The pesticide 3-trifluoromethyl-4-nitrophenol (TFM) is used to control sea lamprey (Petromyzon marinus) populations in the Great Lakes through its application to nursery streams containing larval sea lampreys. TFM uncouples oxidative phosphorylation, impairing mitochondrial ATP production in sea lampreys and rainbow trout (Oncorhynchus mykiss). However, little else is known about its sub-lethal effects on non-target aquatic species. The present study tested the hypotheses that TFM exposure in hard water leads to (i) marked depletion of energy stores in metabolically active tissues (brain, muscle, kidney, liver) and (ii) disruption of active ion transport across the gill, adversely affecting electrolyte homeostasis in trout. Exposure of trout to 11.0mgl(-1) TFM (12-h LC50) led to increases in muscle TFM and TFM-glucuronide concentrations, peaking at 9h and 12h, respectively. Muscle and brain glycogen was reduced by 50%, while kidney and muscle lactate increased with TFM exposure. Kidney ATP and phosphocreatine decreased by 50% and 70%, respectively. TFM exposure caused no changes in whole body ion (Na(+), Cl(-), Ca(2+), K(+)) concentrations, gill Na(+)/K(+) ATPase activity, or unidirectional Na(+) movements across the gills. We conclude that TFM causes a mismatch between ATP supply and demand in trout, leading to increased reliance on glycolysis, but it does not have physiologically relevant effects on ion balance in hard water.
For over 50 years, invasive sea lamprey Petromyzon marinus populations have been controlled in the Great Lakes using the pesticide 3-trifluoromethyl-4-nitrophenol (TFM), which is applied to streams containing larval sea lampreys. The specificity of TFM is due to the sea lamprey's relative inability to detoxify it using glucuronidation; this inability causes death by interfering with the production of ATP, the main energy currency of cells. TFM treatments typically last 12 h, but given the sea lamprey's relative inability to detoxify TFM we predicted that TFM-induced homeostatic disturbances and toxicity would occur following shorter periods of exposure. Accordingly, we exposed larval sea lampreys to the 12-h LC99.9 (i.e., the concentration lethal to 99.9% of the test subjects over 12 h) of TFM for 4 or 6 h and monitored the survival and replenishment of energy stores and metabolite concentrations in surviving sea lampreys over a 24-h depuration period. Minimal mortality (∼20%) was observed during the post-TFM recovery, despite respective 50% and 70% reductions in brain and liver ATP, 70-90% decreases in brain phosphocreatine (PCr), and 30-50% reductions in brain and liver glycogen with corresponding increases in lactate. While relatively resistant to TFM, muscle still underwent a 55% decline in PCr. However, energy stores and metabolites returned to preexposure levels 4-12 h after TFM exposure. We conclude that sea lampreys can rapidly restore homeostasis following shorter-term TFM exposure. The resilience of sea lampreys to shorter-term TFM exposure suggests that there is no merit in reducing TFM treatment times from 12 h, which could lead to "treatment residuals" that survive lampricide treatments. This capacity to reverse TFM-induced perturbations also suggests that larvae seen emerging from the stream substrate late in a treatment, or that find refuge near streambanks or in isolated pools, could be another source of treatment residuals, leading to increased sea lamprey parasitism of sport and commercial fisheries in the Great Lakes.
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