Effects of chronic dietary selenomethionine exposure on repeat swimming performance, aerobic metabolism and methionine catabolism in adult zebrafish (Danio rerio)
- Authors
- Thomas, J.K., Wiseman, S., Giesy, J.P., and Janz, D.M.
- ID
- ZDB-PUB-130222-20
- Date
- 2013
- Source
- Aquatic toxicology (Amsterdam, Netherlands) 130-131C: 112-122 (Journal)
- Registered Authors
- Janz, David M.
- Keywords
- selenium, Ucrit, energetics, swim performance, metabolic rate, aerobic scope, zebrafish
- MeSH Terms
-
- Animals
- Behavior, Animal/drug effects
- Dose-Response Relationship, Drug
- Energy Metabolism/drug effects*
- Environmental Exposure*
- Glycogen/metabolism
- Lactic Acid/metabolism
- Real-Time Polymerase Chain Reaction
- Selenomethionine/toxicity*
- Stress, Physiological
- Swimming*
- Toxicity Tests, Chronic
- Triglycerides/metabolism
- Zebrafish/physiology*
- PubMed
- 23399444 Full text @ Aquat. Toxicol.
- CTD
- 23399444
In a previous study we reported impaired swimming performance and greater stored energy in adult zebrafish (Danio rerio) after chronic dietary exposure to selenomethionine (SeMet). The goal of the present study was to further investigate effects of chronic exposure to dietary SeMet on repeat swimming performance, oxygen consumption (MO2), metabolic capacities (standard metabolic rate [SMR], active metabolic rate [AMR], factorial aerobic scope [F-AS] and cost of transport [COT]) and gene expression of energy metabolism and methionine catabolism enzymes in adult zebrafish. Fish were fed SeMet at measured concentrations of 1.3, 3.4, 9.8 or 27.5 µg Se/g dry mass (d.m.) for 90 d. At the end of the exposure period, fish from each treatment group were divided into three subgroups: (a) no swim, (b) swim, and (c) repeat swim. Fish from the no swim group were euthanized immediately at 90 d and whole body triglycerides, glycogen and lactate, and gene expression of energy metabolism and methionine catabolism enzymes were determined. Individual fish from the swim group were placed in a swim tunnel respirometer and swimming performance was assessed by determining the critical swimming speed (Ucrit). After both Ucrit and MO2 analyses, fish were euthanized and whole body energy stores and lactate were determined. Similarly, individual fish from the repeat swim group were subjected to two Ucrit tests (Ucrit-1 and Ucrit-2) performed with a 60 min recovery period between tests, followed by determination of energy stores and lactate. Impaired swim performance was observed in fish fed SeMet at concentrations greater than 3 µg Se/g in the diet. However, within each dietary Se treatment group, no significant differences between single and repeat Ucrits were observed. Oxygen consumption, SMR and COT were significantly greater, and F-AS was significantly lesser, in fish fed SeMet. Whole body triglycerides were proportional to the concentration of SeMet in the diet. While swimming resulted in lesser concentrations of glycogen in the body, exposure to SeMet in the diet had no significant effect on glycogen content. Exposure to SeMet significantly down-regulated mRNA abundance of protein tyrosine phosphatase 1B (PTP 1B) in muscle, and β-hydroxyacyl coenzyme A dehydrogenase (HOAD), sterol regulatory element binding protein 1 (SREBP 1) and methionine adenosyltransferase 1 alpha (MAT 1A) in liver of adult zebrafish. Overall the results of this study suggest chronic exposure of adult zebrafish to SeMet in the diet can cause both cellular and organismal effects that could affect fitness and survivability of fish.