Toxaphene Effects on Growth and Development of Brook Trout (Salvelinus fontinalis)

1975 ◽  
Vol 32 (5) ◽  
pp. 609-613 ◽  
Author(s):  
Paul M. Mehrle ◽  
Foster L. Mayer Jr.

Twenty-two days before hatching, eyed eggs of brook trout (Salvelinus fontinalis) were placed in a flow-through system and continuously exposed to toxaphene (0, 39, 68, 139, 288, and 502 ng/liter) until they hatched and the resulting fry were exposed for a further 90 days. Hatchability was not affected by toxaphene, but all of the fry exposed to 502 and 288 ng/liter of toxaphene died by 30 and 60 days after hatch, respectively. Growth of fry was significantly depressed at the 139 and 288 ng/liter concentrations 30 days after hatch and at all concentrations after 60 and 90 days of toxaphene exposure.Whole body collagen of fry, as estimated by hydroxyproline, was significantly decreased in the four higher concentrations of toxaphene within 7–15 days after hatch. Backbone collagen was significantly decreased (P < 0.05) in 30-, 60-, and 90-day-old fry exposed to toxaphene, whereas calcium and phosphorus concentrations in the backbone were increased (P < 0.05). The mineral: collagen ratio was significantly increased by toxaphene. The whole body collagen of sac-fry was a good predictor of later growth and development of brook trout.

1988 ◽  
Vol 45 (9) ◽  
pp. 1587-1596 ◽  
Author(s):  
C. M. Wood ◽  
D. G. McDonald ◽  
C. E. Booth ◽  
B. P. Simons ◽  
C. G. Ingersoll ◽  
...  

Brook trout (Salvelinus fontinalis) adapt to chronic sublethal acid/Al stress. The accompanying acclimation confers greater resistance to short-term increases in Al and acidity. Adult trout were exposed in flowing soft water to eight combinations of pH (6.5, 5.2) × Ca2+ (25, 400 μequiv/L) × Al (0, 75, 150 μg/L = 0, 2.8, 5.6 μmol/L). After 10 wk, blood sampling by caudal puncture revealed no significant variations in osmolality, plasma protein, or hemoglobin and only minor differences [Formula: see text] in plasma Na+ and Cl−. Overall, most electrolytes were higher in fish exposed to higher water Al and/or Ca2+; only plasma Ca2+ was directly depressed by low pH. Hematocrit was raised by both low pH and elevated Al. When trout naive to both acid and Al were challenged with pH = 4.8, Al = 333 μg/L under flow-through conditions, there were large negative whole-body Na+ fluxes and marked depressions of plasma Na+ and Cl−, hemoconcentration, and substantial mortality over 48 h. Prior exposure for 10 wk to pH = 5.2 plus either 75 or 150 μg Al/L prevented mortality and ameliorated or abolished these effects through a more rapid recovery of net Na+ balance. Prior exposure to pH = 5.2 alone ameliorated these effects only slightly.


1973 ◽  
Vol 30 (12) ◽  
pp. 1811-1817 ◽  
Author(s):  
Roger O. Hermanutz ◽  
Leonard H. Mueller ◽  
Kenneth D. Kempfert

The toxic effects of captan on survival, growth, and reproduction of fathead minnows (Pimephales promelas) and on survival of bluegills (Lepomis macrochirus) and brook trout (Salvelinus fontinalis) were determined in a flow-through system. In a 45-week exposure of fathead minnows, survival and growth were adversely affected at 39.5 μg/liter. Adverse effects on spawning were suspected but not statistically demonstrated at 39.5 and 16.5 μg/liter. The maximum acceptable toxicant concentration (MATC), based on survival and growth, lies between 39.5 and 16.5 μg/liter. The lethal threshold concentration (LTC) derived from acute exposures was 64 μg/liter, resulting in an application factor (MATC/LTC) between 0.26 and 0.62. LTC values for the bluegill and brook trout were 72 and 29 μg/liter, respectively. The estimated MATC is between 44.6 and 18.7 μg/liter for the bluegill and between 18.0 and 7.5 μg/liter for the brook trout.The half-life of captan in Lake Superior water with a pH of 7.6 is about 7 hr at 12 C and about 1 hr at 25 C. Breakdown products from an initial 550 μg/liter of captan were not lethal to 3-month-old fathead minnows.


