Prolonged Oral Administration of Methyl Mercury Chloride to Rainbow Trout (Salmo gairdneri) Fingerlings

1975 ◽  
Vol 32 (11) ◽  
pp. 2015-2023 ◽  
Author(s):  
G. Wobeser

Rainbow trout (Salmo gairdneri) fingerlings were fed rations containing 4, 8, 16, and 24 ppm mercury as methyl mercury chloride over a 105-day period. Fish receiving the 16- and 24-ppm rations had significantly higher blood packed cell volumes than did controls. Hyperplasia of the gill epithelium was the only morphologic alteration detected in these fish. Individual fish accumulated up to 30 ppm mercury in muscle tissue, but no mortality that could be attributed to mercury occurred.The results suggest that trout can tolerate a large body burden of mercury, if this mercury is acquired over a period of time.


1975 ◽  
Vol 32 (11) ◽  
pp. 2005-2013 ◽  
Author(s):  
G. Wobeser

The median tolerance limit (MTL) for methyl mercury chloride at 24, 48, and 96 h was 0.084, 0.045, and 0.024 mg/liter as mercury, respectively, for fry; and 0.125, 0.066, and 0.042 mg/liter as mercury, respectively, for fingerlings. The MTL (24 h) for mercuric chloride for fingerlings was 0.90 mg/liter as mercury. Fingerlings exposed to methyl mercury chloride concentrated mercury in their tissues much more rapidly than did those exposed to mercuric chloride. The acute toxic action of both compounds was exerted on the gills. Mercuric chloride caused severe epithelial necrosis. Poisoning by methyl mercuric chloride was characterized by epithelial cell swelling and hyperplasia, a marked increase in the number of epithelial cells in mitosis, and terminal epithelial desquamation.





1978 ◽  
Vol 72 (1) ◽  
pp. 17-24
Author(s):  
M. S. Haswell ◽  
D. J. Randall

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.



1982 ◽  
Vol 60 (12) ◽  
pp. 3127-3133 ◽  
Author(s):  
Craig W. Hawryshyn ◽  
William C. Mackay ◽  
Thomy H. Nilsson

Scotopic spectral sensitivity of 15 rainbow trout was determined using a two-choice, operant-conditioning task. Maximum sensitivity occurred at 525 nm and generally declined at longer and shorter wavelengths with evidence of a "shoulder" at 600–650 nm. Fifteen days after injection with either saline control (n = 4) or 4.6–6.2 mg of methyl mercury chloride per kilogram of body weight (n = 9); measurements of response latency and trials to criterion revealed that methyl mercury (MEHG) did not affect memory or motor performance. MEHG did produce significant spectrally uniform decrements in visual sensitivity. These results suggest that MEHG impaired both the scotopic and photopic mechanisms of MEHG-treated rainbow trout.



1983 ◽  
Vol 40 (11) ◽  
pp. 1987-1994 ◽  
Author(s):  
J. W. Hilton ◽  
P. V. Hodson ◽  
H. E. Braun ◽  
J. L. Leatherland ◽  
S. J. Slinger

Juvenile rainbow trout were reared for 24 wk on practical-type diets formulated with fish meals derived from coho salmon (Oncorhynchus kisutch) taken from Lake Michigan, Lake Ontario, and the Pacific Ocean. Levels of contaminants (DDT, chlordane, dieldrin, mirex, and PCBs) increased 10-fold from control and Pacific Ocean salmon-based diets to Lake Ontario salmon-based diets. Rainbow trout accumulated contaminants in direct proportion to dietary levels. However, there were no significant differences in the final body weights, feed to gain ratios, or mortality rates of the trout reared on the different test diets. No signs of abnormal behavior or any indication of histopathological abnormalities were observed in any of the fish. There were no signs of thyroid hyperplasia or any significant decline in serum T3 or T4 levels with increasing dietary contaminant levels. Therefore, rainbow trout do not appear to have been affected by the uptake and accumulation of contaminants. However, the trout did not appear to regulate their body burden of contaminants; this ultimately could prove to be toxic and may adversely affect the ability of these fish to reproduce and survive. The final concentrations of mirex and PCBs in the Lake Ontario-fed fish exceeded the allowed limits to protect human health; therefore, fish meals produced from Lake Ontario salmon are unsuitable as a source of feed for aquaculture of rainbow trout intended for human consumption.



