no morphometric changes but resulted in persistent impairment of Ucrit (critical aerobic swimming speed) by about 10%. This was due to increased oxygen requirements at subcritical swimming speeds (loading stress) and was alleviated when trout were swum at pH 6.5 (zero Al) on day 36. In trout preexposed to sublethal Al, Ucrit was chronically impaired by approximately 16% due to loading stresses and reduction in the maximum rate of oxygen uptake, Mo2max (limiting stress); Ucrit and Mo2max remained depressed even when fish were swum at pH 6.5 (zero Al). Reduced gill area compromises the aerobic scope for activity but may be an unavoidable cost of acclimation to Al.

Branchial Morphological and Endocrine Responses of Rainbow Trout (Oncorhynchus mykiss) to a Long-Term Sublethal Acid Exposure In Which Acclimation Did Not Occur

1993 ◽  
Vol 50 (1) ◽  
pp. 198-209 ◽  
Author(s):  
Céline Audet ◽  
Chris M. Wood
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Chloride Cell ◽  
Chloride Cells ◽  
Physiological Data ◽  
Mucous Cells ◽  
Diffusion Distance ◽  
Cell Numbers ◽  
Rainbow Trout Oncorhynchus Mykiss

Changes in branchial morphology and in plasma Cortisol, adrenaline, and noradrenaline were quantified throughout an 81 -d exposure of rainbow trout (Oncorhynchus mykiss) to sublethal acidity (pH 4.8) in artificial soft water and after a 5-h acid challenge (pH 4.0) of naive fish and 81-d acid-preexposed fish. Changes in branchial morphology at pH 4.8 were generally very mild and characterized by slight increases in filamental mucous cells and decreases in lamellar mucous cells. Chloride cell numbers and branchial Na+–K+- and total ATPase activities did not change. The filamental epithelium thickened, but the water–blood diffusion distance in the lamellae decreased during chronic exposure. Cortisol was significantly elevated throughout whereas catecholamines exhibited relatively little response. Response to acute pH 4.0 challenge was similar in naive and 81-d acid-exposed fish: epithelial damage, increase in visible mucous cells, loss of chloride cells by necrosis, and high cortisol levels but no changes in lamellar or filamental epithelial thickness, diffusion distance, ATPase activities, or catecholamine levels. Previously reported physiological data from these same trout demonstrated that sensitization rather than acclimation had occurred. Therefore, these observations support the view that acclimation does not occur in the absence of significant branchial damage and repair.

scholarly journals Regulation of proliferation and differentiation of adipocyte precursor cells in rainbow trout (Oncorhynchus mykiss)

2008 ◽  
Vol 198 (3) ◽  
pp. 459-469 ◽  
Author(s):  
L Bouraoui ◽  
J Gutiérrez ◽  
I Navarro
Keyword(s):  
Cell Proliferation ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Adipocyte Differentiation ◽  
Nuclear Antigen ◽  
Peroxisome Proliferator ◽  
Endocrine Regulation ◽  
Endocrine Control ◽  
Insulin Growth Factor ◽  
Rainbow Trout Oncorhynchus Mykiss

Here, we describe optimal conditions for the culture of rainbow trout (Oncorhynchus mykiss) pre-adipocytes obtained from adipose tissue and their differentiation into mature adipocytes, in order to study the endocrine control of adipogenesis. Pre-adipocytes were isolated by collagenase digestion and cultured on laminin or 1% gelatin substrate. The expression of proliferating cell nuclear antigen was used as a marker of cell proliferation on various days of culture. Insulin growth factor-I stimulated cell proliferation especially on days 5 and 7 of culture. Tumor necrosis factor α (TNFα) slightly enhanced cell proliferation only at a low dose. We verified the differentiation of cells grown in specific medium into mature adipocytes by oil red O (ORO) staining. Quantification of ORO showed an increase in triglycerides throughout culture. Immunofluorescence staining of cells at day 11 revealed the expression of CCAAT/enhancer-binding protein and peroxisome proliferator–activator receptor γ, suggesting that these transcriptional factors are involved in adipocyte differentiation in trout. We also examined the effect of TNFα on the differentiation of these adipocytes in primary culture. TNFα inhibited the differentiation of these cells, as indicated by a decrease in glycerol-3-phosphate dehydrogenase activity, an established marker of adipocyte differentiation. In conclusion, the culture system described here for trout pre-adipocytes is a powerful tool to study the endocrine regulation of adipogenesis in this species.

Physiological and morphological regulation of acid–base status during hypercapnia in rainbow trout (Oncorhynchus mykiss)

1993 ◽  
Vol 71 (8) ◽  
pp. 1673-1680 ◽  
Author(s):  
Greg G. Goss ◽  
Steve F. Perry
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Chloride Cell ◽  
Morphological Alteration ◽  
Acid Base ◽  
Rapid Reduction ◽  
Fractional Area ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Positive Formula ◽  
Acid Base Status

A kinetic analysis (Michaelis constant (Km) and maximal flux (Jmax)) of the branchial Na+ and Cl− influx mechanisms, along with measurements of blood total CO2 content [Formula: see text], net acidic–basic equivalent fluxes, and gill chloride cell morphology, was performed using rainbow trout (Oncorhynchus mykiss) before, during, and after 96 h exposure to environmental hypercapnia (water [Formula: see text]; 1 torr = 133.3 kPa). Exposure to hypercapnia caused (i) a net acidic equivalent loss (negative [Formula: see text]) that was accounted for entirely by reductions in titratable alkalinity flux (JTA), (ii) an increase in [Formula: see text] from 8.4 ± 0.5 to 20.7 ± 0.4 mmol/L, and (iii) no alteration either in [Formula: see text], [Formula: see text], or [Formula: see text]; [Formula: see text] increased (affinity was reduced). Chloride cell fractional area was reduced by 40% from 174 250 ± 15 650 μm2/mm2 under control conditions to 104 329 ± 17 991 μm2/mm2 after 96 h of hypercapnia. In the posthypercapnic period, there was (i) a net acidic equivalent gain (positive [Formula: see text]) that was accounted for entirely by an elevation in JTA, (ii) a rapid reduction of blood [Formula: see text], (iii) an increase of chloride cell fractional area to control values (179 105 ± 35 233μm2/mm2), and (iv) increases and decreases in [Formula: see text] (564 ± 50 versus 224 ± 21 μmol∙kg−1∙h−1 in the prehypercapnic period) and [Formula: see text] (381 ± 85 versus 585 ± 92 μmol∙kg−1∙h−1), respectively. The results suggest that morphological alteration of the gill chloride cell fractional area is an important response to acid–base disturbances. The results are discussed with respect to the relative roles of morphological alteration of gill chloride cell fractional area and variation in internal substrate (HCO3−) in modifying branchial Cl−/HCO3− exchange for acid–base regulation.

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