1990 ◽  
Vol 47 (8) ◽  
pp. 1593-1603 ◽  
Author(s):  
C. M. Wood ◽  
D. G. McDonald ◽  
C. G. Ingersoll ◽  
D. R. Mount ◽  
O. E. Johannsson ◽  
...  

Water Ca, rather than pH or Al, was the most important factor affecting whole body electrolyte levels in fry exposed from fertilization to swim-up (91 d) to 84 combinations of pH (6.5, 5.2, 4.8, 4.4, 4.0), Ca (0.5, 1, 2, 8 mg/L), and Al (0, 12, 37, 111, 333, 1000 μg/L) in flowing soft water. Aluminum accumulation occurred only at water Al levels > 111 μg/L; Al accumulation was inhibited both by increasing Ca and decreasing pH. Under control conditions (pH = 6.5, Ca = 2 mg/L, Al = 0 μg/L), whole body Na, Cl, K, and Ca levels all increased greatly during development, while Mg decreased. Body Ca levels were elevated up to 3-fold, and Na, Cl, and K up to 2-fold by increasing water Ca at the same pH and Al. Low pH had a small negative influence, intermediate levels of Al (37, 111) a slight positive influence, and higher levels of Al a negative influence on Na, Cl, K, and Ca levels. Whole body Mg showed opposite trends, reflecting delayed development under adverse conditions. At pH = 6.5, the positive influence of increasing water Ca on most whole body ions showed a clear threshold between 0.5 and 1 mg/L. At lower pH, this threshold was shifted to between 2 and 8 mg/L, indicating that Ca levels sufficient to support healthy development at circumneutral pH may prove inadequate under acidified conditions.


1978 ◽  
Vol 35 (8) ◽  
pp. 1084-1088 ◽  
Author(s):  
Wilbur L. Mauck ◽  
Paul M. Mehrle ◽  
Foster L. Mayer

Eyed eggs of brook trout (Salvelinus fontinalis) were exposed to Aroclor® 1254 (0.43–13 μg/L) for 10 d before hatching and the fry for 118 d after hatching. Median hatching time, egg hatchability, and sac fry survival were not affected by Aroclor 1254. At 48 d after hatching, growth was significantly (P < 0.05) decreased by Aroclor 1254 concentrations ≥ 1.5 μg/L, but no significant differences in growth of surviving fry were observed at the end of the 118-d exposure. Mortality occurred in fry exposed to 13 μg/L within 48 d of exposure, and after 118 d of exposure significant mortality occurred in the three highest concentrations. Biochemical constituents in brook trout fry related to growth and development were affected by Aroclor 1254. Hydroxyproline and vitamin C concentrations in sac fry (38 d old) were decreased by ≥ 3.1 μg/L. Backbone development in fry exposed for 118 d was significantly altered. Collagen was significantly decreased in the backbone as was the phosphorous concentration, while the calcium concentration increased. Hydroxyproline concentration in collagen isolated from the backbone was also decreased. The no-effect exposure concentration on backbone composition was < 0.43 μg/L. Whole body residues in fry exposed for 118 d were 40 000 to 47 000 times the concentration in water. Key words: brook trout, Salvelinus fontinalis, Aroclor® 1254, polychlorinated biphenyls, PCB, growth, bone development, vitamin C, collagen


1988 ◽  
Vol 45 (9) ◽  
pp. 1575-1586 ◽  
Author(s):  
C. M. Wood ◽  
R. C. Playle ◽  
B. P. Simons ◽  
G. G. Goss ◽  
D. G. McDonald

