The effect of sublethal cyanide exposure on plasma viteliogenin levels in rainbow trout (Salmo gairdneri) during early vitellogenesis

Female rainbow troutSalmo gairdneri were exposed to 0.01 mg L^–1 hydrogen cyanide (HCN) for 12 days at 12.5 ± 0.5C at the onset of vitellogenesis (May–June). Plasma vitellogenin levels were measured, utilizing a homologous radioimrnunoassay specifically developed for this species. Exposure to HCN reduced vitellogenin levels in the plasma to levels recorded in the control non-vitellogenic group. Similarly, the gonadosomatic index declined steadily throughout the experimental period in vitellogenic females exposed to cyanide while no difference was observed in hepatosomatic indices relative to controls. The high sensitivity of the radioimmunoassay for vitellogenin utilized in this study has permitted a rapid assessment of the effects of low levels of this toxicant on yolk production. The findings indicate that exposure of naturally reproducing female rainbow trout to this low concentration of HCN during early vitellogenesis would eliminate an important source of yolk precursor synthesized in the liver and sequestered by the ovary.     

Effect of increased dietary carbohydrate on selenium metabolism and toxicity in rainbow trout (Salmo gairdneri)

Juvenile trout were reared on either a high available carbohydrate (HC) or low available carbohydrate (LC) diet supplemented with from 0 to 10 micrograms selenium per gram of diet for 16 weeks, to determine if excess liver glycogen deposition affected the metabolism and toxicity of dietary selenium. Trout reared on the HC diet with 10 micrograms selenium per gram diet first demonstrated signs of selenosis and had significantly higher (P less than 0.05) liver selenium levels than trout reared on the LC diet with 10 micrograms selenium per gram diet after 16 weeks, indicating that excess dietary carbohydrate enhances dietary selenium toxicity in trout. The mechanism of the interaction is unclear since neither selenium elimination rates nor carcass and kidney selenium levels were affected by the dietary carbohydrate level. Trout reared on high dietary selenium diets (10 micrograms/g) had an increased incidence of renal calcinosis. In addition, liver copper levels were significantly affected by both dietary selenium and liver glycogen content indicating a significant copper-selenium and copper-glycogen interaction in trout. The development of renal calcinosis and the copper interactions suggest a variety of toxic effects of selenium on trout that may all be responsible for the observed changes in growth and feed efficiency.     

Urea cycle activity and arginine formation in rainbow trout (Salmo gairdneri)

Studies were conducted to determine whether rainbow trout fingerlings possess the ability to synthesize arginine via the urea cycle. Several urea cycle enzymes were detected in trout tissues. An experiment was conducted to determine whether the enzymes increase in response to starvation or in response to dietary protein level (0, 30, 40, 50% protein). Although some effects were observed, they did not appear to be consistent with the function of the urea cycle as a mechanism of detoxifying ammonia in the fish. The activities of kidney arginase and liver and muscle carbamoyl phosphate synthetase (CPS) were higher (P less than 0.05) when protein was omitted from the diet (P less than 0.05) than when it was present but were unaffected by protein level otherwise. The activities of liver arginase and kidney and muscle CPS and ornithine transcarbamoylase (OTC) were higher (P less than 0.05) in starved fish than in fish that received adequate levels of protein. Liver CPS and OTC were lower in starved fish than in fish fed 30% protein. L-[l-14C]ornithine hydrochloride and L-[carbamoyl-14C]citrulline, injected intraperitoneally, were incorporated into tissue arginine, a finding consistent with arginine biosynthesis via the urea cycle. When one-half of dietary arginine was replaced by equimolar amounts of glutamic acid, ornithine or citrulline, glutamic acid markedly reduced growth (P less than 0.05), whereas growth was depressed only slightly by ornithine (P less than 0.05) and not depressed by citrulline (P greater than 0.05). We conclude that trout have a urea cycle that provides for potential arginine biosynthesis.     

