Early Life Stage Mortality Syndrome in Fishes of the Great Lakes and Baltic Sea

<em>Abstract</em>.—Reproductive success and vitamin B<sub>1 </sub>(thiamine pyrophosphate, thiamine monophosphate, and free thiamine) concentrations were assessed in feral female lake trout <em>Salvelinus namaycush </em>from Lake Ontario and Lake Manitou. We monitored fertilization success, survival to hatch, incidence of blue-sac disease, other anomalies, and lake trout early mortality syndrome (EMS). Fertilization and hatching success were high, whereas mortality from blue-sac disease and other anomalies was low in egg batches from both lakes. There was no mortality from EMS in families from Lake Manitou. However, EMS occurred after hatching in the offspring of 48% of the females collected from Lake Ontario. We measured thiamine in liver, red blood cells, eggs, and developing embryos. Relative to fish collected in reference lakes, females in Lake Ontario had depressed hepatic, red blood cell, and egg thiamine concentrations. Although more extensive investigation of thiamine balance is required, it may be possible to use red blood cell thiamine pyrophosphate as a predictive index for EMS susceptibility in offspring. Total thiamine concentrations in developing embryos declined by 50% between fertilization and swim-up. Free thiamine reserves declined most rapidly, whereas levels of thiamine pyrophosphate increased between the eyed embryo and hatch stages. A high proportion (67%) of lake trout families in which the initial egg free thiamine reserves or embryonic concentrations of thiamine pyrophosphate levels were <0.8 nmol/g exhibited EMS. Below this threshold (0.8 nmol/g), the occurrence of EMS was variable (0–100%) and only weakly related to free thiamine concentrations (<em>r</em><sup>2</sup> = 0.32, <EM>P</EM> = 0.014). This observation implies the possibility of additional interactions with other factors.

<em>Abstract</em>.—Dietary amprolium, a thiamine antagonist, was fed to lake trout <em>Salvelinus namaycush </em>broodstock from April to October before spawning to determine its effect on egg and tissue concentrations of thiamine, thiamine monophosphate, and thiamine pyrophosphate. The thiamine concentration of eggs from fish fed no amprolium was 61.8 nmol/g, whereas the concentration of thiamine in fish fed 0.05 and 0.10% amprolium was 4.02 and 1.71 nmol/g (<EM>P </EM>< 0.01), respectively. In lake trout fed 0.10% amprolium beginning in August, egg free thiamine concentration was reduced to 11.6 nmol/g. No sign of early mortality syndrome was observed in sac fry from eggs in this study, which suggests that thiamine concentrations in the egg were not low enough to be below a critical threshold or that factors other than thiamine are involved in early mortality syndrome.


<em>Abstract</em>.—Juvenile and adult lake trout <em>Salvelinus namaycush </em>that were fed semipurified, thiaminedeficient diets or alewives <em>Alosa pseudoharengus </em>containing thiaminase, a thiamine-destroying enzyme, showed no overt symptoms of thiamine deficiency. Growth rates and ovulation rates were similar among all treatments. However, liver thiamine pyrophosphate (TPP), a biochemical indicator of impending thiamine deficiency, in juvenile lake trout fed thiamine-deficient diets was reduced to 35 pmol/ g compared with 59 pmol/g in control groups. Blood TPP in adult female lake trout fed alewives was one-third of that in controls fed a commercial diet. Adult lake trout from Lake Michigan had blood TPP levels similar to those of fish fed the alewife diet in the laboratory. Lake Superior lake trout had TPP levels similar to those of fish fed the control diet in the laboratory. Thiamine synthesis occurred in the intestine of lake trout. At least 81% of thiamine in the posterior intestine was synthesized, presumably by bacteria, when a <sup>14</sup>C-labeled thiamine diet was force-fed to lake trout. Thiamine had a long retention time in the lake trout: at 27 weeks after fish were injected with radioactive thiamine, blood cells retained 11% of the radioactivity that was present at 2 d and liver tissue retained 34% of the 2-d level. Lack of self-sustaining lake trout reproduction by Lake Michigan fish may be related to their lower blood thiamine levels. Thiamine deficiency may cause early mortality syndrome, which is common in Lake Michigan but not Lake Superior fish with higher blood thiamine levels.


