With the exception of mammalian hibernators, entering and emerging from a state of metabolic rate depression is a physiological capacity, alien to warm blooded animals. Many marine ectotherms, including some benthic fish, however, make use of metabolic rate reduction to survive prolonged periods of environmental hypoxia, common in coastal and oceanic habitats. Hypoxic specialist sediment dwellers can survive for several weeks under conditions close to anoxia, and some of these animals even avoid exposure to fully normoxic conditions. We have studied oxidative stress markers in several infauna worms and mud clams, exposed to environmental hypoxia and found them to maintain strong antioxidant capacity.Entering a hypoxic state causes a regulatory response in mammals, involving activation of hypoxia inducible transcription factor HIF-1 α, which is stabilized under severe tissue hypoxia and, after dimerization with HIF-1?, induces up-regulation of genes that preserve functionality in hypoxic tissues. An oxidized tissue redox state and reactive oxygen species are know to prevent HIF-1 α stabilization and interfere with the hypoxic signalling cascade. We were interested in HIF-1 α functionality in hypoxia tolerant marine ectotherms and studied HIF-1 regulation in response to thermal stress and hypoxic exposure in North Sea and polar confamilial fishes (eelpout). We found constitutive HIF-1 α protein levels in fish liver and an increase of DNA binding activity of the HIF-1 dimer under severe cooling in the North Sea eelpout, presumably related to functional hypoxia in liver tissue. Generally, HIF-1 activation was more pronounced at more reduced tissue redox state, however oxidative stress markers were simultaneously increased. Several HIF-1α sequences were since obtained from temperate and polar fish species and will be discussed with respect to the functional peculiarities of the transcription factor in hypoxia tolerant ectotherms.