Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
1977460 | Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology | 2011 | 5 Pages |
Abstract
While swimming endurance (critical swimming speed or Ucrit) 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. Ucrit decreased in both the 6Â mg/L and 12Â mg/L DNP groups, with 12Â mg/L approaching the LC50. 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.
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Authors
Jordan S. Marit, Lynn P. Weber,