Hypoxic response and thermotolerance in fish.


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Doris.Abele [ at ] awi.de

Abstract

Hypoxic response and thermotolerance in fishDoris AbeleAlfred-Wegener Institute for Polar and Marine Research, Bremerhaven, GermanyWe are interested in the cellular mechanisms that support wide ranging latitudinal distribution of marine ectotherms and have studied a new facet of thermotolerance in zoarcids fish, from different climatic regions. The common eelpout, Zoarces viviparus, from the North Sea was compared to the Antarctic eelpout, Pachycara brachycephalum, with respect to cellular oxidative stress parameters and the potential to induce metabolic reorganization during functional hypoxic stress. Functional hypoxia sets on as the final consequence of critical warming in marine ectotherms, and we hypothesized that adaptation to temperature extremes within the thermal tolerance window of a species involves hypoxic signalling, to induce re-organisation of blood supply to central tissues.It turned out very clearly that polar eelpout maintain higher antioxidant defence levels (antioxidant enzyme activities and 3-fold higher levels of liver glutathione) to counterbalance higher tissue oxygen solubility and to protect their susceptible membranes from oxidative damage. Both species have normoxic levels of hypoxia inducible transcription factor (HIF-1α). Acclimation (11 weeks) at above habitat temperature (5°C) in the polar eelpout and also low temperature exposure within the thermal tolerance range of North Sea eelpout (6°C) led to increased HIF-1 DNA binding and dimer formation. We conclude that induction of hypoxia inducible factor plays a role within the physiological stress tolerance program in fish.



Item Type
Conference (Invited talk)
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Published
Event Details
Congress Opening Lecture, Argentinean Congress of Ecology, Cordoba, Argentina, August 2006..
Eprint ID
16236
Cite as
Abele, D. (2006): Hypoxic response and thermotolerance in fish. , Congress Opening Lecture, Argentinean Congress of Ecology, Cordoba, Argentina, August 2006. .


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