Extrathyroidal Effects of Low Concentrations of Thiourea on Rainbow Trout, Salmo gairdneri

1981 ◽  
Vol 38 (10) ◽  
pp. 1283-1285 ◽  
Author(s):  
J. G. Eales

Chronic exposure of fed immature rainbow trout (Salmo gairdneri) to a low ambient thiourea (TU) concentration did not depress circulating levels of T4 (thyroxine) or triiodothyronine, T4 degradation rate, or T4 deiodination rate indicating no significant T4 influence on thyroidal hormone output. However, TU increased the hematocrit and decreased distribution spaces for iodide and T4, indicating direct sensitivity of extrathyroidal processes to TU.Key words: thiourea, thyroxine, hematocrit, iodide metabolism, rainbow trout

1984 ◽  
Vol 41 (11) ◽  
pp. 1678-1685 ◽  
Author(s):  
Michael A. Giles

Rainbow trout (Salmo gairdneri) were exposed to 3.6 and 6.4 μg Cd/L for periods up to 178 d. Transitory changes in plasma calcium and magnesium were observed in fish exposed to 3.6 μg Cd/L although the differences were not significant. Exposure to 6.4 μg Cd/L, however, resulted in significantly lowered plasma sodium, potassium, calcium, and chloride and elevated magnesium concentrations. Analyses of urine indicated that the rate of urine production, osmolality, and sodium, potassium, chloride, magnesium, calcium, and protein concentrations were unaffected by exposure to 3.6 μg Cd/L although slight changes were observed in the first week of exposure. Urine production rate and urinary concentrations of potassium and chloride were unaffected in trout exposed to 6.4 μg Cd/L but sodium, protein, and osmolality were elevated and calcium and magnesium concentrations reduced in these fish. The results demonstrate that the majority of the cadmium-induced electrolyte imbalances do not result from impairment of renal function.


1984 ◽  
Vol 62 (8) ◽  
pp. 1495-1501 ◽  
Author(s):  
J. G. Eales ◽  
Shirley Shostak ◽  
Catherine G. Flood

The effects of the thiols DTT (dithiothreitol) and GSH (reduced glutathione) on hepatic in vitro and in vivo T4 (L-thyroxine) deiodination by rainbow trout held at 11 °C were studied. Hepatic deiodination increased progressively over the DTT range of 0.02–20 mM. GSH was less potent than DTT at low concentrations and strongly inhibited deiodination at high concentrations (> 1 mM). Hepatic deiodination was not increased by 1 mM NADPH or anaerobic conditions and was enhanced and not inhibited by the GSH inhibitor, diamide (2.5 mM), indicating that the low T4 deiodination in the absence of DTT is not due to endogenous GSH deficiency. Intraperitoneally injected GSH consistently increased plasma levels of 125I and [125I]-3,5,3′-triiodo-L-thyronine (T3) in fed or starved [125I]T4-injected trout, suggesting a GSH stimulation of extrahepatic T4 deiodination. However, injected GSH did not elevate plasma T3 concentrations. This was probably due to a demonstrated GSH stimulation of plasma T4 and T3 clearance. Force-fed GSH did not increase [125I]T4 deiodination. It is concluded that exogenous thiols can enhance T4 deiodination both in vitro and in vivo. However, availability of neither endogenous nor dietary GSH appears to regulate T4 deiodination under physiological conditions, including altered nutritional state.


1987 ◽  
Vol 128 (1) ◽  
pp. 255-267 ◽  
Author(s):  
M. G. Vermette ◽  
S. F. Perry

Rainbow trout were infused continuously for 24 h with epinephrine in order to elevate circulating levels to those measured during periods of acute extracellular acidosis (about 5 X 10(−8) mol l-1). Concomitant effects on branchial solute fluxes were evaluated. Epinephrine infusion caused complex and differential adjustments of Na+ and Cl- unidirectional fluxes (influx and efflux) resulting in a significant elevation of the arithmetic difference between Na+ and Cl- net fluxes (JnetNa+-JnetCl-). A significant correlation existed between JnetNa+-JnetCl- and net branchial acid excretion (JnetH+), thereby suggesting a role for epinephrine in piscine acid-base regulation. The stimulation of JnetH+ by epinephrine was due primarily to a reduction in the excretion of titratable acid (JTA) accompanied by non-significant changes in ammonia excretion (JAmm). The results are discussed with respect to a role for epinephrine in regulating acid-base disturbances by interacting with branchial ionic exchange mechanisms.