The relative importance of ionoregulatory and respiratory disturbances in brook trout (Salvelinus fontinalis) under acid/Al stress in soft water is dependent upon water pH and Ca2+ levels. Trout acclimated to Ca2+ = 25 or 400 μequiv/L were fitted with arterial catheters and exposed to acid/Al for 10 d under flow-through conditions. Parameters monitored included pHa, [Formula: see text], [Formula: see text], HCO3−, ΔH+m, Na+, Cl−, K+, Ca2+, protein, lactate, glucose, hemoglobin, and hematocrit. Exposure to pH = 4.8 (no Al) at Ca2+ = 25 μequiv/L caused no mortality and negligible physiological disturbance. Addition of Al (333 μg/L or 12.3 μmol/L) resulted in >80% mortality (LT50 = 39.0 h) preceded by a marked decrease of plasma Na+ and Cl−, a moderate disturbance of blood gases, but no acidosis. At higher Ca2+ (400 μequiv/L), this same exposure (pH = 4.8, Al = 333 μg/L) caused similar mortality (LT50 = 38.5 h) but smaller ionic disturbances, much larger decreases in blood O2, increases in blood CO2, and respiratory acidosis. Exposure to pH = 4.4 (no Al) at Ca2+ = 25 μequiv/L caused 60% mortality (LT50 = 170.0) preceded by marked ionic disturbances and metabolic acidosis, but little change in blood gases. Addition of Al (333 μg/L) increased mortality to >80% (LT50 = 78.2 h) with smaller ionic but greater respiratory disturbances.


1988 ◽  
Vol 45 (7) ◽  
pp. 1212-1221 ◽  
Author(s):  
J. N. Fryer ◽  
W. H. Tam ◽  
B. Valentine ◽  
R. E. Tikkala

Twelve-month-old brook trout (Salvelinus fontinalis) of both sexes were exposed to acidified water (pH 4 5) for a period of 52 d. Ultrastructural morphometric studies of the prolactin cells of the pituitaries of acid-stressed female trout revealed a reduction, after a latent period of about 1 wk, in prolactin cell area, cytoplasmic area and nuclear area which gradually recovered to control values by day 52 of acid exposure. In both male and female trout, acid exposure resulted in significant decreases in plasma osmolarity, and plasma sodium, which gradually returned to control values by day 52 of the study. Total plasma calcium was not altered by acid exposure in either male or female trout. For both male and female trout, acid exposure resulted in transient elevations in haematocrit and a prolonged suppression of blood pH. The whole-body sodium efflux for trout introduced into dechlorinated tap water or distilled water was significantly greater at pH 4.5 than at pH 7.35. Possible relationships between the acid-induced inhibition of the secretory activity of the prolactin cells and impairments in osmotic and ionic regulation observed in acid-stressed trout are discussed.


1989 ◽  
Vol 46 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Lawrence R. Curtis ◽  
Wayne K. Seim ◽  
Lisbeth K. Siddens ◽  
Debra A. Meager ◽  
Richard A. Carchman ◽  
...  

Acidification of streams and rivers associated with rainstorm or snowmelt events is often episodic as are many environmental introductions of toxic substances. We examined the toxicity of continuous or intermittent exposures to sulfuric acid (H+) to brook trout (Salvelinus fontinalis) embryos, alevins, and fry. Acute toxicity tests were conducted with juvenile rainbow trout (Salmo gairdneri). These studies permitted evaluation of key components of intermittent exposures (toxicant concentration, exposure duration, and recovery period) on mortality, reduced growth, and perturbed electrolyte balance. Lethality of H+ markedly changed with developmental stage of brook trout. Resistance of the chorion to H+ penetration probably protected embryonic fish, while hatching and onset of active swimming exacerbated H+ toxicity. Response surface methods demonstrated that between pH 4 and 7, time–concentration relationships for H+ toxicity were greatly influenced by exposure duration and peak concentration but little by length of recovery period. Daily pulses at pH 4 with duration as short 4.5 h produced marked mortality after 90 d. This did not occur after 4–60 d of testing. Whole-body Na+, K+, and Ca2+ concentrations of brook trout were negatively correlated with mean H+ concentrations after 90 d of exposure. Cation depletion appeared to be a more sensitive index of chronic, sublethal H+ toxicity than reduced growth.


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