Document Type


Degree Name

Master of Science (MSc)



Program Name/Specialization

Integrative Biology


Faculty of Science

First Advisor

Dr. Michael Wilkie

Advisor Role



The lampricide 3-trifluoromethyl-4-nitrophenol (TFM) has been used for decades to control invasive sea lamprey (Petromyzon marinus) populations in the Great Lakes, normally with little harm to other fish populations. However, due to the nature of lampricide treatments and the chemical properties of TFM, adverse effects to non-target fishes and non-target mortality occasionally occur. However, investigations of non-target mortality can be complex, particularly if fish deaths are not noticed immediately, due to decomposition of the carcasses. The objectives of this thesis were to expose rainbow trout (Oncorhynchsus mykiss) to TFM in order to: (i) identify forensic markers of lampricide toxicity and (ii) determine the stability of these markers when the fish carcass was decomposing in air or water, at different temperatures (4°C, 15°C or 20°C). To complete these objectives, LC-MS/MS was used to determine the concentration of TFM and the relative amounts of TFM metabolites in the liver and white muscle of rainbow trout exposed to their 9-h LC50 of TFM (the concentration of TFM that results in 50% mortality during a 9 h exposure) for 6 h. These experiments showed that the greatest accumulation of TFM occurred in the liver, in which concentrations were 15-30 fold greater than in the white muscle tissue. These observations were likely the result of the much higher blood flow to the liver compared to the muscle, and the likely presence of organic anion transporters in the hepatocytes of the liver, which would facilitate TFM uptake and other xenobiotics. Although TFM accumulation was greatest in the liver, concentrations were found to be most stable in white muscle during decomposition in both water and air, which was likely due to the muscle tissues relative isolation from the GI tract of the fish and as such the anaerobic bacteria responsible for initiating putrefaction. TFM and TFM-metabolite levels (TFM-glucuronide, TFM-sulphate) were stable in both liver and muscle at 4°C over 72 h in water. However, liver TFM concentration declined by approximately 50% when decomposition took place at 15°C and 20°C. Similar 50 % reductions in liver TFM took place in air, but proceeded more rapidly at warmer temperatures (15°C, 20°C). In white muscle, however, TFM concentrations were stable over the 24 h decomposition period in air, despite significant signs of tissue putrefaction occurring. The metabolites of TFM, TFM-glucuronide and TFM-sulphate, were also detected but much less stable in both liver and muscle, particularly at warm temperatures. It is concluded that white muscle and liver tissue should be collected from the carcasses as quickly as possible following suspected incidents of TFM-induced non-target mortality, and that TFM concentrations in both tissues are reliable forensic markers of TFM toxicity.

Convocation Year