Tritium dynamics in juvenile rainbow trout, Salmo gairdneri

Juvenile rainbow trout, Salmo gairdneri, were maintained in tritiated water, fed a tritiated diet or both, and the specific activity of 3H in the fish was determined during and following 3H exposure. Tissue water 3H-equilibrated rapidly with the ambient water (estimated half-life less than 30 min) and maintained a steady-state specific activity similar to ambient. In contrast, the steady-state specific activity of organically bound 3H was significantly affected by that of the diet. The steady-state specific activity of organically bound 3H of trout maintained in tritiated water but fed non-tritiated diets was approximately 20% of that of the ambient water. This steady-state specific activity was achieved relatively quickly (half-life approximately 1 d) and presumably reflects the exchangeable H of the fish. For trout fed a tritiated diet, in either tritiated or non-tritiated water, steady-state specific activities of organically bound 3H were on the order of 80% of that of the diet. These steady-state specific activities were reached much more slowly (estimated half-lives of 18-32 d) and are likely to represent the accumulation of non-exchangeable 3H in the organic material of the trout.     

The effects of dietary tryptophan levels on growth and metabolism of rainbow trout (Salmo gairdneri)

Groups of rainbow trout (Salmo gairdneri) (mean weight 14 g) were given diets containing 0.8, 1.3, 2, 3, 4 or 6 g tryptophan/kg diet for 12 weeks. By analysis of the growth results, the dietary requirement of tryptophan was found to be 2.5 g/kg diet (equivalent to 50 mg/kg biomass per d). Carbon dioxide expired by trout following intraperitoneal injection of [14COOH]tryptophan contained little radioactivity when dietary tryptophan level was low but, above 2.0 g/kg diet, it increased rapidly with increasing dietary tryptophan level. The break point in the dose-response curve did not, however, coincide with that from the growth results. Changes in concentrations of free tryptophan in blood and liver and activity of hepatic tryptophan pyrrolase (EC 1. 13. 11. 11) in response to changes in dietary tryptophan concentration did not provide reliable indicators for quantifying dietary requirement. Unlike the situation in mammals, blood tryptophan was not protein-bound to any appreciable extent. Tryptophan pyrrolase of trout has properties which suggest it has no apoenzyme form. In fish given adequate levels of tryptophan injected intraperitoneally with a tracer dose of [14COOH]tryptophan, 60% of the dose was incorporated into body protein within 1 d. The turnover of the label in this protein is very slow. Those trout given diets deficient in tryptophan suffered from severe scoliosis and lordosis as well as having increased liver and kidney levels of calcium, magnesium, sodium and potassium.     

Effect of Maillard browning reaction on protein utilization and plasma amino acid response by rainbow trout (Salmo gairdneri)

The effect of the Maillard browning reaction in the diet of rainbow trout (Salmo gairdneri) on growth and amino acid availability was investigated. Chemical and enzymatic hydrolysis methods were applied for the detection of the losses of amino acids in a model protein browning system. Arginine and lysine exhibited the greatest losses in the mixture of fish protein isolate and glucose stored for 40 d at 37 degrees C. The apparent digestibility and absorption of individual amino acids, particularly lysine, was lower in trout fed browned protein than in those fed the control protein. Plasma lysine levels were significantly depressed, while the plasma levels of glucose and most other amino acids were elevated in relation to the loss in nutritive value of dietary protein after browning. The early Maillard reaction derivative of lysine, epsilon-deoxy-fructosyl-lysine, was recovered from browned protein (by using the in vitro enzymatic hydrolysis procedure) and from the plasma of trout fed browned protein. Analysis of plasma free amino acids provided an indication of lysine bioavailability and identified lysine as the first-limiting amino acid in the diets containing browned protein.     

Ammonia toxicity mechanism in fish: Studies on rainbow trout (Salmo gairdneri Rich.)

Salmo gairdneri specimens were exposed for 4–48 hr to various environmental un-ionized ammonia (UIA) concentrations. In the brain of NH₃-treated trout glutamate, GABA, total sugars, ATP, NADH, and succinate decrease, while tissue NH₃ content, glutamine, and lactate increase. In the liver total sugars, succinate, and lactate decrease, while tissue NH₃, glutamine, and the taurine/glycine ratio increase. Such variations depend upon exposure time and environmental UIA level. Ammonia toxicity mechanism in fish is discussed and compared with the one proposed in mammals. Further data obtained from overturned specimens suggest that in these animals a cerebral hypoxic phenomenon also occurs.