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Failure of ATP supply to match ATP demand: the mechanism of toxicity of the lampricide, 3-trifluoromethyl-4-nitrophenol (TFM), used to control sea lamprey (Petromyzon marinus) populations in the Great Lakes.
MedLine Citation:
PMID:  19716611     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
Although the pesticide, 3-trifluoromethyl-4-nitrophenol (TFM), has been extensively used to control invasive sea lamprey (Petromyzon marinus) populations in the Great Lakes, it is surprising that its mechanism(s) of toxicity is unresolved. A better knowledge of the mode of toxicity of this pesticide is needed for predicting and improving the effectiveness of TFM treatments on lamprey, and for risk assessments regarding potential adverse effects on invertebrate and vertebrate non-target organisms. We investigated two hypotheses of TFM toxicity in larval sea lamprey. The first was that TFM interferes with oxidative ATP production by mitochondria, causing rapid depletion of energy stores in vital, metabolically active tissues such as the liver and brain. The second was that TFM toxicity resulted from disruption of gill-ion uptake, adversely affecting ion homeostasis. Exposure of larval sea lamprey to 4.6 m gl(-1) TFM (12-h LC50) caused glycogen concentrations in the brain to decrease by 80% after 12h, suggesting that the animals increased their reliance on glycolysis to generate ATP due to a shortfall in ATP supply. This conclusion was reinforced by a 9-fold increase in brain lactate concentration, a 30% decrease in brain ATP concentration, and an 80% decrease in phosphocreatine (PCr) concentration after 9 and 12h. A more pronounced trend was noted in the liver, where glycogen decreased by 85% and ATP was no longer detected after 9 and 12h. TFM led to marginal changes in whole body Na(+), Cl(-), Ca(2+) and K(+), as well as in plasma Na(+) and Cl(-), which were unlikely to have contributed to toxicity. TFM had no adverse effect on Na(+) uptake rates or gill Na(+)/K(+)-ATPase activity. We conclude that TFM toxicity in the sea lamprey is due to a mismatch between ATP consumption and ATP production rates, leading to a depletion of glycogen in the liver and brain, which ultimately leads to neural arrest and death.
Authors:
Oana Birceanu; Grant B McClelland; Yuxiang S Wang; Michael P Wilkie
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-07-23
Journal Detail:
Title:  Aquatic toxicology (Amsterdam, Netherlands)     Volume:  94     ISSN:  1879-1514     ISO Abbreviation:  Aquat. Toxicol.     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2009-09-15     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8500246     Medline TA:  Aquat Toxicol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  265-74     Citation Subset:  IM    
Affiliation:
Department of Biology, Wilfrid Laurier University, 75 University Avenue West, Waterloo, Ontario, N2L 3C5 Canada. obirceanu@gmail.com
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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