<em>Abstract</em>.—By exposing lake trout <em>Salvelinus namaycush </em>and lake sturgeon <em>Acipenser fulvescens </em>to planar organochlorines in the laboratory, we have revealed a relationship between induction of the Phase I or mixed function oxidase enzyme system and oxidative stress. Indices of oxidative stress in fish exposed to organochlorines include depleted tissue stores of antioxidant vitamins and elevated concentrations of membrane breakdown products. Given the historically different organochlorine contaminant concentrations in lake trout from Lakes Ontario and Superior, an examination of Phase I induction and oxidative stress in these populations was warranted. Lake trout from Lake Ontario had greater hepatic and renal Phase I activity and lower concentrations of the antioxidant vitamin tocopherol than lake trout from Lake Superior. Lipid hydroperoxide concentrations, a measure of oxidative membrane breakdown and general oxidative stress, were also significantly higher in liver of lake trout from Lake Ontario. The relationship between oxidative stress in adult lake trout from Lake Ontario and early mortality syndrome (EMS) of their offspring was also examined. The elevated oxidative stress indices found in adult female lake trout from Lake Ontario were not correlated with the appearance of EMS in their offspring. Concentrations of antioxidant vitamins in embryos and depletion of these vitamins throughout development also did not differ between embryos with EMS and those without EMS. Eggs that later developed EMS were initially lighter in color and had lower total carotenoid concentrations. Additional work concerning the relationships of the various proretinoid forms with EMS is required. Although lake trout from Lake Ontario exhibit some oxidative stress responses, EMS among their offspring does not appear to be directly related to oxidative stress or the depletion of antioxidant vitamins.


2003 ◽  
Vol 37 (17) ◽  
pp. 3864-3877 ◽  
Author(s):  
Philip M. Cook ◽  
John A. Robbins ◽  
Douglas D. Endicott ◽  
Keith B. Lodge ◽  
Patrick D. Guiney ◽  
...  

<em>Abstract.—</em>Muscle and egg samples from returning adult female Lake Michigan coho salmon <em>Oncorhynchus kisutch </em>were collected for thiamine analysis. Three groups of five females having low (2.5%), medium (42.4%), or high (92.6%) mean fry survival were selected for this study. Egg and muscle samples were collected at spawning and analyzed by high-performance liquid chromatography analysis for free thiamine, thiamine monophosphate (TP), and thiamine pyrophosphate (TPP). Egg concentrations of ascorbic acid, iron, zinc, magnesium, and potassium were measured. Twenty-five contaminants were also measured in muscle tissue of adult females. Total thiamine levels in eggs were similar between the medium and high survival groups but significantly lower in the low survival group. Eggs from the high and medium survival groups had higher levels of free thiamine and TP (<EM>P </EM>< 0.01) than eggs from the low survival group. There were no significant differences among the three groups in egg TPP. Muscle concentrations of TPP, TP, and total thiamine were similar among the three survival groups (<EM>P </EM>> 0.10). Correlations between fry survival and egg free thiamine (<em>r </em>= 0.61) and TP (<em>r </em>= 0.52) were observed. Fry survival was not correlated with adult muscle concentration of any form of thiamine or contaminant measured. Among the three groups, no differences in egg concentration were found for ascorbic acid, dehydroascorbic acid, iron, magnesium, zinc, and potassium. This research supports the hypothesis that low egg thiamine is an important factor in early mortality syndrome.


1991 ◽  
Vol 48 (5) ◽  
pp. 875-883 ◽  
Author(s):  
Mary K. Walker ◽  
Jan M. Spitsbergen ◽  
James R. Olson ◽  
Richard E. Peterson

Lake trout (Salvelinus namaycush) eggs containing [3H]TCDD concentrations from 0 to 302 parts per trillion (ppt) were observed through the fry stage for TCDD metabolism, elimination, and toxicity. All radioactive residues extracted from eggs and sac fry were due to TCDD; no metabolites were detected. [3H]TCDD was not eliminated from eggs and sac fry, but was rapidly eliminated from fry (t1/2, 35–37 d). Hatchability was less at egg TCDD concentrations [Formula: see text]; however, the greatest TCDD-related mortality occurred during the sac fry stage. In all TCDD groups (34–302 ppt), sac fry that died developed subcutaneous yolk sac edema prior to death, resembling blue-sac disease. The development of yolk sac edema preceded sac fry mortality, and the severity of edema varied directly with cumulative mortality. Based on TCDD concentrations in the egg resulting from a 48-h exposure, the no observable adverse effect level (NOAEL) for mortality was 34 ppt and the lowest observable adverse effect level (LOAEL) was 55 ppt. The TCDD concentration in eggs that caused 50% mortality above control at swim-up (LD50) was 65 ppt. Lake trout sac fry exposed as eggs are more sensitive to the lethal effects of TCDD than any mammalian, avian, or fish species investigated thus far.


2009 ◽  
Vol 21 (4) ◽  
pp. 262-271 ◽  
Author(s):  
Sergiusz Czesny ◽  
John M. Dettmers ◽  
Jacques Rinchard ◽  
Konrad Dabrowski

Sign in / Sign up

Export Citation Format

Share Document