Mitochondrial Function in Antarctic Nototheniids with ND6 Translocation

Fish of the suborder Notothenioidei have successfully radiated into the Southern Ocean and today comprise the dominant fish sub-order in Antarctic waters in terms of biomass and species abundance. During evolution in the cold and stable Antarctic climate, the Antarctic lineage of notothenioids developed several unique physiological adaptations, which make them extremely vulnerable to the rapid warming of Antarctic waters currently observed. Only recently, a further phenomenon exclusive to notothenioid fish was reported: the translocation of the mitochondrial gene encoding the NADH Dehydrogenase subunit 6 (ND6), an indispensable part of complex I in the mitochondrial electron transport system

Krisenherd Balkan – Krieg zum Frieden? Diskussion mit Hans Koschnick, Peter Lock, Andreas Zumach

Textdokumentation zur Veranstaltung der Osnabrücker Friedensgespräche am 12. Mai 199

Kriegsverbrecherprozesse. Völkerstrafrecht - Anspruch und Wirklichkeit. Diskussion mit Yvonne Featherstone, Hans Koschnick, Wolf-Dieter Narr, Dietrich Rauschning

Textdokumentation zur Veranstaltung der Osnabrücker Friedensgespräche am am 29. Januar 1997 in der Aula der Universitä

Molecular characterisation and expression of Atlantic cod (Gadus morhua) myoglobin from two populations held at two different acclimation temperatures

Much previous research has demonstrated the plasticity of myoglobin concentrations in both cardiac and skeletal myocytes in response to hypoxia and training. No study has yet looked at the effect of thermal acclimation on myoglobin in fish. Atlantic cod (Gadus morhua) from two different populations, i.e. the North Sea and the North East Arctic, were acclimated to 10 and 4 degrees C. Both the myoglobin mRNA and myoglobin protein in cod hearts increased significantly by up to 3.7 and 2.3 fold respectively as a result of acclimation to 4 degrees C. These increments were largest in the Arctic population, which in earlier studies have been shown to possess cold compensated metabolic demands at low temperatures. These metabolic demands associated with higher mitochondrial capacities may have driven the increase in cardiac myoglobin concentrations, in order to support diffusive oxygen supply. At the same time the increase in myoglobin levels may serve further functions during cold acclimation, for example, protection of the cell against reactive oxygen species, and scavenging nitric oxide, thereby contributing to the regulation of mitochondrial volume density

Response of branchial Na+/K+ ATPase to changes in ambient temperature in Atlantic cod (Gadus morhua) and whiting (Merlangius merlangus).

The maintenance of ion and pH homeostasis despite changes in ambient temperature is crucial for ectothermic organisms. Thermal sensitivity of Na+/K+ ATPase mRNA expression, protein expression and activity was determined in gills of North Sea cod (NC) and Northeastern Arctic cod (NEAC), acclimated for 6 weeks at 4 and 10 °C and compared to field samples of North Sea cod (sNC), acclimatized to early spring (4 °C) and summer (18 °C) conditions. The same analyses were conducted in gills of the confamiliar whiting, acclimated at 4 and 10 °C. Branchial Na+/K+ ATPase capacities remained uncompensated at functional and protein levels in NC and NEAC at both acclimation temperatures. Na+/K+ ATPase mRNA expression in NEAC acclimated at 10 °C was about twofold higher compared to NC, indicating some population-specific differentiation at this level. Lower Na+/K+ ATPase capacities in gills of warm-acclimatized sNC at common assay temperatures indicate thermal compensation between seasonal extremes, and post-translational modifications contributed to this mitigation at high assay temperature. Together, cod compensates Na+/K+ ATPase capacities on the warm edge of the thermal window and below 4 °C, respectively. In contrast, whiting Na+/K+ ATPase capacities were cold compensated at 4 °C, supported by 1.5-fold higher mRNA and protein expression. Besides, capacities were lower in whiting compared to NC and NEAC at optimum temperature, which may be advantageous in terms of reduced maintenance cost, but at temperatures ≤4 °C, compensation may represent an energy trade-off to maintain homeostasis. The species-specific response of gadid Na+/K+ ATPase indicates certain threshold temperatures beyond which compensation of the pump is elicited, possibly related to the different biogeography of these species

Adjustments of molecular key components of branchial ion and pH regulation in Atlantic cod (Gadus morhua) in response to ocean acidification and warming.