1984 ◽  
Vol 41 (11) ◽  
pp. 1592-1600 ◽  
Author(s):  
Karl D. Shearer

By examining a group of rainbow trout (Salmo gairdneri) over their life cycle (ova to 1500 g), 1 found that their elemental composition was determined by fish size, stage of life cycle (prefeeding, juvenile, post-juvenile), and reproductive state. Fish were fed practical diets and were reared under hatchery conditions. Whole body elemental concentrations of Ca, Cu, Fe, K, Mg, Mn, Na, P, Sr, and Zn were size dependent prior to sexual maturity. Rates of elemental accumulation in relation to weight gain were higher in juveniles than in adult fish. Reduced somatic concentrations of Mn, Fe, and Zn were observed during gonad maturation in female but not in male trout. Tissue concentrations of some elements remained constant over the duration of the study, while others increased or decreased linearly with increasing fish size. Tables and equations 1 present will enable the normal tissue and whole body elemental composition of rainbow trout at any size to be determined. My results indicate that body burden or wet weight concentration are better indicators of elemental status than dry weight concentration and that comparison of elemental levels between treatment groups in dietary experiments should be made on the basis of a standard-sized fish or by comparing the rates of elemental deposition with growth.



1984 ◽  
Vol 41 (12) ◽  
pp. 1768-1773 ◽  
Author(s):  
S. F. Perry ◽  
P. Payan ◽  
J. P. Girard

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.



1973 ◽  
Vol 30 (10) ◽  
pp. 1575-1578 ◽  
Author(s):  
Kenneth R. Olson ◽  
Paul O. Fromm

Mercury was found in gills of rainbow trout (Salmo gairdneri) which had been exposed to inorganic mercury but not in those exposed to methyl mercury. No specific site for mercury uptake was identified and it is suggested that inorganic mercury enters the gill across the general lamellar surface. High concentrations were found associated with the gill cartilage. Since little ion diffusion occurs during tissue preparation, localization and/or identification of tissues can be accomplished by scans for various elements: sodium (Na), potassium (K), chlorine (Cl), and sulfur (S). The technique is not suitable for identification of highly volatile compounds such as methyl mercury due to the necessity of subjecting tissues to high vacuum conditions, however, we believe electron probe analyses should be useful in studies of active ion transport systems in gill tissue and in investigations of the effects of heavy metal pollutants on fishes.



1988 ◽  
Vol 45 (1) ◽  
pp. 32-41 ◽  
Author(s):  
D. J. Spry ◽  
P. V. Hodson ◽  
C. M. Wood

Rainbow trout, Salmo gairdneri, were fed purified diets with zinc concentrations ranging from deficient to excessive (1, 90, 590 μg Zn∙g−1) and simultaneously exposed to a range of waterborne [Zn] (7, 39, 148, 529 μg Zn∙L−1). After 1 wk, fish fed the deficient diet, at ambient waterborne [Zn], had low plasma [Zn] which decreased further during the 16-wk experiment. Growth ceased after 12 wk; hematocrit and plasma protein were depressed. Both whole body [Zn] and body burden decreased by 16 wk, but most other elements were elevated. Increasing waterborne [Zn] alone increased plasma [Zn], whole body [Zn], and growth in a graded manner and normalized hematocrit, plasma protein, and other whole body elements. Increasing dietary [Zn] to 90 μg Zn∙g−1 at ambient waterborne [Zn] prevented depression of plasma [Zn] and permitted normal growth and whole body [Zn]. Zinc uptake from water, probably across the gills, was independent of uptake from the diet since at any dietary [Zn], increasing the waterborne [Zn] resulted in increased whole body [Zn]. Even when dietary [Zn] was adequate, the waterborne contribution was as high as 57%, and 100% when the dietary [Zn] was deficient. There were no toxic effects on any of the variables measured.



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