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Comp Biochem Physiol C Toxicol Pharmacol. 2014 Mar;160:30-41. doi: 10.1016/j.cbpc.2013.10.002. Epub 2013 Oct 28.

The effects of the lampricide 3-trifluoromethyl-4-nitrophenol (TFM) on fuel stores and ion balance in a non-target fish, the rainbow trout (Oncorhynchus mykiss).

Author information

  • 1Department of Biology and the Institute for Water Science, Wilfrid Laurier University, 75 University Avenue West, Waterloo, Ontario N2L 3C5, Canada. Electronic address: obirceanu@gmail.com.
  • 2Department of Biology and the Institute for Water Science, Wilfrid Laurier University, 75 University Avenue West, Waterloo, Ontario N2L 3C5, Canada. Electronic address: sore1010@mylaurier.ca.
  • 3Department of Biology and the Institute for Water Science, Wilfrid Laurier University, 75 University Avenue West, Waterloo, Ontario N2L 3C5, Canada. Electronic address: mhenry@teraenv.com.
  • 4Department of Biology, McMaster University, 1280 Main Street West, Hamilton, Ontario L8S 4L8, Canada. Electronic address: grantm@mcmaster.ca.
  • 5Department of Biology, Queen's University, 99 University Avenue, Kingston, Ontario K7L 3N6, Canada. Electronic address: yuxiangw@queensu.ca.
  • 6Department of Biology and the Institute for Water Science, Wilfrid Laurier University, 75 University Avenue West, Waterloo, Ontario N2L 3C5, Canada. Electronic address: mwilkie@wlu.ca.

Abstract

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.

© 2013.

KEYWORDS:

3-trifluoromethyl-4-nitrophenol; ATP; Biotransformation; Gill; Glucuronidation; Glycogen; Great Lakes; Hard water; Invasive species; Lampricide; Oxidative phosphorylation; Phosphocreatine; Rainbow trout; Sea lamprey control

PMID:
24177273
[PubMed - indexed for MEDLINE]
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