Marine teleost fish sustain compensation of extracellular pH after exposure to hypercapnia by means of efficient ion and acid-base regulation. Elevated rates of ion and acid-base regulation under hypercapnia may be stimulated further by elevated temperature. Here, we characterized the regulation of transepithelial ion transporters (NKCC1, NBC1, SLC26A6, NHE1 and 2) and ATPases (Na(+)/K(+) ATPase and V-type H(+) ATPase) in gills of Atlantic cod (Gadus morhua) after 4weeks of exposure to ambient and future PCO2 levels (550μatm, 1200μatm, 2200μatm) at optimum (10°C) and summer maximum temperature (18°C), respectively. Gene expression of most branchial ion transporters revealed temperature- and dose-dependent responses to elevated PCO2. Transcriptional regulation resulted in stable protein expression at 10°C, whereas expression of most transport proteins increased at medium PCO2 and 18°C. mRNA and protein expression of distinct ion transport proteins were closely co-regulated, substantiating cellular functional relationships. Na(+)/K(+) ATPase capacities were PCO2 independent, but increased with acclimation temperature, whereas H(+) ATPase capacities were thermally compensated but decreased at medium PCO2 and 10°C. When functional capacities of branchial ATPases were compared with mitochondrial F1Fo ATP-synthase strong correlations of F1Fo ATP-synthase and ATPase capacities generally indicate close coordination of branchial aerobic ATP demand and supply. Our data indicate physiological plasticity in the gills of cod to adjust to a warming, acidifying ocean within limits. In light of the interacting and non-linear, dose-dependent effects of both climate factors the role of these mechanisms in shaping resilience under climate change remains to be explore

Regulation of mitochondrial functioning with temperature in ectothermic animals

Alterations in mitochondrial functions are proposed as key processes in seasonal as well as evolutionary temperature adaptations of ectotherms. Cold exposure frequently induces mitochondrial proliferation to cope with the decelerating effects of low temperatures. In populations of cod (Gadus morhua) along a latitudinal cline differences at the functional level became evident mostly at cold temperature with higher mitochondrial capacities in the sub-Arctic population. In metabolically active tissues like liver, cold acclimation was found to comprise a shift between mitochondrial functions, indicated by increased activity ratios of the mitochondrial key-enzymes citrate synthase (CS) and cytochrome-c oxidase (COX). In all cases transcript levels and functional capacities were not tightly correlated with enzyme activities during thermal adaptation and thereafter, though transcriptional processes are clearly involved and seem to be important to establish the new steady state. However, cold exposure of isolated hepatocytes prepared from the common eelpout (Zoarces viviparus) resulted in increments in CS as well as COX capacities contrasting the situation in whole animal acclimation. This suggests that systemic signals coordinate the pattern of adaptation at the organismic level. As adenosine levels rose transiently during cold acclimation of eelpout in vivo, we tested its role as a regulatory signal during thermal acclimation. In isolated hepatocytes, adenosine had in fact a suppressing effect on COX activity and total RNA contents, but most striking was the activation of COX expression, found for both, mitochondrial and nuclear encoded subunits. Finally, a pattern of expression results which is similar to the one observed in vivo

Assessment of muscular energy metabolism and heat shock response of the green abalone Haliotis fulgens (Gastropoda: Philipi) at extreme temperatures combined with acute hypoxia and hypercapnia.

The interaction between ocean warming, hypoxia and hypercapnia, suggested by climate projections, may push an organism earlier to the limits of its thermal tolerance window. In a previous study on juveniles of green abalone (Haliotis fulgens), combined exposure to hypoxia and hypercapnia during heat stress induced a lowered critical thermal maximum (CTmax), indicated by constrained oxygen consumption, muscular spams and loss of attachment. Thus, the present study investigated the cell physiology in foot muscle of H. fulgens juveniles exposed to acute warming (18 °C to 32 °C at +3 °C day−1) under hypoxia (50% air saturation) and hypercapnia (~1000 μatm PCO2), alone and in combination, to decipher the mechanisms leading to functional loss in this tissue. Under exposure to either hypoxia or hypercapnia, citrate synthase (CS) activity decreased with initial warming, in line with thermal compensation, but returned to control levels at 32 °C. The anaerobic enzymes lactate and tauropine dehydrogenase increased only under hypoxia at 32 °C. Under the combined treatment, CS overcame thermal compensation and remained stable overall, indicating active mitochondrial regulation under these conditions. Limited accumulation of anaerobic metabolites indicates unchanged mode of energy production. In all treatments, upregulation of Hsp70 mRNA was observed already at 30 °C. However, lack of evidence for Hsp70 protein accumulation provides only limited support to thermal denaturation of proteins. We conclude that under combined hypoxia and hypercapnia, metabolic depression allowed the H. fulgens musculature to retain an aerobic mode of metabolism in response to warming but may have contributed to functional loss. Keywords: 1H NMR spectroscopy; Citrate synthase; CTmax; Hsp70; Lactate dehydrogenase; Tauropine; Tauropine dehydrogenas