| Summary: | Previous studies at the Key Lake uranium mill (Saskatchewan, Canada) suggested the complex effluent discharged alters energetic stores of resident fish species. A second study at the same site demonstrated certain fish from lakes downstream of the mill produce larvae with elevated incidence of developmental deformities. The mechanisms by which energy homeostasis is affected in fish downstream of the Key Lake uranium mill are unknown, and the effects of deformities and altered metabolism on swimming ability have not been explored. Therefore, the overall objective of this thesis was to investigate whether effluent exposed fish exhibited differences in swimming performance and energy homeostasis.
To achieve this objective two experiments were conducted. In the first experiment juvenile spottail shiner (Notropis hudsonius) were collected from a lake downstream of the Key Lake uranium mill, and compared to fish collected from a nearby reference lake. In the second experiment larvae were collected from laboratory raised fathead minnow (Pimephales promelas) exposed to 5% diluted uranium mill effluent or control (dechlorinated municipal) water, and reared in the same treatments to 60 days post hatch (dph). No gross deformities were observed in any fish, and only shiner collected from the exposure lake in the field experiment had enlarged heart ventricles relative to body size compared to fish from the reference lake. Swimming performance was similar between shiner from the exposure and reference lakes in the field study, but effluent exposure impaired swimming ability in 60 dph fathead minnow in the laboratory experiment compared to fish from the control water treatment. After swimming performance tests fish were considered fatigued and metabolic endpoints were compared to non-fatigued fish. In both non-fatigued and fatigued shiner, liver glycogen was significantly greater in fish collected from the exposure lake compared to the reference lake. There was no difference in liver triglycerides in non-fatigued shiner between lakes, but liver triglycerides decreased after swimming in the field study reference fish. Muscle energy stores were unaffected by site or swimming in the field experiment. Conversely, whole body triglycerides and glycogen were similar between treatments in non-fatigued fathead minnow in the laboratory experiment. Swimming significantly decreased whole body triglycerides in fathead minnow from both treatments, but whole body glycogen was unaffected. In the field experiment blood endpoints (hematocrit, plasma glucose, lactate) in fatigued and non-fatigued shiner from both lakes further supported the possibility of altered intermediary metabolism or blunted stress response in fish downstream of the Key Lake uranium mill. In the field study, shiner muscle citrate synthase activity (an indicator of tissue aerobic capacity) was similar between lakes, but muscle âhydroxyacyl coenzyme A dehydrogenase activity (an indicator of tissue lipolytic capacity) was elevated. In contrast, laboratory fathead minnow whole body âhydroxyacyl coenzyme A dehydrogenase activity was similar between treatments, but citrate synthase activity was significantly lower in fathead minnow from the 5% effluent treatment.
In summary, shiner from the exposure lake in the field experiment had similar swimming endurance and greater energy stores compared to fish from the reference lake, despite metabolic alterations. Fathead minnow from the 5% effluent treatment in the laboratory experiment had reduced swimming endurance that was matched by reduced whole body citrate synthase activity, but no other metabolic alterations were observed. Therefore, effluent exposure caused metabolic alterations in both fathead minnow and shiner, but specific effects between experiments were inconsistent. Overall, the physiological significance of the metabolic and swimming effects of effluent exposure is unclear, but suggests discharged effluent has the potential to negatively affect wild fish survivability.
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