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.
Rapid evolution of pest, pathogen, and wildlife populations can have undesirable effects, for example, when insects evolve resistance to pesticides or fishes evolve smaller body size in response to harvest. A destructive invasive species in the Laurentian Great Lakes, the sea lamprey (Petromyzon marinus) has been controlled with the pesticide 3-trifluoromethyl-4-nitrophenol (TFM) since the 1950s. We evaluated the likelihood of sea lamprey evolving resistance to TFM by (i) reviewing sea lamprey life history and control; (ii) identifying physiological and behavioural resistance strategies; (iii) estimating the strength of selection from TFM; (iv) assessing the timeline for evolution; and (v) analyzing historical toxicity data for evidence of resistance. The number of sea lamprey generations exposed to TFM was within the range observed for fish populations where rapid evolution has occurred. Mortality from TFM was estimated as 82%–90%, suggesting significant selective pressure. However, 57 years of toxicity data revealed no increase in lethal concentrations of TFM. Vigilance and the development of alternative controls are required to prevent this aquatic invasive species from evolving strategies to evade control.
Bisphenol A (BPA) is widely used in the manufacture of plastics and epoxy resins and is prevalent in the aquatic environment. BPA disrupts endocrine pathways in fish, but the long-term developmental implications are unknown. We demonstrate that BPA deposition in the eggs of rainbow trout (Oncorhynchus mykiss), an ecologically and economically important species of fish, reprograms liver metabolism in the offspring and alters the developmental growth trajectory in two generations. Specifically, BPA reduces growth during early development, followed by a catch-up growth post-juveniles. More importantly, we observed a developmental shift in the liver transcriptome, including an increased propensity for protein breakdown during early life stages to lipid and cholesterol synthesis post- juveniles. The liver molecular responses corresponded with the transient growth phenotypes observed in the F1 generation, and this was also evident in the F2 generation. Altogether, maternal and/or ancestral embryonic exposure to BPA affects liver metabolism leading to development-distinct effects on growth, underscoring the need for novel risk assessment strategies for this chemical in the aquatic environment. This is particularly applicable to migratory species, such as salmon, where distinct temporal changes in growth and physiology during development are critical for their spawning success.
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