Document Type


Degree Name

Master of Science (MSc)



Program Name/Specialization

Integrative Biology


Faculty of Science

First Advisor

Michael Wilkie

Advisor Role

Thesis Supervisor


The primary method of controlling invasive sea lamprey (Petromyzon marinus) populations in the Great Lakes is the application of the pesticide 3-trifluoromethyl-4-nitrophenol (TFM) to larval lamprey nursery streams. Recent evidence suggests that the mode of toxic action of TFM involves the inhibition of oxidative ATP production in the mitochondria. As a result, there is increased reliance on the anaerobic pathways of ATP production which involves the hydrolysis of phosphocreatine (PCr) and anaerobic glycolysis. TFM may also damage the gills, which may disrupt gill-mediated ion regulation and cause internal ion imbalances. While knowledge of TFM toxicity in larval lampreys has been generated in recent years, little is known about how TFM affects the other major stages of the sea lamprey life cycle. Accordingly, a major objective of this thesis was to determine if differences in the basal energy reserves of larval, parasitic and upstream-migrant sea lampreys affected their TFM sensitivity. Exposure of larval, parasitic and upstream migrant sea lampreys to acutely lethal concentrations of TFM [equivalent to the TFM 12-h LC99.9], caused significant reductions in liver ATP concentrations in all three life stages examined, but brain ATP concentrations were unaffected. Brain ATP concentrations were likely buffered by the high glycogen and PCr stores found in this organ system, which underwent respective 30-40 % and 40-50 % reductions during TFM exposure. These findings further support the hypothesis that TFM causes death by interfering with ATP production, leading to a mismatch between ATP supply and ATP demand. To test the hypothesis that TFM-induced damage to the gills also contributes to TFM toxicity, the unidirectional movements of Na+ across the body of larval and upstream-migrant lampreys, and rainbow trout (Oncorhynchus mykiss) were measured using the radio-tracer 24Na+ during exposure to TFM (12-h LC99.9). The effects of TFM on Na+ influx, outflux and net flux were minor, and plasma ion concentrations in parasitic and upstream-migrant sea lamprey were unaltered. These findings suggest that disruption to gill-mediated ion exchange is not the proximate cause of death during exposure to TFM. This improved understanding the physiological effects of TFM on sea lamprey and rainbow trout could help to better predict the effects of TFM on target and sensitive non-target organisms during routine TFM treatments in the field.

Convocation Year