1991 ◽  
Vol 69 (10-11) ◽  
pp. 735-741 ◽  
Author(s):  
J. L. Miguel ◽  
M. I. Pablos ◽  
M. T. Agapito ◽  
J. M. Recio

A method for the purification of ferritin from rainbow trout liver by heat extraction and gel filtration is described. The number of iron atoms varied from 500 to 2000 in purified ferritin. The neutral sugar composition detected was 86 mol of glucose, 24 mol of fucose, 12 mol of galactose, and 8 mol of mannose per mol of ferritin and apoferritin. Release of iron was achieved using low molecular weight chelating agents. The order of effectiveness of chelators was nitrilotriacetate > EDTA > citrate. Removal of the iron does not imply reduction of Fe3+. The rate of release of iron increased with decreasing pH. The slowest release was at pH 7.5. The endogenous chelator is not only sulphydrylic but seems to include carbohydrates that participate in the binding of Fe2+. Trout ferritin exhibits heterogeneity upon isoelectric focusing; four isoferritins with pI values of 4.5 to 4.85 were detected. This heterogeneity represents polymorphic, not polymer, forms. The amino acid composition differs from that of ferritins from other species. High concentrations of glutamic and aspartic acids, alanine, leucine, glycine, and lysine were detected along with low concentrations of methionine and cysteine.Key words: ferritin, isoferritin, rainbow trout.


1986 ◽  
Vol 64 (12) ◽  
pp. 2658-2664 ◽  
Author(s):  
J. G. Eales ◽  
G. Van Der Kraak ◽  
J. P. Chang ◽  
R. J. Omeljaniuk

Plasma levels of 3,5,3′-triiodo-L-thyronine (T3), plasma T3 kinetics, and properties of in vivo T3 binding to saturable hepatocyte nuclear sites were studied in fed immature rainbow trout maintained at 12 °C and then held for up to 14 d at 5, 11–12, or 19 °C. Elevation (19 °C) or depression (5 °C) of plasma T3 occurred during the first 3 h following abrupt transfer from 11 °C, but from 12 h to 7 d, plasma T3 did not differ significantly among the three temperatures. In contrast, the plasma T3 degradation rate increased fourfold from 5 to 19 °C largely because of an increased fractional rate of turnover of the plasma T3 pool. Outer-ring deiodination of T3 was negligible at 5 and 12 °C and slight at 19 °C. Temperature did not influence the proportion of [125I]T3 lost via the enterohepatic route. Uptake of [125I]T3 into the liver and liver nuclear fraction was most rapid at 19 °C, intermediate at 12 °C, and least rapid at 5 °C. Saturable nuclear binding of [125I]T3 occurred at all temperatures. The apparent affinity of T3 for hepatic nuclear sites was similar at 12 and 19 °C but lower at 5 °C; the apparent site capacity underwent no significant change with temperature. In conclusion, over the range of 5 to 19 °C there are marked increases in plasma T3 clearance, rate of T3 uptake from plasma to liver, and rate of T3 uptake by the liver nuclear fraction, but relatively small changes in plasma T3 level, proportion of T3 excreted via the enterohepatic route, and properties of the saturable T3-binding nuclear sites.


1987 ◽  
Vol 128 (1) ◽  
pp. 269-285
Author(s):  
M. G. Vermette ◽  
S. F. Perry

Rainbow trout were infused continuously for 24 h with epinephrine in order to evaluate the effects of elevated circulating levels of epinephrine on selected renal variables. Pronounced effects of epinephrine included elevation of urine flow rate and concomitant increases in the excretion of all measured electrolytes (Na+, Cl-, K+, Ca2+, inorganic phosphate) with the exception of ammonium and bicarbonate ions. Significant reductions in the tubular reabsorption of Na+ and Cl- also contributed to enhanced excretion of these ions. Similarly, epinephrine affected the tubular handling of NH4+ and HCO3- with NH4+ secretion decreasing and HCO3- reabsorption increasing. We speculate that the stimulation of HCO3- reabsorption was a consequence of elevated tubular H+ secretion. Such a mechanism may be important to permit plasma HCO3- retention during periods of internal acidosis. The results are discussed with reference to the role of the fish kidney in regulating acid-base disturbances and the possible interactive effects of elevated epinephrine.


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