PUBLICATION
Acute exposure to 2,4-dinitrophenol alters zebrafish swimming performance and whole body triglyceride levels
- Authors
- Marit, J.S., and Weber, L.P.
- ID
- ZDB-PUB-110405-1
- Date
- 2011
- Source
- Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 154(1): 14-18 (Journal)
- Registered Authors
- Weber, Lynn
- Keywords
- 2,4-dinitrophenol; Critical swimming speed; Swimming motion; Whole body triglycerides; Acute toxicity; Zebrafish
- MeSH Terms
-
- 2,4-Dinitrophenol/toxicity*
- Animals
- Dose-Response Relationship, Drug
- Environmental Monitoring/methods
- Lipid Metabolism/drug effects
- Motor Activity/drug effects*
- Swimming/physiology*
- Triglycerides/metabolism*
- Uncoupling Agents/toxicity
- Water Pollutants, Chemical/toxicity
- Zebrafish/metabolism
- Zebrafish/physiology*
- PubMed
- 21406246 Full text @ Comp. Biochem. Physiol. C Toxicol. Pharmacol.
Citation
Marit, J.S., and Weber, L.P. (2011) Acute exposure to 2,4-dinitrophenol alters zebrafish swimming performance and whole body triglyceride levels. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP. 154(1):14-18.
Abstract
While swimming endurance (critical swimming speed or U(crit)) and lipid stores have both been reported to acutely decrease after exposure to a variety of toxicants, the relationship between these endpoints has not been clearly established. In order to examine these relationships, adult zebrafish (Danio rerio) were aqueously exposed to solvent control (ethanol) or two nominal concentrations of 2,4-dinitrophenol (DNP), a mitochondrial electron transport chain uncoupler, for a 24-h period. Following exposure, fish were placed in a swim tunnel in clean water for swimming testing or euthanized immediately without testing, followed by analysis of whole body triglyceride levels. U(crit) decreased in both the 6mg/L and 12mg/L DNP groups, with 12mg/L approaching the LC(50). A decrease in tail beat frequency was observed without a significant change in tail beat amplitude. In contrast, triglyceride levels were elevated in a concentration-dependent manner in the DNP exposure groups, but only in fish subjected to swimming tests. This increase in triglyceride stores may be due to a direct interference of DNP on lipid catabolism as well as increased triglyceride production when zebrafish were subjected to the co-stressors of swimming and toxicant exposure. Future studies should be directed at determining how acute DNP exposure combines with swimming to cause alterations in triglyceride accumulation.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping