Oxidative Stress During Stressful Heat Exposure and Recovery in the North Sea Eelpout Zoarces Viviparus L.
From: Alfred-Wegener Institute for Polar and Marine Research, Physiology of Marine Animals, Am Handelshafen 12, 27570 Bremerhaven, Germany.
The Journal of experimental biology
- Publish Date: Jan 2006
- ISSN: 0022-0949
- Volume: 209
- Issue: Pt 2
- Pages: 353-63
- Medium: Print
- Language: English
- Citation (JAMA): Heise Katja, Puntarulo Susana, Nikinmaa Mikko, et al. Oxidative Stress During Stressful Heat Exposure and Recovery in the North Sea Eelpout Zoarces Viviparus L.. J. Exp. Biol. Jan 2006;209:353-63
Abstract
The interplay between antioxidants, heat shock proteins and hypoxic signaling is supposed to be important for passive survival of critical temperature stress, e.g. during unfavorable conditions in hot summers. We investigated the effect of mild (18 degrees C), critical (22 degrees C) and severe (26 degrees C) experimental heat stress, assumed to induce different degrees of functional hypoxia, as well as the effect of recovery following heat stress on these parameters in liver samples of the common eelpout Zoarces viviparus. Upon heat exposure to critical and higher temperatures we found an increase in oxidative damage markers such as TBARS (thiobarbituric reactive substances) and a more oxidized cellular redox potential, combined with reduced activities of the antioxidant enzyme superoxide dismutase at 26 degrees C. Together, these point to higher oxidative stress levels during hyperthermia. In a recovery-time series, heat-induced hypoxia and subsequent reoxygenation upon return of the fishes to 12 degrees C led to increased protein oxidation and chemiluminescence rates within the first 12 h of recovery, therein resembling ischemia/reperfusion injury in mammals. HSP70 levels were found to be only slightly elevated after recovery from sub-lethal heat stress, indicating minor importance of the heat shock response in this species. The DNA binding activity of the hypoxia-inducible transcription factor (HIF-1) was elevated only during mild heat exposure (18 degrees C), but appeared impaired at more severe heat stress. We suppose that the more oxidized redox state during extreme heat may interfere with the hypoxic signaling response.
Mesh Headings (Keywords): Animals, Blotting, Western, Electrophoretic Mobility Shift Assay, HSP70 Heat-Shock Proteins, Heat, Hypoxia-Inducible Factor 1, North Sea, Oxidative Stress, Perciformes, Superoxide Dismutase, Thiobarbituric Acid Reactive Substances
Check for Full Text / PubMed Unique Identifier (PMID): 16391357
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.