Oxidative stress during stressful heat exposure and recovery in the North Sea eelpoutZoarces viviparusL.

Abstract

SUMMARY 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°C), critical (22°C) and severe(26°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°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°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°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.

Effects of seasonal and latitudinal cold on oxidative stress parameters and activation of hypoxia inducible factor (HIF-1) in zoarcid fish

“…We have investigated the HIF response to cold shock in North Sea eelpout (Heise et al 2006a) and found HIF-1 DNA binding in liver tissue (the only organ we investigated) significantly enhanced following 2 h cold exposure to 1 and 5°C, compared to control fish kept at 12°C. In contrast, 2 h of heat shock above 20°C failed to have an effect on eelpout HIF (Heise et al 2006b). Based on these previous findings, we hypothesized that HIF-1 signalling could especially be involved in the physiological regulation supporting seasonal and regional cold tolerance in fish.…”

“…Calculation of the percentage intensity was based on densitometry of gel images, with the sum of all four bands taken as 100% value. Control experiments for testing the specificity of the human EPO enhancer by adding an excess of unlabeled probe or by adding antibody (against the N-terminus of rainbow trout HIF-1a, see above) are described in our previous study on Z. viviparus (Heise et al 2006b). No antibody was available which recognised the HIF-1a protein in liver samples from P. brachycephalum.…”

“…Similarly, warming from 12 to 18°C (but not to above 20°C) stimulated enhanced HIF-1-DNA binding in the temperate eelpout (Heise et al 2006b). It therefore appears that HIF-1 could be a common regulator for the adjustment of tissue oxygenation towards the border of the thermal range of a fish but no longer at extreme temperatures.…”

Oxygen- and capacity-limited thermal tolerance: bridging ecology and physiology

“…The range of active thermal tolerance (see Glossary) is limited on both sides by pejus temperatures (T p ; the box lists processes supporting active tolerance, which become constrained beyond T p ). Towards warm and cold extremes, the transition to passive thermal tolerance (see Glossary) is indicated by a decline in (venous) P O2 (solid black arrows), causing oxidative stress (Heise et al, 2006), heat shock response and, finally, transition to anaerobic metabolism (e.g. Kyprianou et al, 2010;Pörtner and Knust, 2007;dashed black arrows).…”

“…due to warming) until reaching different capacity limits (under routine conditions, indicated by breakpoints, BP). Through similar principles and differences in thermal responses (Q 10 ), OCLTT distinguishes stenotherms from eurytherms (here exemplified through narrow versus wide temperature ranges and differences in the temperature dependence of the workloads; see Pörtner, 2006). In each case, the thermal window width of functional scope is represented by the length of the dashed arrows.…”